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What are the effects of combining rapamycin with dietary restriction?
Are the effects additive or subadditive? In many ways, rapamycin acts like a CR mimetic, but even CR can only go so far.

Please explain the question more clearly without reliance on jargon

To clarify; administration of rapamycin (a drug) to lab organisms (including mice [1]) extends lifespan. Similarly, restricting the intake of nutrients to the minimum without causing malnutrition also extends lifespan in lab animals (including primates [2]).
Rapamycin inhibits the mTOR pathway (mammalian Target Of Rapamycin) - specifically mTORC1 (Complex 1) - which influences protein synthesis, autophagy and inflammation (among others). Upstream factors of mTOR include nutrient availability and insulin signaling (see "Deconvoluting mTOR biology" for good review [3]).
It has been hypothesized that the lifespan-extending effects of caloric restriction (CR) are mediated by mTOR (one can see why - mTOR is affected by nutrient availability). In fact it may depend on the method of CR;
Greer et al [4] report that different methods of CR in C.elegans, for instance feeding them a diluted food source, or conversely feeding them on alternate days, do not necessarily require the same genetic pathways. Not only this but CR combined with a genetic mutant (eat-2) have additive lifespan-enhancing effects.
So whilst the evidence is not concrete, and I look forward to other studies in mammals similar to the one by Greer et al, it looks as though rapamycin and CR have similar but not exactly the same effects on lifespan; rapamycin specifically inhibits an individual pathway which is involved in many processes, and some of its effects are not necessarily desirable (e.g. rapamycin inhibits the immune system [5]). On the other hand, CR (most of the different types) seems to be mediated by mTOR - this difference is critical: mTOR is not necessarily inhibited by CR, it is just required for its effect.
Therefore combining rapamycin and CR is unlikely to have an additive effect as rapamycin may override any influence CR has on mTOR signaling, but I have not seen a study in which this has been tried. Combing different methods of CR (or developing drugs to do just that) may well have additive lifespan-enhancing effects.

Harrison DE, Strong R, Sharp ZD, et al. Rapamycin fed late in life extends lifespan in genetically heterogeneous mice. Nature. 2009;460(7253):392-5.
Colman RJ, Anderson RM, Johnson SC, et al. Caloric restriction delays disease onset and mortality in rhesus monkeys. Science (New York, N.Y.). 2009;325(5937):201-4.
Weber JD, Gutmann DH. Deconvoluting mTOR biology. Cell cycle (Georgetown, Tex.). 2012;11(2):236-48.
Greer EL, Brunet A. Different dietary restriction regimens extend lifespan by both independent and overlapping genetic pathways in C. elegans. Aging cell. 2009;8(2):113-27.
Thomson AW, Turnquist HR, Raimondi G. Immunoregulatory functions of mTOR inhibition. Nature reviews. Immunology. 2009;9(5):324-37.


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Effect of extracellular molecules on membrane potential
I am reading about the effect of extracellular potassium and chloride on the membrane potential, and now a question has come to my mind about what would happen if we added some molecules that have no charge to the extracellular? (consider that only K+ and Cl− can cross the membrane.)
I think that membrane potential and volume does not change, but I'm not sure about that.

@MCM I cannot add comment after the great answer of MCM. Thank you alot. Then this means the volume also increase?

I'm wondering if you don't mean increase the volume of the cell - in which case, in extreme conditions where the cell cannot maintain water and salt concentrations, the cell would lose volume as water and salts move out. In a hypotonic solution (much more water than solutes), the cell would lyse as osmotic pressure favors water moving into the cell.

The absolute answer would depend on a lot of factors, but the basics of it would be that - Yes, the volume does change and Yes, it would have an affect on the membrane potential.
By adding mass to any liquid solution, you are changing the volume. Plain and simple. Liquids are not compressible, and the only way to maintain volume while adding mass would be to increase the density of the liquid. [Edit] I'm wondering if you don't mean increase the volume of the cell - in which case, in extreme conditions where the cell cannot maintain water and salt concentrations, the cell would lose volume as water and salts move out. In a hypotonic solution (much more water than solutes), the cell would lyse as osmotic pressure favors water moving into the cell
The membrane potential would change, but how much depends on a lot of factors. It would most likely change due to the movement of ionic solvents down their concentration gradients. Osmosis would move water out of the cell and into the extracellular environment, and ultimately reduce the membrane potential as more water outside the cell would essentially decrease the molarity of the solution. The cell would have to pump more ions out in order to regain the membrane potential.
The exception might be if you added so many hydrophobic molecules outside the cell that you basically saturate the environment, which could prevent exchange of all charged or partially charged atoms and molecules.

"The cell would have to pump more ions out in order to regain the membrane potential." So any change would be transient?

@AlanBoyd - Correct. The cell has the ability to open or close ion channels (free exchange down the gradient), and decrease or increase ion pumps (active transport). If the solution is hypertonic, the cell can open channels until the membrane potential is regained. If the solution is hypotonic, the cell can expend energy via ion pumps to move atoms into solution. This is particularly pronounced in neurons, where signal propagation relies on the membrane potential's existence (and is a little bit higher than your average cell). Barring extreme conditions, of course. Cells can't always cope.

A bit of an addendum: The cell almost never completely shuts down ion channels or pumps. The membrane potential is balanced between the two (and some other players).

I'm no electrophysiologist, but I do know that the membrane potential is determined by the distribution of ions across the membrane: mostly Na+, K+, Ca2+ and Cl-.
An uncharged molecule will only influence membrane potential if it has an effect upon the distribution of these ions. One example of such a molecule is valinomycin, a neutral ionophore which permeabilises membranes to K+ ions. Another example is ouabain which inhibits the Na+/K+ pump that is in part responsible for establishing resting membrane potential.
But in general the addition of uncharged molecules will have no direct effect upon membrane potential.
(I expect that there will be someone along shortly to explain why it is much more complicated than this.)
edit: It turns out that MCM got here before me!

Remember also that plenty of molecules have receptors on the membrane that can cause membrane potential to change, directly or indirectly.

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sort: votes


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What is the distinction between F' plasmid and R plasmid?
Is there a difference between an F' plasmid that has taken up a chromosomal gene that conveys antibiotic resistance, and an R plasmid? Is a bacterium containing an R plasmid and yet lacking an F+ plasmid capable of horizontal gene transfer by conjugation?

