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Are there any substance that are more dangerous at low dose than at higher dose?
It is commonly admitted that

The dose makes the poison

which means as a person, the more I take a substance, the more risk I take for my health.
There is even an indicator called LD50 (see Median Lethal Dose), which specifies the 'lethal dose' at which 50 percent of subjects will die.
This might seems a stupid question but: are there any substances for which it is more dangerous to take at low dose than at higher dose? For example, you have to ingest at least 1µg of XXX because if you ingest less you will have health problem...

Oxygen comes to mind. A low dose is much more harmful than a large one :).

sugar, water, protein, ... these all have an optimal range of healthy doses- too much OR too little can be harmful.

Dihydrogen Monoxide is a brutal killer.

All of these substances in lower than required concentrations are not of themselves toxic, but rather prevent a subsequent reaction from occurring and is (indirectly) lethal. As such, not real answers. ;)

@Konrad offers the most accurate and direct answer to OPs question. Michael Kuhn gives an important epidemiological example of indirect toxic effects. This indirect argument can also be extended to every substance within or used by our body, and therefore not very constructive.

several ingested poisons can be more harmful in low doses because in large doses they naturally trigger a vomiting response.

Yes. Taking antibiotics (and by extension antivirals and antineoplastics) at low doses is dangerous, as this creates an evolutionary pressure to evolve antibiotic resistance (or rather, incorporate through horizontal gene transfer). This is dangerous because an infection resulting from these bacteria will then be harder to treat.
In the paper "Experimental evolution of resistance to an antimicrobial peptide", Perron et al. gave E. coli the chance to evolve resistance against a novel antibiotic. When given a high dose initially, most bacteria died. When exposed to low doses, the bacteria evolved resistance in 600 to 700 generations.
For the same reason it is strongly advised to finish a course of antibiotics even after symptoms fade.

+1 although I don’t think this is what OP was referring to because the effect is indirect rather than there being a toxic effect of the antibiotic of the host which decreases with increased dose.

I agree, but my answer is true to his original question

This is a bit of a news flash - the answer is probably yes.
Reading through recent Nature articles this one popped up: Toxicology the learning curve.
Where there are some intriguing examples of low concentration only toxic effects.
It might be worth a read. The preface gives a review of the idea, going back to the 16th century physician Paracelcius that the toxic properties of anything increases monotonically with dosage.  This is reflected in most of the answers and its one of the few things which toxicologists universally expect to see.
A research group at U Missouri-Columbia is claiming that endocrine disruptors have non-monotonic toxicology curves, meaning that toxic effects actually decrease with greater dosage.

Nature is kind enough to allow access to this image.  The three curves on the right show a decline in drug effect as concentration increases.
Endocrine hormones act at very low dosage - testosterone, estrogen, pituitary and thyroid hormones are some examples.  We'll probably be hearing more about this in the future, rather than less.
While this is still controversial, its made news because it is the sole class of compounds which really behave this way.  notably the first curve is for BPA (Bisphenol A) - the plastcizer which is common in pool toys and toy inflatable balls and drink bottles but the FDA has flagged for closer study.

No. The influence of dose–response relationship on toxicity is one of the fundamental properties of (bio)chemistry, and follows directly from the fact that concentration influences the reaction rate: a chemical reaction between two or more agents is a stochastic process where agents have a certain chance of interacting based on physical proximity (and other factors). The higher the dose, the higher the chance of two agents meeting, and a reaction taking place.
This has two interesting consequences:

Homeopathy doesn’t work.
Although not all substances show a clear dose–response curve (simply because they are always reactive no matter their dose), toxicological studies which fail to show a dose–response relationship are met with scepticism. A recent example of this is the GMO toxicity study undertaken by the French scientist Séralini. One of the many flaws in this paper cited by other scientists was precisely this lack of dose–response relationship.

Example of something always reactive no matter the dose?

@David No, sorry. “no matter the dose” is also stretching it a bit – you always need some minimal amount, it’s just that the steepness of the curve varies.

thanks for the clarification; as written it can be interpreted as "homeopathy" doesn't work, except when it does. On another note (more as a clarification for readers than as a correction to you) the GMO study is a poor example to use. Because of the many flaws, any inference is limited (e.g. my primary conclusion is that there is insufficient information to conclude anything about the relationship dose-response relationship).

No. The influence of dose–response relationship on toxicity is one of the fundamental properties of (bio)chemistry...?!?

@Lo Unclear? It means that things get more toxic with increased dose, never the other way round.

@Konrad Rudolph: there are plenty of example of substances having different effects at different doses (steroid hormones, for instance), and dose-response relationships are not always going up. A diet low in vitamines is as bad as a diet high in vitamines

"concentration influences the reaction rate": Usually, but there are zeroth order reactions. Of course not forever, it stops if the reactant is gone, but reactions exist that have a fixed rate for a large range of concentrations.

I think the best answer is right now would be
Probably no, but we're not certain
The question of non-monotonic dose-response is still being discussed and debated. You will find a good example of this at EFSA

First of all, that is an excellent question! Secondly, please excuse the lack of thorough sourcing for this post. I only like to share some pointers...
Q: Can substances do more harm in a mammal at a lower dose than at higher dose?
A: Yes.
Some may know the example of the blood thinner, and widespread NSAID Acetyl-salicylic acid (Aspirin). I will use this example because Aspirin is one of the most known and used drugs in the world, with a long and interesting history. As being part of the class of nonsteroidal anti-inflammatory drugs (NSAIDs) it has recently gotten a bad wrap for blocking an enzyme which is crucial for prostaglandin synthesis and processes that maintain  a healthy stomach wall in the presence of an potentially harmful bacterial and chemical milieu. On a sidenote, as an acid, Aspirin actually hardly dissolves directly in the acidic stomach.
To quote wikipedia (DOR: 28/09/2012):

Salicylates are excreted mainly by the kidneys as salicyluric acid
  (75%), free salicylic acid (10%), salicylic phenol (10%), and acyl
  glucuronides (5%), gentisic acid (< 1%), and 2,3-dihydroxybenzoic
  acid.[148] When small doses (less than 250 mg in an adult) are
  ingested, all pathways proceed by first-order kinetics, with an
  elimination half-life of about 2.0 to 4.5 hours.[149][150] When higher
  doses of salicylate are ingested (more than 4 g), the half-life
  becomes much longer (15–30 hours),[151] because the biotransformation
  pathways concerned with the formation of salicyluric acid and salicyl
  phenolic glucuronide become saturated

Aspirin can interfere with a lot of drugs, including Ibuprofen. The known list of drugs is so high, in part due to the widespread application of aspirin, and in part due to the chemical composition of this very small drug with two functional groups. A functional group is a sort of chemical feature that determines how and with what probability a chemical interacts in a given milieu.
As a certain metabolic degradation pathway may get saturated, other pathways can take over and lead to different potentially harmful metabolites resulting in damage to the excretion/clearance organs such as the liver (hepatotoxic) and kidney (nephrotoxic).
A metabolite is the product of metabolism ( a weak back-referencing definition). metabolic pathways are a sequence of chemical reactions within a cell, and metabolism is the entire set of metabolites and pathways.
Liver/Kidney Toxicity is believed to result from an interplay of a) high concentrations of metabolites or direct toxins (=parent chemicals) within specialized high-concentration-forming cells, and b)  the non/covalent  binding of cellular macromolecules to interfere with their normal function and/or production of reactive oxygen species (ROS).
Another example (from memory) is the interaction pharmacokinetics of theobromine (from cacao) and other xanthines (unverified).
There are many more examples. I hope this example and mechanism serves you well as a starting point...

From a biochemical standpoint:

In fact drugs may act differently at different concentration thresholds at different times at different places within an organism and its cells that make it up. Evolution exploited this very early on and used it for things like body segmentation along defined axis during development.
Drugs may interact with each other differently at different levels of concentrations, say as binary, ternary, and higher order complexes. The rate of formation of such complexes is denoted through the dissociation constant - which is a type of equilibrium constant such as pH is.
The dissociation constant describes the propensity of a chemical species to separate reversibly and, - this is crucial! - is concentration dependent. This is accounted for by the use of so called activities or the apparent concentrations, as a result of incomplete hydration of the chemical and other effects of a "crowded environment". Now don't just think of chemicals, but macromolecules as well. In immunology for instance new molecular features can arise on the surface of a macromolecule, due to the association (complexation) with a small molecular drug. This in turn can lead to an immunological reaction, even anaphylaxis ( a so called Type I hypersensitivity reaction) and ultimately shock. Such drugs are classified as haptens.

Important in an organisms sensitivity and susceptibility to drugs however, is the current allometric growth rate and types of organs and cells available. As such a fetus is more susceptible than an adult.
I hope a simple yes accompanied by this admittedly to-long to really read post gave you some insight into what scientist across many, many fields are dealing with. Naturally, the issue is more complex.
Personally I believe the issue of dosing and drug reactions will improve significantly over the coming decade...

Maybe I'm misreading your post, but I don't see any example of a substance that is more harmful at lower doses in your post.

I may be missing something here, but I can find no mention of how lower doses of aspirin are more harmful than higher ones in your answer. I assume that one of the metabolites it gets broken into activates a different pathway and can lead to toxicity. Is that what you mean?

Correct, I didn't include a specific example only an example mechanism. Substances acting differently at different levels is well known within the concerned fields of science. Substances/Drugs which are toxic at low levels cannot be approved nor are they generally appealing for studies. Substance's "dualism" can offset the LD50. The post also doesn't discuss how substances can be toxic at low dose or discerns entantiomeric purity (e.g. thalidomide) and/or entantiomer-specific pathways. Specific examples may best be extrapolated from systems-biological and/or chemotherapeutics literature...