Can’t help myself …relevant (but here the better word would be “explanation”). Ed Yong thinks to, too.

Explanation isn't really the word I'm looking for, as I do know what the terms mean individually, but not in relation to each other. I'll edit it to read "distinction".

If I understand the nomenclature correctly, an R plasmid is just any plasmid containing an antibiotic (R)esistance gene (eg. Amp, Kan, Cm, etc.). It's a bit of an outdated name from when people didn't know how exactly the plasmids conferred such resistance.
An F-plasmid is any plasmid that contains the genes necessary for (F)ertility, eg:horizontal gene transfer via the tra operon.
The two do not have to appear together -- eg: Many F plamids will contain resistance genes (along with other random chunks from the genome), but resistance doesn't always have to be part of the payload. Likewise, it is common in labs to build pure resistance vectors that lack any horizontal transfer capability in order to select for particular clones.

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Do wolves bury food like dogs?
Many breeds of domestic dogs seem to like burying food, presumably in preparation for leaner times.
Assuming that dogs evolved from animals similar to the modern wolves through a mix of natural and artificial selection, is this burying behavior novel in dogs, or inherited from wild wolves? Do wild wolves also habitually bury food, and return to their caches when hungry?

The habit of burying food in modern dogs is an instinct that came from the grey wolf (Canis lupus) long ago, and originates from a phenomenon called surplus killing, where a carnivore would kill more than it could eat, and often use it at a later time.

Many, if not all, carnivores possess behaviour patterns which allow utilization of a kill at a later time, or allow other members of the same social unit or offspring to use the food.

When the prey is small enough to transport, and there are pups, it is often returned to the den.

Pups will usually remain in their den for the first three or four weeks of their lives before mother allows them to venture forth into the light. During this time the mother is quite dependant on her mate and other pack members to bring her food in the form of meat that is often regurgitated for her.

It is then fed on by the litter, and the excess buried for later use.
This is called 'caching', and is still seen today in the domestic dog (Canis familiaris).


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Why doesn't honey spoil quickly?
Why is it that honey can last for decades and not spoil like other foods? Is there any chemical in honey which gives rise to this amazing feat?

see http://biology.stackexchange.com/questions/19744/sugar-as-a-defence-against-bacteria

Based on Alan Boyd's link I think this is a dupe.

One reason is that sugar has a pH of 7, while honey has a pH of 3.26 to 4.48, a killing field for bacteria. Also, bees process honey by means of an enzyme called glucose oxidase, AKA 'Penicillin A' (formerly) or 'Notatin', which reduces atmospheric O2 to H2O2 (Hydrogen peroxide), forming an antimicrobial barrier on the honey surface. Also, bacteria become desiccated in honey because of the hygroscopic effects of the sugar (mostly supersaturated in honey). Basically, related, but not a duplicate question.

@daniel pls reopen the post. as J. Musser mentioned, it's definitely not a duplicate.


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How do we know the presence of light when our eyes are closed?
Last night I laid on my bed and tried to go to sleep with the light off.
I closed my eyes (but hadn't gone to sleep). My younger brother touched the wireless mouse (which had laser) for the laptop.  He wiggled the mouse and it's laser contacted my closed eye . I knew some light was thrown on my face, and it's color was red. The laser on the mouse was actually red. So my question is, when my eyes are not functioning (not seeing, closed) how did I come to know that there was a light aimed at my eyes, and it was red?

There are two reasons for light to appear red through the eyelids.

Eyelids get a rich supply of blood which contains iron (in hemoglobin). The iron in blood absorbs all colors of light but reflects red light. (reference)
Our tissue transmits red wavelengths of light very well, but it doesn't transmit blue or wavelengths of light towards the blue end of the spectrum very well. So, the blue light is absorbed by the skin, while the red light travels through. When this light hits our eye through our eyelids, it is mostly red. (reference).

Also, as Rickard Sjogren said, the eyelid is a thin membrane and allows light to pass through.

Short answer, your eyelids does not block all light. Since they are only a thin layer of skin, the light is able to pass through although not completely obviously. Since the eyes are still completely functional when you close them, only covered by the eyelids, you are able to see when light strikes your face.

Most people can see a bright torch (flashlight in US English) or desk lamp through their hand, which is a good deal thicker than eyelids. If anything, the surprising thing is how dark it is with your eyes closed.

@pete kirkham very interesting point ! Why dont u convert this into a question ?


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How many times can a human get chicken pox?
How many times can a human get chicken pox?
For example: I got chicken pox, and recovered. If I was infected with HIV, and I am exposed to chicken pox again, can it infect me second time?, According to what I've heard, chicken pox comes only one time, because of the immune system of humans. But if I am infected with HIV and so definitely have immune system damage, will chicken pox come a second time, or will the immune system still protect the body from chicken pox?

after INFECTED with HIV,i am guessing shingles will come instead of chicken pox. but i have a doubt in this.

Suggestion: I think this question would be more useful for future reference if rephrased along the lines of: Can immunocompromised individuals be infected multiple times by diseases that you normally only get once in your life?

Usually you get chicken pox only once in your life, the recurring form are usually shingles.  But: It can happen (also in people which are not immunocompromized). I know two persons which got chicken pox twice and which are otherwise normal in regards of their immune system.
Persons with an HIV infection are more at risk here. They can develop both forms and depending on how much their immune system is already affected by the HIV infection can develop severe forms of the infection. It might be necessary to treat them with antiviral drugs. So it is clearly recommended to ask a MD about this. See here for more details.


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How did these apples grow together?
I came through this pic while scrolling through facebook, and it was a bit strange to me.
As far as I know apples have a corymbose type of inflorescence, in which a single pedicel ends in a single thalamus.
And I am totally sure that the edible part, which is fleshy in the apple, is thalamus. How did this fruit came into existence?
I want a biological answer for this query.

They are basically conjoined apples which share a common stalk. They are rare but do happen. Here is an article of one discovered in a backyard.

conjoined apple discovered in a store (reference)
It apparently happens because of bad weather conditions, stress and insect damage. Fused fruits are also found in the case of cherries, watermelons, peaches etc.

Inadequate pollination because of heat and other adverse growing
  conditions causes that section of the fruit in which the seed did not
  develop to not grow and fill out. Also, the fruit primordium
  (embryonic growing point) can be damaged or altered by environmental
  factors and cause strange growth forms. Of course, Siamese twins or
  two fruit growing together is also rather common(reference).

Read more about them on article 1 and article 2.

that was very well explained thanks for this answer.


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When is the lactase in lactose-free milk active?
Recently we have started suspecting that one of our children has hypolactasia (lactose intolerance), and so accordingly I have had my first exposure to lactose-free dairy- and dairy-like products. In addition to soy milk and almond milk, we have recently purchased actual dairy milk that was labeled lactose-free. This gave me the impression that they had used some process to remove the lactose, but looking at the ingredients more closely, it seems that they simply added lactase enzyme to the milk to assist breaking down the sugars.
My question is this: when is the lactase enzyme active? Does the lactase activity begin right as it is added to the milk, or will it not become active until ingested?
Essentially, I'm wondering if this type of milk can/should be used in cooking or baking. High temperatures will certainly denature the lactase enzymes in the milk, but if the lactose has already been broken down, this shouldn't be a problem.

Having done an inordinate number of rather mind-numbing A.S. practicals involving milk and enzymes the year before last, in my experience lactase always began breaking down the lactose immediately and converting a boiling tube worth of milk in less than 50 minutes at below room temperature.
To further allay your concerns, this website suggests that most Lactose Free milk has undergone UHT treatment - therefore cooking shouldn't be a problem as the enzymes have presumably been added before the pasteurisation, and are therefore denatured - I can't see why you'd then go to the extra trouble of adding the lactase aseptically after pasteurisation; and if the lactase shows in the ingredient list it presumably wasn't done with immobilised enzymes in the factory.

I would just add that lactase has an optimum temperature of action of 25 °C and an optimum pH of 6. So, for sure the stomach (very low pH) is not the good place for it to function.


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Why does a gene have two alleles?
Why does a gene have two alleles?
When there is a gene for producing the color pigment for a flower, why are there there two alleles, producing either same color or different color (homozygous and heterozygous)?

To sustain our species

I'm not sure exactly what question you're asking.

Have you done any research at all?

So which factor decides a specific allele to be expressed and the other allele to remain repressed

Allele is a variant form of a gene. How many alleles there are depends on number of copies of the gene and number of variants. In theory you can have 5 identical copies or single copy and single allele (Y-linked genes come to mind).
Regulation is very complicated, I'll refer you to reading on recessiveness, dominance. Barr bodies also have to do with various expression profiles in same thing.

A flower (or a person) has two alleles for a gene because it inherits one set of chromosomes from one parent and another, comparable, set of chromosomes from the other parent.  Hence there are two copies of each gene, and so there are two alleles for each gene.

So which factor decides a specific allele to be expressed and the other allele to remain repressed

In a heterozygous diploid cell, typically both alleles are expressed (parental imprinting is a well-known exception to this statement).  However, if, as in Mendel's pea plants, one allele is wild type and one is mutant, than whichever allele is dominant will be expressed (or in other words  have a visible phenotype that you can score).  Co-dominance is a rare exception to this statement--if two alleles are co-dominant then each homozygote has a different phenotype, but the heterozygote has a third phenotype. For example, the mating type locus in baker's yeast.


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Why does allele linkage cause disproportionate phenotypic ratios?
I was learning about allele linkage in Biology class and I got confused by the resultant phenotypic ratios.
Say you have a dihybrid cross BbGg x BbGg.
The Punnett square would look like the following (sorry for bad formatting):
     BG...... | Bg.... |  bG.... |  bg

BG   BBGG       BBGg      BbGG      BbGg
---  -----------------------------------
Bg   BBGg       BBgg      BbGg      Bbgg
---  -----------------------------------
bG   BbGG       BbGg      bbGG      bbGg
---  -----------------------------------
bg   BbGg       Bbgg      bbGg      bbgg

So:
This would result in a a 9:3:3:1 phenotypic ratio. (Dom/Dom : Dom/Rec : Rec/Dom : Rec/Rec)
However, if the alleles B/b and G/g were on the same chromosome, the ratios turned out to be around 4:1:1:4 in an example (still Dom/Dom : Dom/Rec : Rec/Dom : Rec/Rec)
The stated reason was that there would only be Dom/Dom and Rec/Rec, and the Dom/Rec and Rec/Dom only showed up due to crossing over. However, this begs the question: Why could Dom/Rec and Rec/Dom not have occurred prior to recombination? My reasoning is that just because the alleles are on the same chromosome does not mean that they must both the autosomal chromosomes for the allele must have either a dominant genotype or recesssive phenotype. That is, before crossover, there should still be a 9:3:3:1 random distribution between phenotypes represented by genotype sets (BbGg/BBGg/BbGG/BBGG):(Bbgg/BBgg):(bbGg/bbGG):(bbgg).
Note: when I say dom/rec for example, I mean that for the first allele the character represented by BB or Bb was expressed, and the "rec" means that for the second allele the character represented by gg was expressed. I am assuming autosomal dominance for simplicity.
If anything is unclear, don't hesitate to comment. I'm pretty tapped out right now. Thanks, hob

What do you mean by "if the alleles B/b and G/g were on the same chromosome"? Are you saying that the parental genotype is BG/bg? Chromosomes are inherited as a unit. Without crossing over, if the parental genotype is BG/bg, only either BG or bg can be passed on. This means the offspring could be BG/BG, BG/bg or bg/bg.

No, I mean that allele1 that encodes for B or b and allele2 that encodes for G or g are on the same chromosome. Thanks!

I think you have the wrong terminology. You,re saying that the genes which encode for B or b and G or g are on the same chromosome. This is the situation I described in my first comment. The answer to your question depends on what the parental genotypes are.

Could you be more specific as to what your question is?