The question is not about substances acting different at lower concentrations but specifically about being more harmful/dangerous at lower concentrations. Your examples don't fit that, strictly speaking you're not answering the question that has been asked.


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Are all healthy animals more likely to defecate near the end of a rest-cycle?
Just what the title states.
It stems from observation & personal experience that a person/dog/cat/monkey is more likely to relieve oneself immediately after it wakes up from the peak-sleep cycle of it's body-clock. Is this observation true? What causes this behaviour ?

I think we can actually go farther than mere behavioral argumentation. The separation of the autonomous nervous system into parasympathetic and sympathetic is, one the one hand, associated with the sleep/wake cycle, on the other with parasympathetic/sympathetic activity (low/high epinephrine secretion). This duality certainly applies to all vertebrata (i.e. big animals), as fight & flight is associated with all vertebrata, see e.g.
http://en.wikipedia.org/wiki/Fight_or_flight_response
In other words: from the existence of fight or flight in all vertebrata I infer the existence of a dual autonomous nervous system (parasympathetic and sympathetic) in all vertebrata, although there may be other proof. Since in sleep the parasym. NS is active, the bowel moves. Conclusion: the bowel moves in the sleep of all vertebrata.

I'm sorry, I don't understand your answer. Could you elaborate please?

I have added a reformulation. Better now?

I'm prefixing this one by saying that I don't actually agree with you (also, I think the old nut that the plural of "anecdote" is not "data").
That having been said: wouldn't the simplest explanation just be "because it was likely a long time since the animal's last 'relief'" since it's been sleeping for XXX hours? Or would you argue that this observation is also true after, say, a 20 minute nap?
Also, what does this have to do with a nervous system?

Accepted this may be anecdotal; I'll update the question on this & remove the note on the nervous system too. But I would argue the second paragraph with the clarification that an animal/being is more likely to defecate after the typical 'night/rest' cycle which is the 'deepest' such sleep cycle.

Digestion is an energy consuming process. It is, therefore, often followed by a period of rest. Animals will, consequently, often digest during sleep. It follows that they will eliminate the waste products of digestion upon awakening.
Given the above, I doubt there is a causal link between sleep or rest and the need to commune with nature, water a tree, appease the porcelain god, or whatever your preferred euphemism happens to be, soon after awakening.

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Arabidopsis thaliana RCSB active site gene mutant
I'm looking for an Arabidopsis thaliana gene listed in RCSB with a clear mode of function and active site. In addition it needs to have an obvious phenotype when knocked out like severely retarded growth, lethal or near lethal. The gene also has to be exclusive to plants so RNA polymerase wouldn't work.
I found this paper in plant physiology but I'm having trouble finding those genes with an obvious active site.
Thank you very much

I can tell you generally how to go about it.
Go to table S2 from the paper and download the spreadsheet.  You can search RCSB for each gene symbol. There are 2400 individual genes and there are probably over 1000 alias genes, so that's a lot of searching.  You can do this en masse by using a python script and a library like BioPython, or you can put each symbol into the search box at RCSB.org and see if a structure comes up.
You can and should look over that table for phenotypes you think you can actually work with.  Many of the phenotypes in the paper might require a microscope or a good deal of experience with arabidopsis.  E.g. "Embryo defective; Preglobular / Globular" what does that mean?  You can also write the authors for advice but they might be too busy to get back to you.
Cutting down your search like this before you do it would be very helpful.  The number of genes with both an accessible phenotype and a structure will probably be a relatively small list (50?).
Relatively few arabidopsis protein structures are solved, so you will have to do homology modeling - aligning any protein structure sequence(s) you find with the A. thaliana sequence, and deciding where the active site or disruptive mutation would be in the plant gene.
Example: CHY1(CoA Ester Hydrolase) must be solved - searching for "CoA Ester Hydrolase" at rcsb I find a three structures.  the human structure 2DQZ has a lot of annotation associated with it.  This class of enzymes has been studied for a while, so the active site probably has been studied.  A pubmed search should give a lead on where the active site research has been done.  using BLAST to align the structures to the arabidopsis gene or to all other CoA Ester Hydrolases would be an important step to take too.
Hope this helps.

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How are different types of cells created from zygote?
In the process of mitosis that starts from zygote, how do different cells appear? What happens that some cells become one type and some another?
For example, is there a cell that divides into a blood cell and a skin cell?

The word you want to search for is "differentiation". http://en.wikipedia.org/wiki/Cellular_differentiation

differentiation starts

@Memmin Thanks for giving me the right term, thus the right direction. Sometimes not knowing the terminology is the whole problem.

I'm not sure about the first developmental stages but, given you already have hundreds of cells with slightly different physiology, the next developmental stages like dev. of neural tube happen through excretion of translation factors and growth factors in several cells. Each of those cells that are in a region where more than one excretion overlaps get a higher dose than the others. This is the signal for the cell to differentiate into another type, by changing its physiology. Such factor excretions are important events, and the genes encoding for the factors are evolutionally highly conserved (so called homeobox proteins).
However, this has nothing to do with mitosis. The newly divided cell does not decide on its own but reacts to a stimulus, like skin cells develop into skin cells because they are on the outside of the cell ball. Excreted factors do the fine tuning.

I was looking for differentiation in the early development stages. But nonetheless, thanks for the info.

The process of formation of different types of cells that differ in morphology and function is termed as cell differentiation. In multi-celled organism, each task of life is carried out by different types of  specialized cells say nerve cell for transmitting impulses, muscle cells for coordinating movement and these cells differ in their appearance and function, but originated from the same parental cell, the zygote. These specialized cells are formed by a process called differentiation.
Cell differentiation is the process by which genetically identical cells of an embryo become specialized.

From a fertilized egg, at least 250 distinct types of differentiated cells are present in adults.
Zygote->determination ->differentiation

Cell specialization involves the preferential synthesis of some specific proteins like antibodies in plasma cells or Hb in erythrocytes.
The genome is the same in all cells of our body, but only certain genes are turned on and other genes are switched off and this lead to specialization. That is, genes active in the neurons may not be active in muscle cells. For instance, genes for actin and myosin filaments are present in all animal cells, but these genes are active only in muscle cells.
http://www.biologyexams4u.com/2012/08/cell-differentiation.html


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Do Yeast Insertion constructs revert?
If I insert a new gene with a yeast integrating plasmid and select with a drop out culture once, can I assume that the newly integrated gene will stay in the strain without putting selective pressure on it?  (i.e. can i use normal liquid culture and plates after getting the yeast with the newly integrated strain?

Can you give a little more detail about what exactly you did - what is the structure of the YIp, and did you cut it before transformation?

Thanks @AlanBoyd - I will need to get a YIp - if there are some that are more persistant than others I would like to know about it. your answer is helpful here. I'm considering how to adapt a LEU2 based plasmid that currently have. Just getting into yeast though and I'm really naive.

Disclaimer: I only work with bacteria. This seems analogous to antibiotic selection in E. coli, and as such, selection pressure is needed to maintain the engineered yeast population to be assured that you aren't incubating environmental strains.

It depends upon exactly what you have done.
The standard way of using a yeast intergrating plasmid (YIp) is for it to integrate into the genome by recombination between a piece of yeast DNA that the YIp carries and the same DNA in the genome. This is often, but not necessarily, the selectable marker. So for example a YIp carrying the URA3 gene as its only yeast DNA will integrate at the URA3 locus (probably mutant to allow selection for Ura+, so more correctly ura3).
If the YIp is linearised by cutting at a site within the URA3 marker this will direct insertion and will increase the transformation efficiency.
Once insertion has taken place, the configuration at the integration site is:
chromosome...URA3...other YIp sequences...ura3...chromosome
This is inherently unstable because a looping-out event can take place via recombination between the URA3/ura3 regions. So removing selection means that you run the risk of losing the insert. Furthermore, it is possible for looping out to occur leaving the URA3 allele behind instead of the ura3 allele. So you can lose the vector even when selection is maintained (but this will depend on the exact nature of the mutation).
More complex configurations are possible where the targetting sequence is separate from the selectable marker, and where digestion removes a whole chunk of the targetting sequence before transformation. So for example if the TRP1 gene was used for targetting a plasmid with the URA3 marker in a TRP1 ura3 strain you would get:
chromosome...TRP1 fragment A...URA3+other YIp sequences...TRP1 fragment B...chromosome
the resulting transformant is now Ura+ because of the integrated URA3 plasmid, but some TRP1 DNA is now missing (the DNA that was excised when the plasmid was digested) so the strain is trp1. The appearance of this Trp- phenotype indicates that the transformation has probably occurred by the pathway described.
In this case the inserted plasmid is much more stable because those two remaining fragments of TRP1 DNA are not identical, so there is no possibility of looping out.
In summary, if your transformant has the insert carrying the "new gene" flanked by a repeating sequence then it is unstable, otherwise it is ok to remove selection. In the first case, if the new gene is at all deleterious then there will be a strong selective pressure in favour of cells which have lost the insert.
Addendum
You can avoid using YIp plasmids altogether by integrating your new gene at any locus using long targetting primers, as shown in the Figure below.
Design primers to amplify your gene as usual, but synthesise them with 40 bp 5' extensions corresponding to two sequences at the extreme ends of the integration site (URA3 used here for illustration purposes). The resulting fragment can then be used in a transformation and will integrate at the URA3 site by homologous recombination, replacing the resident DNA. The advantage of using URA3 for this is that you can select for integrants as Ura- cells by resistance to fluoorotic acid (FOA). Although you can probably select directly for this, I have always co-transformed the fragment together with another selectable plasmid (LEU2, TRP1 etc., but not a CEN plasmid) Then your e.g. Leu+ transformants can be screened for those that have also become FOAR. This co-transformation happens at quite high frequency because the cells that do take up DNA take up a lot of it. Once you remove selection for the co-transforming plasmid it will soon get lost, leaving you with a clean non-reverting integrant.
It's been a while since I did this sort of thing - probably there are even smarter methods around now.