I found the explanation at this site helpful:
http://www.ndsu.edu/pubweb/~mcclean/plsc431/linkage/linkage1.htm
I don't have a clear sense of what you mean when you ask about assorted phenotypes occurring before recombination ("crossover"). All of your examples deal with diploid organisms. If they are multicellular then the cells that can undergo meiosis are highly specialized, and eventually become haploid. As the chromosomes are prepared they tend to become compact, and are often not expressed. So it is difficult to assess the phenotype of those haploid cells. The rest of the cells in the organism are diploid  and at least some of them can express the alleles that give rise to the phenotypes that you are scoring.
At the moment of fertilization there is no further recombination, as the zygotic cells undergo mitosis.  There is no segregation, no independent assortment, no linkage (that you can measure--the genes are still arrayed along their chromosomes). Each mother cell divides to give two perfect copies of itself. Then the daughters divide, etc. Even in the cells that are going to become germ cells, they divide by carbon copy mitosis right up until they enter meiosis.
So there is no mechanism that would lead to genotypes different from the genotype of the zygote (until meiosis).

But in the genotype of the zygote, it would be possible for it to be bG, for example, right? Therefore after meiosis, bbGG would occur without crossing over, which means that the thing I was taught about BBGG and bbgg being the only possibilities before crossover would be false, right?

As your Punnett square shows, when a bG sperm fertilizes a bG egg then yes, 100% of the viable zygotes will also be bG.  In the notation you are using, to indicate both alleles of each gene, you would write it as bbGG as you have. IF the B gene and the G gene are not on the same chromosome (unlinked), THEN you could draw it like this: b/b; G/G. In contrast, if the B gene is linked to the G gene on the same chromosome, then you could draw it like this: bG/bG. The bbGG notation you have been using does not distinguish between these two different situations.

authors: Даниела Ангелова


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Book recommendations for algorithms used in evolutionary biology
Do you have recommendations for a book that presents the different algorithm used in theoretical evolutionary biology?
I don't mean evolutionary or genetic algorithms (otherwise this question would not be a good fit for Biology.SE) but algorithms applied to evolutionary biology. I am not interested in statistical procedures and algorithms to reconstruct phylogenetic trees, to annotate DNA sequences or to find out synonymous changes by comparing sequences of closely related species. I am not interested in introductory book on programming.
I am interested to computational modeling applied population genetics, kin selection, game theory, population range expansion, simulating sexual reproduction, selection for different sex determination system, evolution for robustness/evolvability, evolution of codon usage, evolution of genetic code, evolution of cognition, evolution of multicellularity, …
I don't quite know if one book that encompass all these subjects exist. If not, I wold welcome suggestions of book that present the algorithmic used in some but not all of these subjects.
Searching a bit in amazon, I easily found tons of book but don't quite know if they fit my expectations. Below are some examples
Evolution as computation
Individual based modeling and ecology
Models and algorithm for genome evolution
modelling for field biologists
Practical computing for biologist
Evolution as computation
Genetic and evolutionary computation
Genetic algorithms+ data structures = evolution programs
The missing algorith
Cellular Model: Mathematical and theoretical biology, Algorithm, Data structure, Bioinformatics, Computational biology, Artificial life, Computer simulation
Natural-Artificial-Models-Computation-Biology
An-Introduction-Genetic-Algorithms-Paper

Derek Roffs modelling evolution and another book I'm trying to think of (maybe by Otto) touch on some of these subjects.

Rather than asking people to click 10 links, can you add the titles as a list (with links)?

I have to agree, I didn't bother to check them all (because I'm reading on an iPhone)

@GriffinEvo I don't think Sarah Otto ever wrote a book about algorithmic. She wrote this book which is about mathematical modeling. The equivalent of this book but with the tools of algorithmic rather than mathematics would be a good answer to my question.

What you are describing usually falls under the category of computational biology or just mathematical biology. Unfortunately, the biggest part of this field is bioinformatics, or the application of statistical and/or dynamical programming techniques to sequence data. You exclude this in your question, and I would agree with you that it is a "boring" topic from a theoretical biologist's perspective, because it mostly uses computer science in a very standard way as a tool for experimental biologists.
As you noticed, it is also standard to use computational models in theory papers as a way of simulating things. I think this is the sort of resources you are asking for. Unfortunately, specific algorithms are seldom standardized or reused in this area. Typically, each paper (or sequence of related papers) uses their own models.[1] As you read a lot of papers, you will find some common themes, but these are just standard ideas of theoretical biology expressed as simulation. I doubt that comprehensive books exist, and even if some do their utility is not clear to me due to a lack of specific algorithm (re)use.[2] However, the most commonly used techniques are to either to solve differential equations numerically (which most would classify as mathematical modeling) or run agent-based or population-based models. General resources on these exist, and here are some discussions for the latter other SEs:

Simulation modeling of diseases.
Sources for Algorithmic Evolutionary Game Theory.
Canonical reference on agent-based computing.

Finally, do not confuse 'computational modeling in theoretical biology' with 'algorithmic biology'. Algorithmic biology is a new field that views ecological and evolutionary dynamics as computatioanl proccesses. Instead of using mathematical tools borrowed from physics (as is standard with the dynamic systems approaches to mathematical biology), it uses the tool of theoretical computer science (note that this is a type of math that has very little to do with programming the laptop infront of you). I know of only two books in this field:

Gregory Chaitin "Proving Darwin: Making biology mathematical" - Although Chaitin had contributed significant and original thoughts to computer science in the past, I would strongly advice against this book because it misses the point from both the biological and computer science point of view.

Leslie Valiant "Probably Approximately Correct: Nature's algorithms for learning and prospering in a complex World" - in this book (based on earlier papers), Valiant recasts evolution as a type of machine learning. This is very interesting from a mathematical point of view, although it might not connect directly enough to biologically relevant questions (see also some of the discussion in Kaznatcheev (2013) and Kaznatcheev (2019)) and misses the computational power of frequency-dependent selection (see Kaznatcheev (2020)). But I would recommend reading this book.

Notes

In general, I consider these sort of models as heuristics and I am skeptical of their usefulleness beyond rhetorical devices/examples.
I think that literature reviews would be interesting computational modeling in specific subfields. In fact some colleagues and I have wanted to do this for the smaller area of evolutionary game theory (This answer can serve as a starting point for some algorithmic considerations of EGT).

Have you looked into "Fundamental of Molecular Evolution" by Dan Graur & Li.
Another suggestion in line of population genetics and different evo. theories would be -
Evolutionary Genetics: Concepts and Case studies
(Multi-author book. Editor Fox & Wolf)

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text:
Should I dilute DNA with water or elution buffer?
I've extracted DNA using a kit and final step is eluted with buffer. If I must dilute my DNA samples, do I use the same elution buffer or can I use milliq water?

Just a note, the Qiagen TE buffer has significant UV absorbance around 230nm. Been too long since I did that spectra to remember exactly how much or what wavelength, so just be aware of that if you need spectroscopic measurements of your DNA. Absorbance at 260nm should be fine.

I would generally recommend using the elution buffer (which is typically Tris-EDTA buffer) or TE-Buffer, as the pH and the conditions stabilize the DNA for a longer time, which is especially interesting when you want to store your DNA.
It also dependent on your downstream application - when they recommend diluting the sample in water (or another buffer) I would follow this advice. In my experience TE buffer is perfect for all molecularbiology applications (cloning, digestion, amplification, PCR, etc.). The EDTA will of course complex bivalent cations, but since the concentration in the buffer is only 1mM and the DNA solution is usually diluted further in PCR or digests, this plays no role in real life applications.

The Quiagen kits I'm familiar with explicitly state that you can use water instead of elution buffer for elution. The choice of continuing to use buffer or water is yours and depends on what you want to do with the DNA and whether the buffer interferes with later steps. Using the buffer is probably safer for long-term storage, but I don't know how much this really matters (I never had any problem storing DNA in water).
If you dilute with water you'll obviously end up with a weaker buffer that might not be able to keep the pH at the specified value. So if you need your DNA at the elution buffer pH, you shouldn't dilute it.

Just to add to the above responses, you are better off not use MQ because if it is contaminated with DNases, then it will digest your construct if it reaches room temperature or 37 oC as you are melting the frozen construct in your hand! TE-buffer is the standard buffer for DNA elusions but make sure your column is compatible with it. For transfection based experiments TE works fine for me!


text:
Self pairing in DNA
I know that ssRNA molecule can fold over itself (e.g. in t-RNA). Can DNA do the same? Is there any example of this in nature?
Why is this phenomenon more common in RNA than in DNA?

Are you talking about single stranded DNA?

You may also be interested in DNA supercoiling.

Does this answer your question? Can DNA produce ribozyme-like structures?

DNA can adopt secondary structures like RNA, the main difference is that DNA is usually present as double-stranded DNA while RNA is in most cases present as single-stranded RNA. Double-stranded DNA won't easily adopt any other conformation than the well-known double helix as this one is more stable than possible structures each single strand could adopt on its own.
One example that occurs in nature are G-Quadruplexes which for example occur in telomeres.
There are also artificially created DNA enzymes (also called DNAzymes or deoxyribozymes) that adopt tertiary structures like ribozymes do. But there are no known DNA enzymes that occur in nature as far as I know.

Could you add a link for the DNA (deoxy)-ribozymes? Sounds cooks and I had not heard of them.

@terdon I've added a Wikipedia link. The first one was created by Ron Breaker (who's more famous for having found most of the riboswitches we know so far), if you're looking for some newer papers on this I'd look for Scott Silverman, he has written a few reviews on the topic.

Good answer; might benefit from mentioning ssDNA viruses as the most common natural occurrence of ssDNA, as well as other dsDNA conformations (A, B, Z)


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Excretion of monovalent and divalent ions in sharks
I have heard that sharks excrete $\ce{Na+}$ and $\ce{Cl-}$ by their gill surfaces but divalent ions like magnesium are excreted through feces. What could be the reason behind this?

You want the reason as in why such a behaviour would have been evolutionary beneficial or adaptively useful or as to what anatomical mechanisms make divalent ion removal through gills (or vice versa) not possible?

@SatwikPasani I actually want the physiological mechanism but I'll love to learn any evolutionary advantage.

divalent cations tend to form less soluble salts than monovalents, such as calcium phosphate. If you tried to excrete these through the gills it would probably lead to the build up of calcified deposits on the gills and damage the tissue and decrease gas transfer surface area. This isn't a problem if you dump the cations into solid waste.

@user137 Thanks. Why dont you convert this into an "answer" and add some references ?

The main reason seems to be a mechanism to save water and allow the excretion of higher concentrations of the ions. See the image (from here):

The urine enters the glomeruli at a relatively low rate and with a low magnesium concentration. The paper cited below mentions a concentration of 1.5mM. First organic compounds as glucose are recovered actively, water follows the molecules passively. Then more ions as Ca$^{2+}$ enter in the proximal segment II. In the distal segment finally sodium and chloride are actively transported out while water passively leaves the segment. The divalent ions (magnesium, calcium) are left in high concentrations (the paper below says that the Mg concentration is now around 130mM). This helps concentrating these ions for excretion while loosing as little water as possible at the same time. Sodium and chloride are actively regulated in the gills.
For a short overview, see the link at the image above, for a detailed view, have a look at the following publication: "Kidneys sans glomeruli".

Could there be a reason why this happens for calcium and magnesium not for sodium and chlorine ?

I have only found a hypothesis. First it seems a matter of energy (the transporters actively use ATP) and the nutrition. There is a paper about this, but I haven'T got hands on it.


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Concentration of DNA by isopropanol
I have read that DNA can be concentrated by addition of isopropanol.
What does "concentrated" mean? What does isopropanol do on a molecular level to concentrate DNA?

What you are asking about is the precipitation of DNA (or any other nucleic acid) by isopropanol (or ethanol, which is more common). To do so, you add salt (usually slightly acidic sodium acetate) which makes sure that the phosphate backbone of the DNA is saturated with sodium ions to make it less soluble. Then you add the organic solvent, which precipitates the DNA from the solution by changing the polarity of the solution. This makes the ions form salts and the DNA precipites. The principle is explained in the Wikipedia article on ethanol precipitation. Finally the solution is centrifuged to collect the DNA at the bottom of your reaction tube and to be able to take off the supernatant.

Small addition: Isopropanol having a bigger alkyl group makes the solution more organic in nature compared to ethanol. Why isopropanol and not n-propanol is perhaps because it is easy to manufacture isopropanol. n-propanol is better at precipitating smaller nucleic acids.

It is because isopropanol is less toxic in the handling than n-propanol. n-propanol can cause severe eye damage and is generally more toxic than ethanol or isopropanol.

Point taken. but it is also easy to manufasture isopropanol :P

@Chris.. I am not sure why you say n-propanol is more toxic. It can be easily metabolized to propionic acid. This article says that isopropanol is more toxic in terms of longlasting effects.