Thanks Alan - I think this is helpful - Sounds like I can keep the selected strain in cold storage and only replate it once in a while if I avoid the repeats in my construct.  If I use a Leu2 knockout sequence I have maybe I can avoid this problem I hope.

Yeast integrating plasmids are known to be stable, even in absence of a selective medium but can revert like most homologous recombination plasmids.
Quoting from the book Yeast Gene Analysis (pg476):

YIps are generally more stable than YRp or YEp plasmids. As a result
  it is safe to grow most YIp-bearing strains in rich media, although it
  is good practice to store them under selective conditions. The
  stability of YIp-bearing strains depends on the nature of the
  integration event. For example, if the YIp generates a tandem repeat
  upon integration into the genome, this can  revert to wild-type by an
  intramolecular homologous recombination event.

-> hence use markers regularly and frequently.
Sources:
Mick F. Tuite, Yeast Gene Analysis Vol 26 (Academic Press, 1998 ) p.476

Thanks @LoSauer This was helpful so I'm upvoting though Alan's response is a little more detailed for the 'official' answer.


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Why do grapes not pea shrink when placed in strong sugar solution?
I tried an experiment. First, I placed grapes in pure water(hypotonic solution). The grapes burst because of endosmosis. Then, I placed new set of grapes in strong sugar solution(fully saturated) but they did not shrink. And then when I placed it in strong salt solution(fully saturated), they did shrink a little. Why does this occur?
How is this possible?

What is a strong sugar solution? Grapes contain ~15-20% of sugar.

According to Wikipedia fully saturated sucrose solution should be 2000g/L, way above the 15-20% sugar content of grapes. Interestingly the versions of this experiment that I can find online all use salt for a hypertonic solution. Of course this could be just because it is cheaper than sugar.

Why are we so sure that osmosis can happen in both directions in grapes?

@rwst - The grapes are probably dead, so any trans-membrane pumps would most likely be inactive. That leaves pores and other entry points for water to equilibrate. There's also evidence in the experiments above; because of the membrane potential maintained by ion concentrations (fewer in the cytosol) the saturated salt solution would cause water to leave the grapes and also cause the smaller ions to enter the grapes to dissipate the membrane potential. Sugar isn't small, though, and requires active transport (to the best of my memory).

Well, without the details of your experiment to cross-check with the sugar and H2O content of your average grape, I'd say the saturated solution probably approximated the natural molarity of sugar in the grape. At least to the point it didn't make any advese effects noticeably on your time scale.
That seems the most apparent solution to me. I suppose it's also possible (though I don't know the mechanics behind it) that hypertonic solution might have acted as a preservative - similar to jam. It's not just water which will attempt to reach an equilibrium, but all compounds that can pass through the membrane - perhaps sucrose/fructose/glucose can do so, maintaining the structural integrity of the grape.
Both are guesses until you reveal more information, though.

please see the question now .... I have added some more information and then help me!

It is important to note that osmotic pressure is a colligative property, which means that it does not depend on the identity of the solutes, but simply their concentration. This also means that in considering the grape, we have to estimate the concentration of all solutes, not just the one you used to make the (possibly) hypertonic solution.
I'll assume the sugar used was sucrose, which is the common table sugar. I guess I should also mention that I'll assume the salt was NaCl, which is the common table salt.
Wikipedia says that the solubility of sucrose is 2000 g/L. As the molar mass is 342.3 g/mol, the concentration is approximately 5.8 M.
NaCl on the other hand, has a solubility of 359 g/L. At 58.44 g/mol, the concentration is approximately 6.1 M. However, the Na+ and the Cl- dissociate in water, so the concentration is effectively double when counting solutes. That gives 12.2 M, which is much higher than a sugar solution. This accounts for why grapes would shrivel in a salt solution more than in a sugar solution.
As to why the grapes did not shrink in a sugar solution - I don't think it is unreasonable for a grape to have total solute concentration in the range of 5.8 M. Estimates of the sugar concentration in a grape are given in % w/w. Clearly grapes are denser than water (you can test this by putting a grape in water and seeing it sink). Therefore if you were to calculate in % w/v, you would find it to be more concentrated than a the same % w/w solution in water. Moreover, according to this site grapes have a significant amount of glucose and fructose. These are monosaccharides, as opposed to sucrose which is a disaccharide. This means for the same mass of "sugars" there are more individual sugar molecules, resulting in more osmotic pressure.
In sum, I think the sugar solution is probably isotonic, not hypertonic.

i tried this experiment but failed.
The reason for our failure in this experiment might be as follows:
 1. The grape coating might be immpermeable.
 2. It may happen that the solution might not be hypertonic but isotonic(equal concen. of solutes in both)
 3. The salt solution might be less dilute than the sugar one.
i am just a student but giving my point of veiw....

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How stable is in vivo whole cell patch clamping?
For a head fixed animal, how stable is the current state-of-the-art whole cell recording from a cortical neuron? The animal's breathing, and heart beat must move the neuron relative to the recording device quite a bit, and I was wondering how stable the seal would be. How long can one hold a cell, and what is the typical quality of such recording?

After talking to a few electrophysiologists, I found out that they have very diverse opinions.
It seems that a common way of stabilizing the movement of the brain with respect to heart beat is to press the brain with some softish-rigid material like agar. Also, draining the CSF could help but then this cannot be done without sacrificing the animal.
The quality of the patch degrades over time, and it could be held for an hour or more (anecdotal).


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Does sleep in humans re-structure based on the expected sleep time?
I've read about anecdotal evidence that human brain has a fairly good internal clock that can be used to judge the amount of time that has passed. I'm wandering if there are any mechanisms in the human brain by which the brain can make adjustments to biological processes, based on the expectation of getting so many hours of sleep in the upcoming night. In this case, an alarm clock is not used.
For example, a person typically sleeps for 8 hours a night. On one day, that person realizes that he/she will sleep for only 5 hours that night, has there been any studies that demonstrate that the person's sleep would be "different" from the regular sleep? Will the person's sleep on that night be just a "cut short" version of regular sleep, or will the sleep be restructured to accomodate sleep time restriction?
For example a person's normal sleep cycle is 90 minutes long, so in 8 hours there would be about 5 complete cycles. Would there be any observable adjustments to the sleep cycle length or the amount of deep/REM sleep within the cycle, if a person expects to sleep only 5-6 hours or 10+ hours?
Thank you for your input!

From my personal experience, I can tell you one thing for sure: If, before going to sleep, I know that I have to wake up early or sleep less, and I think about this positively and say something like "ok, buddy, this time you've got just 4 hours to sleep. we need to get as much rest as possible. prioritize sleep over all other for these 4 hours. and don't get surprised being awoken after 4 hours of sleep. so make your cycles well fit this period to get as much rest as possible." - and play with these thoughts and anticipations, you know, it works. Maybe its more about auto-training, but still..

I haven't heard of studies like the one you're proposing, but you can test this hypothesis on yourself with this app.
Knowing you need to sleep less than your usual amount will probably affect the quantity and quality of your sleep, but not because of an "internal clock". Most likely, whatever you need to wake up early for will cause you some anxiety, which will affect both sleep duration and quality.

you are suggesting my own app... :)

:D It's a nice one.


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How are there multiple varieties of the potato?
The potato appears to propagate by growing an 'eye'/'bud' which eventually grows into a new plant. So there would probably be single representative of the potato species in the world with all others being genetically identical.
Yet wikipedia indicates there are several closely related species of the potato; apparently as a result of selective breeding. To my understanding (which is probably wrong) there is only a single potato that grows the eyes without the need for a second parent - so there should probably only be the same genes repeated in each potato/plant.
What am I missing here? Why are there multiple varieties of the potato?

Spontaneous mutations?

This question is more interesting that first meet the eye (ho-ho).

You're missing that potatoes also reproduce sexually.
They're flowering plants, and they produce seeds that are not genetically identical to their parent plants.

I've never seen them flower ... and i missed it on the wikipedia page too.

Wikipedia describes the flowers, fruits, and seeds, and goes on to say "All new potato varieties are grown from seeds, also called "true seed" or "botanical seed" to distinguish it from seed tubers."

Well, uvesten is correct in saying that potatoes are flowering plants and as such they can reproduce sexually. However, as everyone mentions potatoes can, like many plants, reproduce asexually by putting out clones.
Since clones are (by definition) genetically identical to the parent plant, this would seem to rule out the possibility of producing different varieties (or even species) from clonal propagation.
But! this very interesting study by Jiang et al. looked at Arabidopsis lineages (Brassica family). They found:

"in vitro regeneration of Arabidopsis plants results in a high frequency of heritable phenotypic variation "

That is, regenerant Arabidopsis plant lineages displayed extensive phenotypic somaclonal variation - the cloned "offspring" were not genetically identical. They attributed most of this genetic variation to an increased base substitution frequency in the regenerant offspring but there may also be unknown epigentic factors as well.
Jiang et al. summarise:
...

... somatic mutation rates are characteristically higher than germline rates in multicellular organisms [26] and has important particular potential consequences for the evolution of plants, given that they frequently adopt life cycle strategies that involve regeneration from somatic tissues.

So, perhaps some of the variation we see in plant species which commonly propagate asexually actually arose during this process and not via sexual reproduction ... ? This would be good news for houseplants which are nearly always propagated asexually.
However, I am not sure whether this extends to potatoes.
Jiang et al. 2011, Current Biology, 21, 1385, Regenerant Arabidopsis Lineages Display a Distinct Genome-Wide Spectrum of Mutations Conferring Variant Phenotypes

Thank you, Poshpaws (+:
This is what I seem to experience as the potato plants hereabouts spring from the bud on the tuber


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If the brain has no pain receptors, how come you can get a headache?
I've read many years ago in books, that the brain has no nerves on it, and if someone was touching your brain, you couldn't feel a thing.
Just two days before now, I had a very bad migraine, due to a cold. It's become better now, but when I had it I felt my head was going to literally split in half, as the pain was literally coming from my brain.
So it lead me to the question: How come people can get headaches if the brain has no nerves?

The brain does not. However, the skull, muscles, and skin surrounding it to. :) Pressure differentials (your sinus cavities expand  beyond your nose!) and sore muscles (especially neck muscles) can cause or contribute to headaches.

The brain "has" nerves, depending on how you define it: http://en.wikipedia.org/wiki/Cranial_nerve more accurately as January notes it lacks nociceptors.

Brain, indeed, cannot feel pain, as it lacks pain receptors (nociceptors). However, what you feel when you have a headache is not your brain hurting -- there are plenty of other areas in your head and neck that do have nociceptors which can perceive pain, and they literally cause the headaches.
In especially, many types of headaches are generally thought to have a neurovascular background, and the responsible pain receptors are associated with blood vessels. However, the pathophysiology of migraines and headaches is still poorly understood.

So if I tear my head apart leaving brain miraculously intact I'll never get headache again? What part of my skull gets pain from stress? And which one is hurt by not sleeping? I think most headaches are not explained by skull being hurt.

"...with blood vessels" - would like to how vessels being contracted or dilated relates to pain.

You are correct in that the neurons themselves do not sense pain. However, the brain contains layers of coverings, blood vessels, the scalp and some muscles. All of these other structures have pain receptors. The coverings of the brain are called meninges and consist of the dura, arachnoid and pia. The dura in particular has a lot of pain receptors and may be responsible for many headaches. As a neurosurgeon I have seen this first hand during awake brain surgery when we open the dura. The patient usually doesn't report any pain when you drill a hole in their skull. However, they start to report dull pain or headache when you stimulate or touch the dura.

@ area51 - "The patient usually doesn't report any pain when you drill a hole in their skull" ?

They're probably under a local anesthetic, but it would be less shocking if that was noted explicitly.

The local anesthetic only numbs the scalp not the bone. Generally patients don't experience bone bain when drilling the bone. The next layer encountered is the dura. We generally don't number the dura and patients may report a dull pain or headache when manipulating or cutting the dura.

That the brain doesn't have pain receptors has somewhat drifted into the corpus of general knowledge, perpetuated by pamphlets, books and documentaries.
Your question caused me to look up wikipedia. Citing:

A headache or cephalalgia is pain anywhere in the region of the head
  or neck. It can be a symptom of a number of different conditions of
  the head and neck. The brain tissue itself is not sensitive to pain
  because it lacks pain receptors. Rather, the pain is caused by
  disturbance of the pain-sensitive structures around the brain. Nine
  areas of the head and neck have these pain-sensitive structures, which
  are the cranium (the periosteum of the skull), muscles, nerves,
  arteries and veins, subcutaneous tissues, eyes, ears, sinuses and
  mucous membranes.


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Adipocyte Density
People who are overweight and wish to lose weight, often do so because they are concerned about looking too big.  Their increased size is attributed to an increased volume of fat.
When people try to lose weight however, they often quantify their goals in terms of weight, not volume.
So my question is, is the volume of an adipocyte cell always directly proportional to the weight of the fat stored within the cell?
If not, what factors would increase/decrease the size of the adipocyte cell for a given mass of stored fat?

Chris asked, "what factors would increase/decrease the size of the adipocyte cell for a given mass of stored fat?"
For an obese person, subcutaneous and visceral fat is composed of 40% immune cells, while that number is ~10% in lean individuals. There is much interplay between adipocytes and immune cells via adipokines and cytokines. Examples include ADIPOQ (adiponectin) and IL1 (interleukin 1). Thus, agents that reduce the inflammation state of the adipose tissue are also likely to have an effect on adipocyte size. This nonetheless is secondary to diet and diet composition as an adipocyte is nearly all lipid droplet and that lipid droplet stores fat - either from the diet directly or converted into fatty acid from simple carbohydrates in the diet.

Is the volume of an adipocyte proportional to the mass of fat that it stores?
The answer is: yes.
Since fat is stored in a lipid droplet within the adipocyte, it is already in the densest form possible. In other words there is no way to make the stored fat more compact, so that a given mass of stored fat takes up less volume.
Response to comment from Chris:
I think you are perhaps being a little pedantic here. Anyway the graph below conveys my view, together with your refinement. So yes, adipocyte volume changes in proportion to mass of fat stored. (The line on my graph should be at 45 degrees, but I drew it by hand so it may be a little out.) There is no way to escape the increase in volume when fat is stored.

Adipocyte volume isn't directly proportional to adipocyte fat content.  Because this would mean 0 fat = 0 volume.  But even with no fat, adipose cells still exist and occupy volume.  Are you however suggesting the change in adipocyte volume is proportional to the change in fat stored within?

Adipocytes (fat cells) change in size quite a bit with nutrient and particularly fat uptake.
Take a look at this paper which is about identifying adipocyte sizes from histological slides.
  In the cross section they are sometimes 10+ times larger.  When you add depth to the equation there is quite a bit of range in the fat cell must be substantial.
On the other hand, white fat cells do multiply and it is thought that when fat cells are engorged, they secrete growth factors that encourage adipocyte division.
So its not just the adipocytes getting larger, but there are also more fat cells over time if there is extra fat storage needed.
Its particularly of note that Insulin like growth factor 1 (IGF-1) is one of the factors identified that signals adipocytes to divide, coupling fat tissue multiplication with metabolic factors just as you might expect, possibly participating in the development of insulin resistance as the tissue expands.

Very interesting!


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What determines the fate of a cell with respect to differentiation?
I have been reading about Townes and Holtfreter's work in 1955, in which cells are dissociated from a blastocyst in an alkaline solution then mixed together and spontaneously reaggregates based on type, so epidermal cells around the outside and neural plate cells in the middle.
I understand enough about cell adhesion to understand why the cells will seem to attract cells of their own type, but would like to know how they can initially detect what to become and where they are needed in a specialised form, without something acting like a brain telling them what to become and where to go.
If the selection from the available types is random, as I suspect, what happens to blastocysts with too much epidermal tissue or vice versa? I'm struggling to imagine how organisms like this can develop without something taking the lead and actively coordinating what goes where.

Cell differentiation, cell fate and cell mapping is an interplay of accessible evolutionary strategies/programmes and responses to dynamic environmental cues such as specialized hormones (e.g. morphogens) and physical parameters and constraints. That is putting it very broadly. It is a complex issue, if L. Wolpert's PLOS assays are any indication. I compiled a few links to get you started.
Specifically, reappraising the topic of your cited classical experiment are R.Moore et al:

The classical cell sorting experiments undertaken by Townes and
  Holtfreter described the intrinsic propensity of dissociated embryonic
  cells to self-organize and reconcile into their original embryonic
  germ layers with characteristic histotypic positioning. Steinberg
  presented the differential adhesion hypothesis to explain these
  patterning phenomena.....

(Source: Robert Moore, Kathy Q. Cai, Diogo O. Escudero, Xiang-Xi Xu, Cell Adhesive Affinity Does Not Dictate Primitive Endoderm Segregation and Positioning During Murine Embryoid Body Formation, Genesis. 2009 September; 47(9): 579–589)
Regarding: ...without something taking the lead and actively coordinating...
On a hunch that you are not talking about complexity, attractors and polarity, I would like to share a few words. You may completely disregard them if you'd like.
My personal experience (from my country) is that few biologists delve into "that" branch of EvoDevo, because a profound understanding involves calculus, modeling and a knack for theoretical biology. Yet, afaik few struggled comprehending the evolutionary logic of making an organism based on Albert's book chapters alone.
See:

Reaction–diffusion system
Cell fate determination
Fate mapping
Asymmetric cell division
Pattern formation
Alberts Molecular Biology of the Cell describes this very well (can be accessed online for free)

I personally recommend G.Müller's authored/coauthored papers:
(open access)
http://homepage.univie.ac.at/gerhard.mueller/publications-papers.html
Disclaimer: I am not specialized in the field of EvoDevo or Theoretical Biology.
Views expressed here are my own.