This is mostly about potential eye damage though n-propanol (by splashes). This MSDS says for example "Eye contact with n-propanol may cause severe irritation with corneal injury, which may result
in permanent impairment of vision, even blindness."


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Proportion of amino acids from a random polymer of U and C

A protein synthesis assay was carried out in vitro. A
  polyribonucleotide containing U and C in proportion 1:5 (positions of
  U and C are random) was used as a template. Which amino acids and in
  what proportions will be incorporated into the synthesized polypeptide
  molecules?
А. 1Phe : 5Pro : 3Leu.
B. 1Leu : 1Pro : 1Ser : 1Phe.
C. 1Phe : 5Ser : 5Pro : 5Leu.
D. 1Phe : 25Pro : 5Ser : 5Leu.
E. 5Leu : 5Pro.

First thing I am not sure is whether only U and C is there. I have tried solving this sum taking both the conditions into consideration . I also tried solving it from options but could not succeed.

The first thing to mention is that this is the type of experiment that Marshall Nirenberg performed in order to break the genetic code, and for which he got the Nobel prize in 1968. We stand on the shoulders of giants.
If the ratio is U:C, 1:5, then it is easy to calculate the probability of encountering each of the 8 possible codons composed by just U and C. So for example:
the probability of UUU is (1/6)3
the probability of UUC is (1/6)2*(5/6)
and so on.
Here's a Table that gives all of the values and demonstrates that the answer is (D).


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How does the cornea breathe during sleep?
The cornea is not supplied with blood vessels and so exchanges gases directly with the atmosphere. So how does it breathe during sleep when our eyes are closed?

As you noted, the cornea needs oxygen, yet it's not vascular. It needs to get it's oxygen supply from diffusion. In the daytime, diffusion occurs from air through the tear film covering the cornea.
The cornea spends about a third of it's lifetime under closed lids. At night, the tear film remains intact and is continuously replenished. The inner aspect of your eyelids, called the palpebral conjunctiva, are highly vascularized, with capillaries just below the surface (and accessory tear ducts and tiny mucosal glands to keep it moist).
When you sleep, oxygen (and nutrients) diffuses from the palpebral conjunctival capillaries through the tear film to your cornea.
The blood vessels in the palpebral conjunctiva are more permeable than most other capillaries and contribute fluid and nutrients to tears by leaking plasma. The surface epithelial cells are also a source of tear fluid because of a special arrangement of the cells such that there is more intercellular space allowing fluid, antibodies, and other plasma constituents to the surface of the conjunctiva.
This very issue was of great concern to ophthalmologists when people started wearing extended-wear contact lenses.
The Conjunctiva and Lacrimal System (www.eyecalcs.com/DWAN/pages)
Organization of Capillaries in the Primate Conjunctiva
The Conjunctiva—Structure and Function (oftalmologia/enciclopedias)
The oxygen tension and temperature of the superior palpebral conjunctiva
Facts About the Cornea and Corneal Disease (cool article)

If the palpebral conjuctiva doesn't work properly, can it cause blindness ?  Are there any reported cases ?

@biogirl - yes, it can and does cause blindness, most commonly in dusty, sandy, dry climates.


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Can cell exist without Ribosomes?
Last night I came across a question that goes as follows:-
Cells cannot exist without
a) cell wall
b) cell membrane
c) mitochondria
d) ribosomes
I am getting confused with option B and option D

If RBC is lacking ribosomes then where the antigen proteins on RBC are coming from ?

The most essential thing for a cell to survive is a membrane. Without a membrane there is no boundary between cell and its surroundings. A selectively permeable membrane is needed for cells (from single celled organisms to elephants and giraffes and whales) to survive. Cells will die quickly on removal of cell membrane.
The RBCs are good example of cells without mitochondria or ribosomes which survive for 120 days.

Please read the article on Erythropoiesis for detailed information on how RBCs form and how they have proteins in their surface.
In short, the RBCs acquire the surface proteins during their formation period in the bone marrow. Inside the bone marrow the premature RBCs have nucleus, ribosomes, mitochondria, etc... and produce all the required structural and functional proteins. On maturing they loose the nucleus and cell organelles and contain only hemoglobin in their cytoplasm.

If RBC is lacking ribosomes then where the antigen proteins on RBC are coming from ?

I have edited my answer @DhrubaBanerjee Please see if it answers your doubt. Please read the article on Erythropoiesis

There is no cell without a membrane :P (A cell by definition has to have a membrane). Self sustaining cells do need ribosomes but they can survive without mitochondria (prokaryotes anyways don't have one and there are eukaryotes without mitochondria such as Entamoeba)

Good one @WYSIWYG. Really good, lol

There exist some accounts of temporary stages that lack a cell membrane. If these represents a form of cell question of definitions. SSee e.g. http://www.biomedcentral.com/1471-2180/11/255

@fileunderwater very interesting. Thanks for the link.

@fileunderwater The statement in that article seems doubtful. First they say "protoplasts" and then they say "without a membrane". Protoplasts are plant cells without walls but they still have membranes. Without a membrane (long enough to be called a stage) the cell would have no boundaries and therefore the definition of a cell no longer holds (more like a cell lysate)

@WYSIWYG I cannot really evaluate this research, and was just curious about what papers are out there. There are a couple of other articles as well, e.g. http://www.ncbi.nlm.nih.gov/pubmed/12111719 and http://jcs.biologists.org/content/114/11/2009.short. As I said, whether these are cells is a question about how you define a cell. It seems like they survive for ~10h before a new membrane is formed (a "gelatinous envelope" is formed before that though). Quote: "Nucleocytoplasmic aggregates,  ... released after injury ... are membraneless structures that can survive in seawater for 10–20 min."

@fileunderwater Interesting. This means that the enzymes can function in seawater and also there should be some way of preventing diffusion of cellular material(the gelatinous envelope perhaps)

@WYSIWYG Yes, also interesting with regard to the origins of life, since it shows another way that replicating structures can be compartmentalised (at least temporarily).

Cells can survive without ribosomes, but they would accumulate damage and be unable to restore worn out or exhausted supplies of any proteins they may require. The ribosome is necessary to be able to perform protein translation from RNA. Thus, if the cell can survive without protein, then it would be able to survive without ribosomes. No known organism that exists today meets that definition, if I am not mistaken. However, at some point, it is theorized that the earliest cells were able to perform replication and metabolism without the use of protein. So, it is likely, but not something that is seen in life today.
Nicholas H. Barton Derek E.G. Briggs Jonathan A. Eisen , David B. Goldstein and Nipam H. Patel.(2010). Evolution. Cold Stone Harbor Laboratory Press.

Nicholas H. Barton Derek E.G. Briggs Jonathan A. Eisen , David B. Goldstein and Nipam H. Patel.(2010). Evolution. Cold Stone Harbor Laboratory Press.


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What is "chain identifier" in PDB?
The PDB file format is explained here. My question is what "chain identifier" is exactly? What is the difference between two residues which have the same sequence number but different chain identifiers?

The "chain identifier" does exactly what it says: it identifies the polypeptide or other molecular chain. For some structures, there is only one, so you'll only see an identifier A. However, many structures show two or more proteins bound together, or an enzyme complexed to a substrate, or a small molecule inhibitor in a binding pocket - there are many different possibilities. Each individual chain of atoms has its own identifier.
For example, 1VKX shows my favorite transcription factor NF-κB bound to the κB DNA enhancer sequence. There are four chains in the structure: two polypeptide chains, the p65 subunit A and the p50 subunit B, and two DNA chains C and D, one for each strand (forward and reverse).


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Why do cucurbits produce so much fluid when their stems are cut?
When carrying out some germination tests on species in the Cucurbitaceae, I notice that young plants of this family produce a lot of clear fluid when they are dissected. Most plants I dissect do not produce any fluid, even ones which appear to be turgid and have large cells. Why do cucurbits do this, and what's the fluid?

So do daffodils.

Members of the Cucurbitaceae family (squash, pumpkin, cucumber, melon etc.) are unique* in that they possess two distinct phloems, see figure below. The fascicular phloem (FP) is the main transport conduit, and more closely resembles the phloems of other plant families. Its role is to transport photosynthates and other nutrients (Turgeon & Oparka, 2010).The extra fascicular phloem (EFP), is more minor and has an atypical composition for a phloem. Although we have been aware of this dual phloem system for centuries (Crafts, 1932; Fischer, 1883, 1884, 1886), it is often ignored!!
The minor strands of EFP have been found to be the source of the extreme bleeding observed in cucurbits (Zhang et al., 2010). However this excessive bleeding has meant that cucurbits are a very popular model plant for phloem composition studies, since copious amounts of phloem contents are easily accessible. This is problematic since we now know that the exudate originates from the atypical EFP strands, making it a poor model (maybe is isn't even a phloem at all)!
The reason that the EFP does not block upon wounding is that it lacks blocking and sealing mechanisms (such as P proteins and pectins), which usually exist in order to protect the phloem from damage or disease, and to prevent the loss of vital metabolites. The fact that these are not present in EFP, along with the fact that EFP is rich in defensive proteins (Walz et al., 2004), may suggest a defensive role for this secondary phloem. Its anatomical placement around the vital vascular transport conduits supports this idea.

*No others are known, but could definitely exist.
Bibliography

Crafts, A. S. “Phloem Anatomy, Exudation, and Transport of Organic Nutrients in Cucurbits.” Plant Physiology 7, no. 2 (1932): 183–225.
Fischer, A. “Das Siebröhrensystem von Cucurbita.” Berichte Deutsche Botanische Gesell 1 (1883): 276–279.
Fischer, A. “Neue Beiträge Zur Kenntniss Der Siebröhren.” Berichte Über Die Verhandlungen Der Königlich-Sächsischen Gesellschaft Der Wissenschaften Zu Leipzig, Mathematisch-Physische Klasse 38 (1886): 291–336.
Fischer, A. Untersuchungen Über Das Siebröhren System Der Cucurbitaceen. Berlin, 1884.
Turgeon, R. and Oparka, K. “The Secret Phloem of Pumpkins.” Proceedings of the National Academy of Sciences 107, no. 30 (2010): 13201 –13202.
Walz, C. and Giavalisco, P. and Schad, M. and Juenger, M. and Klose, J. and Kehr, J. “Proteomics of Curcurbit Phloem Exudate Reveals a Network of Defence Proteins.” Phytochemistry 65, no. 12 (2004): 1795–1804.
Zhang, B. and Tolstikov, V. and Turnbull, C. and Hicks, L. M. and Fiehn, O. “Divergent Metabolome and Proteome Suggest Functional Independence of Dual Phloem Transport Systems in Cucurbits.” Proceedings of the National Academy of Sciences 107, no. 30 (2010): 13532.

Looking through some papers it is not clear to me that botanists actually know why this should be the case, and I am sure that you are more qualified than me to comment on this Richard! However, there's some discussion of this in Zhang et al. (2012).
These authors argue that the "exudate from curcubits is copious" because of physiological adaptations due to their growth habit - i.e. they are vines and as such often require the structural support of other plants. Vines compensate for a lack of a supporting stem structure by having xylem vessels that are wider than comparable freestanding species  and "high hydraulic conductivity" (which is a measure of how readily water will flow through pores - in the case of curcubits - very readily). Similarly, sieve tubes and sieve pores are very wide compared to species in other families. Since these sieve tubes have such a large cross-section, they do not readily self-seal.

The Origin and Composition of Cucurbit Phloem Exudate
C Zhang, X Yu, BG Ayre, R. Turgeon - Plant Physiology, 2012 - Am Soc Plant Biol. 158, 3

See also:

Why vines have narrow stems: Histological trends in Bauhinia (Fabaceae), Ewers, F., Fisher, J, Oecologia, 1991, 88, 2


text:
Is it necessary to conduct a power analysis before beginning an experiment?
I know that power analysis is the statistically valid way to ensure you use the correct numer of samples or repeats in an experiment. But I have never seen any biologist actually conduct a power analysis. Mostly, researchers seems to use a rule of thumb (three technical, three biological replicates is a common one).
Should I be doing a power analysis each time I design an experiment, or can I just use one of the common biology rules of thumb? If not, what are the consequences for the validity of my results? And is there a situation where I will be required to use power analysis, which makes it advantageous to get used to doing it now?