I would like to add to Lo Sauer's nice answer but give a slightly different perspective.
What you referred to as the "brain" of the cell, is mostly its regulatory program. An abstract way to think about the regulatory program is like a computer, or mathematical function, which gets input (in the form of signal molecules inside and outside the cell) and calculates an output (behavior - which genes/proteins to activate, for example) based on this input. This is usually how cells make decisions, both in differentiation and when reacting to the environment.
Of course the really interesting part is how the regulatory program is implemented. It seems that most of it is encoded in the DNA, although there is also a significant role for epigenetics factors (non-DNA factors that are inherited from the zygotes). As you can imagine this regulatory program is highly complex and is being studied by many groups, mostly using genomic experimental and computational techniques. It is currently far from being understood at a comprehensive level.
You can read about specific simple examples in some of the places Lo Sauer mentioned, for example Drosophila embryo segmentation/pattern formation.


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methods for targetted deletion of genomic regions?
I would like to know what are currently used methods for targeted deletion of genomic regions in mammalian organisms or cell lines. I have heard of Zinc-Finger nucleases as a recent genetic engineering method, but I don't know if there are other methods, more efficient or better tailored, for the deletion of specific regions.

please consider setting for an answer. thank you

I can only provide you with a few pointers from memory, as an ad hoc search for "review of dna cutting techniques" was not prolific.
Please consider the provided information with precaution and only for pointers to help you do literature research.

cre/lox system and variants (best known), belong to SSRs (Site specific recombinases)
various Restriction enzyme based systems (see Homing Endonucleases)
meganuclease based tools
aptamer based
based on hybridizing n-mer probes which yields a reactive species nicking the DNA at the probe's-site when introduced to certain chemicals such as oxoacids
light twizzers and lasers /purely proof of concept (perhaps already commercialized?)
ZFNs and variants / protein based-probes . http://en.wikipedia.org/wiki/Zinc_finger_nuclease

There are definitely published reviews on this exhaustive topic, notwithstanding the dozens of books.
I would estimate that there are at least 10 commercial methods, and almost 100 methods in total when theoretical and proof-of concepts are included.
Naturally (literally!), the vast majority of methods will be based on the noncovalent interaction of an n-mer "homing construct"/probe a)attached to an nuclease or b)an
attachment site for a nuclease or c)participate in the reaction for the formation of a reactive chemical species to break the sugar-phosphate backbone.
I would speculate that most other methods are likely not practical in terms of either efficiency and/or affordability.
To learn about the applicability of the respective methods relating to your field of research, and be provided with an overview of the pros and cons of the methods, you will still need to find a good review paper.


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Brain response frequencies while sleeping
I'm not sure if this is the right place to ask this but Biology seemed to fit best.
I'm trying to find out what frequencies the brain responds to best while sleeping.
The reason for this is recently I attended a lecture where it was stated that the brain hears low frequencies/deep noises better, meaning fire alarms for example might not be as effective as we think.
However I remember there was an episode of The Big Bang Theory where they said high pitch noises are heard better while sleeping as a built in response to, for example, a baby crying. Now I know this is just a TV show but I presume they must have some basis for the remark since they do have science advisors, it also just seems to make more sense.
Does anyone know which is correct or better yet can point me in the direction of some research to help.

Just to point out that the big bang theory episode states that women are more likely to respond to high pitched sounds such as a baby crying. I have no idea if it is true but it makes perfect evolutionary sense.

On a less serious sidenote: I know Francis Crick was an advocate of his brain@40Hz theory. / I would advocate for the Sceptics.SE site, which deals with scrutinizing notable sources...

Sleep as you may know is divided into 2 broad categories which are the REM (Rapid Eye movement) and NREM (non rapid eye movement). NREM is further divided into 3 stages (reference). You never know which stage of sleep you are in when you are subjected to a particular frequency of sound. Your response to different sounds differ in your different sleep cycles.
The present 3 stages in NREM sleep is an update by The American Academy of Sleep Medicine (AASM) in 2007 (reference).The original 4 stages in the Rechtschaffen and Kales (R&K) standardization of 1968 (reference) has been used to explain the effect of disturbances in different sleep cycles

Stage 1 is still the phase of sleep from which it is easiest to wake
  someone up.
People in Stage 2 sleep are unlikely to react to a light or a noise,
  unless it is extremely bright or loud.
During Stage 3, the muscles still have some tonus, and sleepers show
  very little response to external stimuli unless they are very strong
  or have a special personal meaning (for example, when someone calls
  your name, or when a baby cries within earshot of its mother).
Stage 4 is the stage of sleep that accomplishes most of the body’s
  repair work and from which it is most difficult to wake someone up (reference).

A study conducted to measure brain activity while sleeping subjects were subjected to varying degrees of sound found that some people did you wake up after being hit with 70db of sound while others woke up even at sounds between 40 - 50 db (reference). This could lead to new behavioral or drug therapies for people with sleep disorders.
A review on the affect of low frequency sound on sleep could not reach any significant conclusions warranting that more search needs to be conducted in the field.(reference).
You will be interested to know that different sounds have been found to wake up men and women. A list is available here. Differences between the sleep of men and women are listed in this article.


text:
Why was polyploidy not lethal in certain octodontid rodents?
As discussed in Why is polyploidy lethal for some organisms while for others is not?, polyploidy is normally lethal in mammals.
However, two species of Octodontidae (South American rodents), are tetraploid due to a recent doubling of all chromosomes:

Tympanoctomys barrerae: 4x = 102
Pipanacoctomys aureus: 4x = 92 (apparently some chromosomes were lost after the polyploidy event)

See the paper discussing T. barrerae, the first of these tetraploid rodents discovered.
According to the Wikipedia article, both are believed descended from the same species, Octomys mimax (or possibly now-extinct close relatives thereof), which has 2x = 2n = 56 chromosomes, half those of T. barrerae.
What was special about Octomys that allows it to survive polyploidy, unlike most mammals?
Interesting:

The sperm head of Tympanoctomys is is by far the largest naturally occurring in mammals, and its size is causally related to the double genome size it has to accomodate.

Actually, that is not what is discussed in the question you linked to. The following is a quote from the very comprehensive accepted answer (emphasis mine):

Polyploidy arises easily in both animals and plants, but reproductive
  strategies might prevent it from propagating in certain circumstances,
  rather than any reduction in fitness resulting from the genome
  duplication.

In fact, try rereading that answer and the references therein, it answers your general question.
There is a popular theory (mostly accepted) that there have been whole genome duplication events (WGDs) in the vertebrate ancestry. If true, it means that all mammals are the descendents of polyploid ancestors. For a very nice review of WGDs in vertebrate evolution, see here [1]. Octomys is simply the only known mammal with a more recent WGD event. As for what makes it special (taken from [2]):

Our data demonstrate that parental-specific silencing of at least one
  gene and normal X chromosomal dosage mechanism are conserved in the
  tetraploid genome. We hypothesize a concerted action of genetic and
  epigenetic mechanisms during the process of functional diploidization
  of this tetraploid genome.

1) Van de Peer Y, Maere S, Meyer A., The evolutionary significance of ancient genome duplications., Nat Rev Genet. 2009 Oct;10(10):725-32.
2) Bacquet C, et al., Epigenetic processes in a tetraploid mammal, Mamm Genome. 2008 Jun;19(6):439-47.

I would say in practice that it is more complex than this. Trichrisomy (extra chromosome) is often (not always) fatal or causes significant negative phenotype (Downs syndrome for instance) in humans.  Genome duplication has occurred several times in the course of evolution, but it is still very rare in animals.  Plants are much more resilient to polyploidy than animals.

@shigeta, true but the main difference here is that polyploidy at the species level (such as WGD) is very different to individual aberrations such as Downs'. Individuals are very sensitive to changes in ploidy, however, changes in gene or even chromosome copy number have occurred multiple times in multiple lineages. Clearly they were accompanied by compensatory changes elsewhere to allow the species to deal with the change in ploidity. I think it is not reasonable to compare trichrisomy or Down's to WGD events.

the point is taken that while its not disputed that occasionally animals tolerate genome duplication, its still not clear to me that the whole genome duplication is tolerated by all animals.  there may be something particularly permissive in these rodents given the frequency seen in that branch...


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Multi-nucleated cells: advantages and examples?
This question arises because I saw that monocytes and leukocytes are commonly called 'mononuclear cells' in the scientific literature. The implication of course being that other immune sub-types are multi-nuclear!
I know of granulocytes (e.g. neutrophils) that are classed as 'polymorphonuclear' because their nuclei are segmented, and can alter their shapes, and muscle cells that fuse together to form one long cell (muscle fiber) with multiple nuclei. What other examples of multi-nucleated cells are there?
I am also interested in the advantages gained by cells having multiple (or segmented) nuclei?

Technically, all the granulocytes (neutrophils, eosinophils, and basophils) have multiple lobes/segments, not multiple nuclei. Syncytia in cardiac muscle cells is important for coordinated contraction. Not sure about the rest..

@jello yes I realize that polymorphonuclear does not mean multiple nuclei, but 'mononuclear' does imply that 'ploynuclear' cells exist, and I am sure that muscle fibres do have multiple nuclei, because multiple cells fuse together. I'm interested to know the advantages of multiple nuclei, and what other cell types have it. Thanks

Muscle cells are the only cells I know of that are polynuclear. With respect to monocytes, a concise review of their nomenclature can be found in this paper by L Ziegler-Heitbrock, P Ancuta, S Crowe, et al. (Blood, 2010). Apparently it has had quite a complex and confused biochemical characterization, but the article states the name indeed derived from its single lobed, mononuclear morphology. This is in distinction to other phagocytes which have multi-lobular nuclei (polymorphonuclear cells).
With respect to advantages, a multinucleated cell makes sense when the speed of intracellular signalling is important (e.g., calcium diffusion). It may also be useful in the case of cells when the cell needs to coordinate the synthesis of large amounts of protein.

Hepatocytes (liver cells) are also often binucleated, which I remember reading probably has something to do with the liver's filtering capabilities - backup code or excess code to handle harmful substances.

That's an example I was not aware of, but very interesting.

Another example of multinucleated cells is osteoclasts, which are specialized derivatives of macrophages that degrade bone matrix.  They form by fusion of mononucleated progenitors and can accumulate many nuclei in a single large cell.  In cell culture with mouse macrophages, it's common to obtain individual osteoclasts with 50-100 or more nuclei each.

Can you back your answer up with a reference?

Multinucleate cell angiohistiocytoma (MCAH)
Osteoclasts
muscle fiber
granulocytes
Types of giant cells
A.  Physiological giant cells:
•   Osteoclast
•   Megakaryocytes
•   Striated muscle
•   Syncytiotrophoblast
B.  Pathological giant cells:
•   Langhan's giant cell
•   Foreign body giant cell
•   Touton giant cell
•   Tumor giant cell
•   Warthin–Finkeldey giant cell
Liver cells
Skeletal muscle
Some cardiac muscles

As such, your answer is incomplete because you haven't mentioned any advantages. It also needs references.

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


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Is it possible to increase lifespan through controlled evolution?
A few years back when I was reading The Selfish Gene by Richard Dawkins, there's this short passage where he theorizes about a way to achieve an increased lifespan through controlled evolution.
The theory goes like this: we don't tend to have medical problems until after 30 because we all tend to reproduce before that age.  Thus, people who tended to die before 30 never passed on their dying-prone genes.
So, if you didn't let people reproduce before a age X (where X starts at 30) and then slowly move that age up, you could use evolution to increase lifespan.
The ethical issues notwithstanding, is there any reason why this wouldn't work?  If it would work, how long do you think you would need to sit at each value of X?  How far apart do you think each value could be?  Finally, how many generations, using this technique, would it take before someone would live to be 1000 naturally?

The well quantifiable subject of say e.coli evolution is a totally different matter than say human evolution on aging, no less. This subject in the way it is phrased may be better suited for skeptics.SE (which is meant to discuss the information provided by notable sources).

@LoSauer I see no great difference between E. coli and human evolution. They same forces drive both of them. Granted the human genome is orders of magnitude more complex than that of E. coli but nevertheless, the governing principles of evolution are the same in both cases.

@terdon bacteria have a lot more lateral gene transfer and can acquire plasmids to add new chromosomal material.  They also have co-regulation through operons.  Prokaryotic and eukaryotic selection and evolution are remarkably different, at least to the level of mechanisms described in this question.

All true @shigeta, I am just saying that the driving force of selection still depends on the time that an individual reproduces, whatever way it does so, be it sexual or budding or whatever. In any case, this is a discussion I would love to have over a beer some time but not really appropriate for the comments of the poor OP's question. Unfortunately. Maybe we can continue it in chat at some point?

@terdon wish we could get a beer.  not only would the conversation be welcome, but that could mean I was in France!  Its been a while :)

before that age -> after that age, perhaps?

I think this would probably work.  The grandmother effect, which is one of the main theories for human longevity after fertility might indicate that human lifespan would increase if the children come later.
Just have to disclaim here: We will never do this.  Many unthinkable consequences would result...
If you simply forbid anyone to have children before they are 40 or 45 (fertility doesn't drop until age 35 or so), forbid invitro fertilization and medical assistance to conception we would probably be looking at a prolonged lifespan.  Infertility rates in women at age 40 are not clear, but one estimate is that 40% of women can have children at 40 years of age.  If we want to seen an effect early, we would push the age up a year or two.  Forbidding in vitro fertilization and other medical assistance to offspring we could look like a 80-90% cut of people - lots of people would never have children.  This might make people unhappy an destabilize the social fabric.
Its not clear how long this would take.  The generation time would go to 40 years from about 20 now - 40 to get to childbearing age, but results would take 80 years - when we find out how the children would fare.  Given the C elegans longevity experiments and the fact that we are starting with 8 billion people, we probably would find some great late age breeders who may also live long.  But for the longevity phenotype to set in it would take several generations as we are looking for an indirect effect: later breeding causing longevity.  The Belyaev experiments which produced domesticated foxes by strong selective breeding took some 30ish generations to complete though they saw a significant effect in just 10.  It could take a similar numbers of selection rounds in this cse.  4-500 years. Ethical issues aside, this is why most geneticists study flies.
There would also be a lot of other negative socioeconomic consequences to this thought experiment.  One good thing is that the population of the earth would plummet - many people would be eliminated from the gene pool, though eldercare would be a major part of the world workforce.  Lots of work, not clear who is going to pay for it, but low unemployment and low low wages may result.

So you see Mister President, this is quite a distinct possibility, though some sacrifices would have to be made.
The science of human eugenics is not scientifically wrong, but selective animal breeding and lab experiments don't usually evaluate or care about the consequences of large peturbations in the gene pool.
You would also have a lot more autism and Downs syndrome and other congenital defects which tend to show up in offspring of older parents. These issues might improve with application of biotechnology which screens weak sperm and eggs without ruining the effect you are looking for, maybe not.
Since we are selecting against fecundity, the human race could be dogged by fertility problems or chronic genetic diseases which the genetic contribution of some of the more robust people in the gene pool being removed and the tendency to such age-related birth defects might not go away given the drastic selection pressure we are putting on the gene pool.
Other consequences you might not expect; some physical traits associated with longevity and prolonged fertility would cause us to look more alike and not necessarily in a good way.   Browse the internet; its probable that we would get shorter and possibly uglier?
There are many more direct ways to increase the human lifespan - better diet, exercise, the elimination of poverty, vaccinations, proper medical care, access to clean drinking water and a lower birth rate (fewer children not later) all are known to directly effect longevity, having more than doubled the human life expectancy in the past few hundred years.

What a great answer. +1

A potential side effect of the selection would be a substantial delay of the age of puberty, as to, say, 30, which would effectively extend childhood.  Longer lives are usually correlated with later age of sexual maturation.

@mgkrebbs yup this is one possible part of an outcome.  All of this can be imagined when one looks at what happens to domesticated foxes - they became more juvenille in appearance when they were genetically tame.  would all people also start to look older when they are younger?  not sure, but stimulating to think about.

This has been done in fruit flies. At least two labs have used selection to breed longer-lived  flies.
Rose, M. Laboratory Evolution of Postponed Senescence in Drosophila melanogaster. Evolution (1984).
Luckinbill, L. et al. Selection for Delayed Senescence in Drosophila melanogaster. Evolution (1984).
We won't do this to humans, because eugenics is evil.
The "methuselah flies", as Rose calls them, live about twice as long. I don't know how long it would take to get them to live 10 times as long. In any breeding program you run up against the problem that eventually you'll run out of standing genetic variation to select from, and you have to wait for new mutations to appear.
But obviously selection can eventually lead to the evolution of much longer life. This has happened many times in evolutionary history, for example.

Eugenics is just a method, why would it be inherently "evil"?


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What gives things their colour?
My 6 year old daughter asked me 2 biology-related questions yesterday and I tried my best to answer them with the aid of YouTube videos.  One of the questions (I may post the other one too) was

How do we see colour?

I showed her a video on YouTube where it was explained that light hits an object and if that object is a tangerine then that object will absorb all colours except orange and will reflect orange and that's why we see it as being orange.  I then repeated this explanation and she said.

But how do we see different colours?

I then showed her a video describing corneas, vitreous humours, lenses, optical nerves and so on.  I think I lost her.  I got a bit lost too.
Now I have two problems, which I'd like to ask to you all as questions

I do not know how to explain to a 6 year old how we are able to perceive colour.  Does anyone know how this can be explained?
I have never quite understood this idea that an object has a colour depending on the light that hits it.  Okay, I understand that in low light objects have a different colour because there is a not much light hitting it and that different objects absorb different wavelengths of light and therefore appear as different colours.  What I don't understand is that if I place a bar of gold a bar of silver side by side in the same lighting conditions they do have different colours, so therefore there must be something inherent in these object that give them different colours.  What is that something?

That "something" is just the absorption and emission of this light energy within the bonds and structures of whatever you happen to be looking at.

Also, related: http://biology.stackexchange.com/questions/1446/why-can-cones-detect-color-but-rods-cant?rq=1

this question has two pretty formidable parts - 1) how do we perceive color and 2) what optical properties of matter give them their color. @LanceLafontaine's answer does a good job with this. (2) is a very big question, depending on the level of detail at least as much chemistry and physics as it is biology.

my daughter asks formidable questions.  I just hope she doesn't ask me how babies get inside their mummy's tummy's.

I hope I'll have the time to whip up an answer later, but I just wanted to make the point that objects do not "have" color. We "perceive" them as colored. Try holding a gin&tonic under a neon (UV) light (it will appear bright blue) or placing a blue object under a streetlight (it will appear green).

But you see this is exactly what I don't get.  Holding a gold bar under neon lighting, I assume, produces a different colour to holding a silver bar under the same neon light.  Therefore, objects do have a property, lets call it shuyutokiwomatatalilibo, for the sake of argument, that makes it appear to have a different colour to other objects.

I do not know how to explain to a 6 year old how we are able to perceive colour. Does anyone know how this can be explained?

Well, depending on the depth you want to introduce her to, it can be difficult to explain to adults - much less children. You explained the basics well enough. Without going to the molecular mechanisms, here's a useful diagram:

Light will pass through the eye and Retina until it hits the Cones and Rods. That produces a reaction (which I'll address next) - which then causes signals to either resume or cease (Rods are, ironically, shut off by light - not turned on). These signals pass through Ganglion cells, through the Optic Nerve, and interpreted by the brain. When some cells are switched on, like a 3-Way traffic stop, they will prevent the information from other cells being transmitted.
A simple way of explaining it might be that inside our eyes are millions of teeny-tiny molecules that act like light-switches, and the brightness and color of light determine which of the "light-switches" are on or off.
If you want to go further into the actual mechanisms (or just have the background knowledge for future reference) the next diagram shows the mechanism itself (and the original in full-size since the one shown is squished if you prefer):

The big things to note above is the change from cis-Retinal to trans-Retinal which occurs after a Photon is absorbed. This causes signaling molecules to go a bit wild, open ion channels, and the depolarization of the membrane propagates the charge down the cell - much like a neuron.

I have never quite understood this idea that an object has a colour depending on the light that hits it. Okay, I understand that in low light objects have a different colour because there is a not much light hitting it and that different objects absorb different wavelengths of light and therefore appear as different colours.

Well, let me stop you here. Low-light is a different situation than colored-light. Let's get the basics down:
Photons are absorbed by the electrons of the atoms that compose the molecules of an object. Whatever Wavelength of light is not absorbed by the electrons is reflected, and it's this Wavelength that we perceive as the color of the object as our Cones absorb the reflected light.
Photons can also be emitted when an electron moves to a lower-energy state. The Wavelength emitted by the electron is directly related to the difference between the High and Low energy states, as this diagram shows fairly well:

The emitted photons are the object's "Incandescence" - which is when an object produces a color of light by itself. The color you perceive is NOT going to change if the object emits incandescent light because the object is generating its own light. Neon signs are a great example: The gases being subjected to a current emit light, and will appear whatever color it's supposed to be whether or not it's a blue moon or sunset.
Photons which are reflected and not emitted - i.e. almost everything that doesn't have a power source - as I said above, are then absorbed by our Cones and our brain interprets the signals to produce a color.
The reason why objects that reflect light can change color is because not all environmental light is the same. Red objects will appear Black under Blue light because Blue light doesn't contain Red Wavelengths - there's nothing to reflect, so the object absorbs all of the available Wavelengths - the very definition of Black!
A lot of our color perception depends on ambient light, and most of the time - thanks to the Sun - that is a full-spectrum white light. Which brings me to answer the last bit of your question:

What I don't understand is that if I place a bar of gold a bar of silver side by side in the same lighting conditions they do have different colours, so therefore there must be something inherent in these object that give them different colours. What is that something?

Yes, there definitely is something inherent in both objects. That is: Their electron configurations absorb different chunks of the spectrum, and accordingly reflect different chunks of the spectrum. Although that's still a bit simplistic, since metals have some unique properties that other Elements do not. Their electrons exist in more of an "ocean" than around central atoms, but that's a whole other question.
As a fun bit of Trivia to impress your daughter when she's old enough, it's always a fun fact to know that the color Yellow is completely constructed in your head.
The human eye only has Rho (Red), Gamma (Green), and Beta (Blue) color receptors which have the following absorption pattern (from photo.net):

What everybody sees as "Yellow" is actually when both the Green and Red receptors are activated at the Wavelength where they intercept above, which your brain interprets as "Yellow":

Because your brain does a lot of processing, despite having only three color receptors we can perceive millions of colors (and shades/tones). Now for a while everywhere you look you'll be utterly amazed at what's going on, and you rightfully should be. ;-)


text:
"Acellular" designation for organisms
Why do some biologists refer to single-celled organisms such as Amoeba and Paramecium as
acellular (i.e., without cells) rather than unicellular (i.e., one cell)?

Can you point us to an example of this?

From Wikipedia:
Some biologists refer to wholly syncytial organisms as "acellular" because their bodies contain multiple nuclei which are not separated by cell walls.
As Albano pointed out, "cell walls" should probably be "cell membranes".
Paramecium and some types of amoeba like the Chaos genus have multiple nuclei so they fall under this definition.

Our own cells are not separated by cell walls either. This is an error in Wikipedia. It should probably read "cell membranes".

@S.Albano yes you are right it should probably be cellular membranes.

@Bitwise, I stand corrected thank you. Comment removed to avoid confusion.


text:
Does cooking or ripening reduce the concentration of solanine in nightshade?
I recall a story from one of my Botany professors where he encountered a woman picking Solanum dulcamara (nightshade) berries. When he asked her what she was doing with them, she responded that her husband had her make a pie from them every year.
As her husband was presumably still alive, and since I regard this particular professor as reliable, what would have removed enough solanine from the berries to avoid ill effects? Does the concentration decrease upon ripening, or would cooking destroy the toxin? Would that also be why we fry green tomatoes?
(As a disclaimer, no-one should eat plants that are known to be poisonous. Even though some people don't react to poison ivy, it is still a bad idea to rub it all over your body.)

Did you mean Solanum viride or Solanum viridifolium?

The common name is green nightshade. I am guessing viridi, but I will check in Flora of the Pacific Northwest.

Actually, it doesn't show either of those in my area. I don't have one to key out, but the illustration for S. dulcamara looks like the correct one.

Do you have a reference for the diminishing of the alkaloids during ripening?

If you ask Dr. Duke's phytochemical database, by far the most solanine is found in green potatoe fruits (their skin), with much less in leaves and tissues. Similar values are seen in green tomatoes, with dozens of mg per 100g fruit. There is no value for Solanum dulcamara (doesn't mean there is nothing in it) but it appears to have small quantities of atropine. Furthermore, Wikipedia gives for solanine a minimum toxically effective dose for humans of 200 mg---that's where dizzyness and dispnoe starts---, and gives for children a lethal amount of S. dulcamara of 30-40 unripe berries or less. The amount of solanine increases (in potato) when temperature goes up, because it is produced by plants as an antifungal against rot. Ripening in S. dulcamara and, as we know all ourselves, potato and tomato, destroys solanine, so fully ripe berries seem to be okay. Solanine does not degrade when cooked but is lost with the cooking water. For an account of solanine poisoning from potatoes see e.g. this free paper. Newer potato varieties have much less solanine than those from former times.
http://www.ars-grin.gov/duke/
http://de.wikipedia.org/wiki/Solanin
Know your databases!

The database link is good. My background is in taxonomy and phylogenetics, so I am at a loss for knowing where to look up things that are not gene/protein sequences or species identification. It is unfortunate that the evidence in the answer for reduced levels in nightshade after ripening is all implicit. I would have thought there would be some information about levels, or lack thereof in the ripe berries.

First of all there is no solanine in green tomato, there wasn't, and there never will be.

Steroidal glycoalkaloids (SGAs) extracted from tomato leaves and
  berries (Lycopersicon esculentum Mill.) were separated and identified
  using optimized reversed-phase liquid chromatography with electrospray
  ionization (ESI) and ion trap mass spectrometry (ITMS). The ESI source
  polarity and chromatographic conditions were evaluated. The ESI
  spectra contain valuable information, which includes the mass of SGAs,
  the mass of the aglycones, and several characteristic fragment ions.
  Cleavage at the interglycosidic bonds proximal to the aglycones is the
  most prominent process in the ESI process. A protonated molecule,
  [M+H]+, accompanied by a mixed adduct ion, [M+H+Na]2+, was observed
  for α-tomatine (i.e., m/z 1034.7 and 528.9) and dehydrotomatine (i.e.,
  m/z 1032.6 and 527.9) in positive ion mode spectra. The structures of
  these tomato glycoalkaloids were confirmed using tandem mass
  spectrometry. The identification of a new α-tomatine isomer
  glycoalkaloid, named filotomatine (MW 1033), which shares a common
  tetrasaccharide structure (i.e., lycotretraose) with α-tomatine and
  dehydrotomatine, and soladulcidine as an aglycone, is described for
  the first time. It occurs in significant amounts in the extracts of
  wild tomato foliage. Multistage mass spectrometry both of the
  protonated molecules and of the doubly charged ions was used for
  detailed structural elucidation of SGAs. Key fragmentations and
  regularities in fragmentation pathways are described and the
  fragmentation mechanisms involved are proposed.

2005 - Analysis of tomato glycoalkaloids by liquid chromatography coupled with electrospray ionization tandem mass spectrometry

Your bitter nightshade really has solanine content:

Alkaloids are well known for their antimicrobial activity. Though all
  natural alkaloids come from plants, not all plants produce alkaloids.
  Plants of the Solanaceae family are known for their high alkaloid
  content. Alkaloids are found in all plant parts like roots, stems,
  leaves, flowers, fruits and seeds. In the present study, those plant
  parts of Solanum dulcamara were selected which have been reported to
  produce a high content of a specific alkaloid: solanine (from unripe
  fruits), solasodine (from flowers) and β-solamarine (from roots).
  These alkaloids were extracted from various parts of S. dulcamara by
  well-established methods and were screened for their antibacterial
  activity. Human pathogenic bacteria, viz., Enterobacter aerogenes,
  Escherichia coli, Staphylococcus aureus, were selected for the study.
  All three alkaloids inhibited the growth of E. coli and S. aureus.
  However, no significant activity was observed against E. aerogenes.
  Minimum inhibitory concentration and minimum bactericidal
  concentration were also evaluated.

2009 - Biological activity of alkaloids from Solanum dulcamara L.

The glycoalkaloid content usually decrease by ripening, so that the animals can eat them safely and deliver the seeds. At least that's my observation. So there is a good chance that the ripe fruits are edible...
If they are not, it is hard to get rid of the solanine. Solanine is heat stable it decomposes over 200°C (about 240-260°C afaik) and it is not (poorly) water soluble. So cooking in hot water does not help.

Reduction in concentration of α-chaconine (CHA) and α-solanine (SOL),
  toxic glycoalkaloids in potatoes, during cooking by 3 procedures was
  investigated. Raw or cooked potato samples (2 g) were extracted twice
  with 5% acetic acid solution. The extract was purified on Sep-Pak C18
  and CHA and SOL contents were determined by HPLC. Recoveries of CHA
  and SOL from raw potatoes were 96.5 and 98.2%, respectively, vs. 96.2
  and 96.7% from cooked potatoes. >93.9% of CHA and 95.9% of SOL
  remained in potatoes after boiling. Contents of both were reduced by
  15% on microwave treatment. On deep-frying alkaloid contents varied
  according to temperature. At 157°C, both alkaloids were unaffected; at
  170°, potatoes showed a large variation in residual alkaloids. At
  210°, alkaloids were partially decomposed; after 10 min heating, 64.9%
  of CHA and 59.7% of SOL remained. It is suggested that the critical
  temperature for decomposition of both alkaloids in potatoes may be
  around 170°. Results confirmed the relatively high stability of CHA
  and SOL in potatoes under normal home cooking conditions.

1990 - Effect of cooking on contents of α-chaconine and α-solanine in potatoes.

Deep frying over 200 °C might help, because it degrades the glycoalkaloids and probably moves them from the fruits to the oil, but be aware that this is an old article... Teflon will burn over 270°C afaik, and you should check the smoke point of the oil, because most of them have in a range of 150°C to 250°C. I guess there are other methods which I don't know of, but I think you don't want to eat that pie... ;-)


text:
Mutation in axillary buds of trees overcoming self-incompatability?
I seem to recall from either reading or lecture that there have been instances of trees that are self-incompatible accumulating enough mutations in an axillary bud that the resulting branch was able to pollinate flowers on other parts of the tree. Unfortunately, I do not have a source for this information.
Are there recorded instances of this happening, or is this a figment of my fevered brain?

You may be remembering the line of work since reviewed here: https://www.nature.com/articles/hdy2013114 (Scofield DG. 2013. A definitive demonstration of fitness effects due to somatic mutation in a plant. Heredity 112:361–362.) Maybe you can clarify the question further, as well, if you are still interested one decade after the op?

Recently, samples from different parts of cottonwood trees have been sequenced (Nature News). The conclusion:

“The variation within a tree is as great as the variation across unrelated trees,” says Ken Paige, an evolutionary biologist at the University of Illinois at Urbana-Champaign, who led the team that made the discovery.

This doesn't say anything about overcoming self-incompatibility, and it probably depends on the mechanism of self-incompatibility if it can be overcome by accumulating mutations.

Going through my old Botany textbooks. It would appear that for at least one mechanism for self-incompatability, it would require between one and three de novo mutations. Perhaps for some mechanisms it would be more likely, and perhaps someone has come across this in the wild, but for now this works for me. :)


text:
Does drinking coffee have negative effects?
From what I collected, coffee is a magical potion that lets you feel energetic, and essentially not-sleepy. But are there any tradeoffs? I mean, if it was so beneficial, wouldn't the human body produce caffeine naturally?

First of all, the fact that a substance is beneficial does not mean that our body will, perforce, produce it naturally. Think of oxygen and water for example1.
As for the negative effects of coffee drinking, yes there are many although coffee has both a positive and a detrimental effect on human health. The main active ingredient in coffee is caffeine which can have the following negative effects:

Caffeine can increase blood pressure in non-habitual consumers.
High blood pressure is associated with an increase in strokes, and cerebral
vascular disease, which in turn increase the risk of multi-infarct dementia.
Caffeine may reduce control of fine motor movements (e.g., producing shaky hands)
Caffeine can stimulate urination.
Caffeine can increase cortisol secretion, some tolerance is developed.
Caffeine can contribute to increased insomnia and sleep latency.
Caffeine withdrawal produces headache, fatigue and decreased alertness.
Caffeine is addictive.
High doses of caffeine (300 mg or higher) can cause anxiety.
High caffeine consumption has been linked to an increase in the likelihood of experiencing auditory hallucinations. A study conducted by the La Trobe University School of Psychological Sciences revealed that as few as five cups of coffee a day could trigger the phenomenon.
High caffeine consumption accelerates bone loss at the spine in elderly postmenopausal women.

The list above comes from the very comprehensive wikipedia page on the health effects of caffeine. In fact, wikipedia is particularly good on this subject, see the following pages:
http://en.wikipedia.org/wiki/Caffeine
http://en.wikipedia.org/wiki/Health_effects_of_caffeine
http://en.wikipedia.org/wiki/Health_effects_of_coffee
1 Our bodies do produce both Oxygen and water as byproducts of various reactions but nowhere near enough to satisfy our need for these substances.

I understand the need of writing a generic answer but... it all depends on doses, frequency of assumption and the person who drinks the coffee. Caffeine has very different effects at the molecular level depending on its concentration, so it is very difficult to generalize. For instance, 300 mg of caffeine are ~4 cups of espresso, which you generally don't drink at the same time.

@nico, of course it does, everything is dosage dependent. However, the question was not about what the effect of a specific dose of coffee is, it was about coffee in general. All I said was that caffeine can produce the listed effects. if you can give an answer listing different effects of long term cofee consumption at different doses please do, considering how much of the stuff I drink, I would very much like to read it :).

As always, it depends.
To be more precise, let's presume you are asking about habitual coffee consumption. Thus, for people asking: "I really like to drink several cups of coffee per day, but I have heard this might be unhealthy. Should I be worried?"
Based on my reading of O'Keefe, J. H. et al. (2013), overarching results indicate you should not be overly worried (but exception cases will follow):

a growing body of data suggests that habitual coffee consumption is neutral to beneficial regarding the risks of a variety of adverse CV outcomes including coronary heart disease, congestive heart failure, arrhythmias, and stroke. Moreover, large epidemiological studies suggest that regular coffee drinkers have reduced risks of mortality, both CV and all-cause. The potential benefits also include protection against neurodegenerative diseases, improved asthma control, and lower risk of select gastrointestinal diseases. A daily intake of ∼2 to 3 cups of coffee appears to be safe and is associated with neutral to beneficial effects for most of the studied health outcomes.

However, you might want to be cautious in regards to:

... potential risks (which are mostly related to its high caffeine content) including anxiety, insomnia, tremulousness, and palpitations, as well as bone loss and possibly increased risk of fractures.

And ...

Those with dyslipidemia may consider brewed and filtered coffee as opposed to preparations made from boiling beans without filtering.

So if you have trouble sleeping, already have an overly anxious personality, are prone to fractures, or have dyslipidemia, you might want to consult your doctor about your coffee intake.
A systematic review and meta-analysis investigates the effects of coffee on blood pressure and cardiovascular disease (CVD) in hypertensive individuals (Mesas, A. E. et al., 2011) and concludes:

The results of this review have clinical implications for the control of hypertensive patients. On the one hand, the acute increase in BP may temporarily increase the risk of a cardiovascular event (10, 11). This is consistent with the increased risk of coronary disease and stroke in the hours after coffee consumption. Thus, hypertensive patients with uncontrolled BP should avoid consuming large doses of caffeine. ... However, we found no evidence to justify avoidance of habitual coffee consumption in well-controlled hypertensive patients; therefore, in these patients, medical recommendations should prioritize modification of other lifestyles, such as quitting smoking, controlling weight, and increasing physical activity.

O'Keefe, J. H., Bhatti, S. K., Patil, H. R., DiNicolantonio, J. J., Lucan, S. C., & Lavie, C. J. (2013). Effects of habitual coffee consumption on cardiometabolic disease, cardiovascular health, and all-cause mortality. Journal of the American College of Cardiology, 62(12), 1043-1051.
Mesas, A. E., Leon-Muñoz, L. M., Rodriguez-Artalejo, F., & Lopez-Garcia, E. (2011). The effect of coffee on blood pressure and cardiovascular disease in hypertensive individuals: a systematic review and meta-analysis. The American journal of clinical nutrition, 94(4), 1113-1126.

Likely another relevant recent meta-analysis (I haven't read it): Poole, R., Kennedy, O. J., Roderick, P., Fallowfield, J. A., Hayes, P. C., & Parkes, J. (2017). Coffee consumption and health: umbrella review of meta-analyses of multiple health outcomes. Bmj, 359, j5024.

There are copious studies on the health effects of coffee. The overall conclusion is that people who drink coffee have slightly less health issues than people that don't.
BMJ:
The umbrella review identified 201 meta-analyses of observational research with 67 unique health outcomes and 17 meta-analyses of interventional research with nine unique outcomes. Coffee consumption was more often associated with benefit than harm for a range of health outcomes across exposures including high versus low, any versus none, and one extra cup a day.
https://www.bmj.com/content/359/bmj.j5024
For adults consuming moderate amounts of coffee (3-4 cups/d providing 300-400 mg/d of caffeine), there is little evidence of health risks and some evidence of health benefits. https://www.ncbi.nlm.nih.gov/pubmed/16507475