You've already gotten a decent answer to this, but I'll provide my own thoughts on the subject.
Yes
It's necessary. It is absolutely something you should do before beginning an experiment, and preferably something you should do in collaboration with the person who is going to be helping you analyze your data. To address a couple points:

You'll see all kinds of researchers doing all manner of sloppy things when it comes to statistics and data analysis. Reading some journals makes me groan. You won't necessarily find it a problem for your field, but one should ask oneself if the goal is merely not to get called out by your peers, or to actually run a well designed experiment.
The consequences to the validity of your results lie in an increased risk of Type II error - the incorrect failure to reject the null hypothesis, or in slightly clearer English, finding no effect when an effect exists in reality. Which means, if you run an under powered study, you run the risk of doing the entire experiment, finding nothing, and being wrong. The consequences of that are myriad - first, it likely harms your chances to get published, as null results are often quite difficult to get into press. Second, if it does get into press, you've managed to get an incorrect finding into the literature, which will then be propagated in meta-analysis, reviews, and the minds of impressionable future readers. And then there's the chance you'll abandon a potentially productive line of inquiry because you couldn't be bothered to do power analysis.
One thing to also consider is that not having conducted power analysis somewhat limits your ability to chase after interesting sub-findings. If you've built your experiment on a shaky foundation, and then want to do a second analysis on a sub-set of your results, you almost certainly don't have the power for it.
There are times when you'll be required to do power analysis. If you do research that's clinically relevant, and you ever want it to appear in one of those journals, you may very well be required to show you had a properly powered experiment. And many grant applications require you do so. Even if they don't require it, some people will do a napkin math estimation of your power if they don't see it appearing in your application anywhere.

sjcockell is partially correct. To do power analysis, you at least need to have some notion of the effect measure you're likely to see. And these are indeed just estimations of what you'll see. But in nearly all circumstances, you'll likely have some ideas already. Are there similar experiments you can draw from? Your own pilot studies? A "feel" born of experience in your particular system?
It's also trivially easy to calculate power under a number of difference scenarios, to ensure your experiment is sufficiently powered if things go considerably worse than expected. For example, in a study I once did the power calculations for, we weren't sure what the ratio of exposed to unexposed subjects would be. So I ran it over a large range:

Which left me with the confidence that even if I was in my "worst case" scenario, I'd have reasonably good power at realistic effect sizes.
That's the true strength of power calculations. They'll tell you things about your study. What you need. What doesn't matter. Whether or not before you spend time and money pursuing an idea if you have a reasonable chance at success. Sit down with someone, take an hour or two (at most for a simple experiment) and do it right. Or ask CrossValidated for advice.

Great answer, thanks. I accepted this one because it answered the precise points in my question.

In order to calculate power, you need to know the variance of the data being collected. You can only estimate this prior to actually gathering the data itself, so any a priori power calculation is itself just an estimate.
This is why sometimes you will see small studies being conducted as pilot studies (for example, see (1)), which enable variance to be more accurately determined, and a true power calculation to be performed.
Knowing the power will enable you to state the probability that the effects you are observing are real (at a given sensitivity). The better idea you can get of this False Discovery Rate, the more solid the conclusions you can draw will be (so it is almost always a good idea to calculate it, but it is not always a feasible thing to do).
(1): Power and sample size estimation in microarray studies, Lin et al., BMC Bioinformatics 2010, 11:48.

Thanks for your answer. That covers quite well why one might do a power calculation. How commonly are they used though? They are not usually mentioned in papers - is that because they're too commonplace to mention or because nobody does them?

I think it is often because they are not done as much as perhaps they should, not because they are done and left unreported. On a related note, in the course of doing some work this afternoon I discovered http://www.poweratlas.org/ - of which I was previously unaware.

OK, I'll make sure I always do them in future  - I'd prefer to set an example than follow a lazy trend. I will actually be doing a lot of transcriptomics in the next year or so, so that link will come in very useful when thinking about power analysis for it.

@sjcockell: the link is for comressing machines now...

Due to my own woeful ignorance on the subject, I have been reading up on statistical methods recently. From what (little) I understand, the real answer to this question is:
Yes, but only if you are doing Neyman-Pearson hypothesis testing
and
Absolutely not, if you are using Fisher p-values
That is, the question isn't formulated correctly, because power analysis is only valid under one statistical framework (Neyman-Pearson). And you are probably not using that framework.
In my experience, most experimental biologists use Fisher's p-value, which gives the probability of the data (or more extreme data) assuming that the null hypothesis is true. Under Fisher's framework, among other drawbacks, there is no quantitative measure of the test's power. However, it has the benefit that it allows scientists to do something close to what we would like to do--that is to draw conclusions from evidence obtained in individual experiments.
The Neyman-Pearson framework does included the idea of a test's power, because you must formulate an alternative hypothesis as well as desired alpha and beta error rates before starting your experiment. However, it mostly denies us the ability to make inferences from individual experiments, and for that reason appears less suited to experimental science. To quote from Goodman (see below), under Neyman-Pearson, "we must abandon our ability to measure evidence, or judge truth, in an individual experiment."
There is no clear right frequentist framework, although what is clear is that you cannot mix Fisher and Neyman-Pearson. Finally, although it doesn't really address your question directly, it seems wrong not to mention Bayesian methods as an alternative to these two frequentist frameworks, which comes with its own baggage.
Further reading from people that understand this much better than me:
Michael Lew's answer to "Setting the threshold p-value as part of hypothesis generation" at Cross Validated
Michael Lew's answer to "What are common statistical sins" at Cross Validated
Hubbard, Raymond, and M. J Bayarri. “Confusion Over Measures of Evidence (          p’S) Versus Errors (α’S) in Classical Statistical Testing.” The American Statistician 57, no. 3 (August 2003): 171–178.  (Working Paper PDF)
Arguments for Bayesian statistics:
Goodman, Steven N. “Toward Evidence-Based Medical Statistics. 1: The P Value Fallacy.” Annals of Internal Medicine 130, no. 12 (June 15, 1999): 995–1004.
Jaynes, E. T. Probability Theory: The Logic of Science (Online version of some parts)


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What is the name of this type of inflorescence?
I was having a look at a rhizophora plant (from the mangrove family), and I got curious about its inflorescence. I can't make out what kind of inflorescence it is.
Here is a photo of the inflorescence.

Does anyone know which kind of inflorescence it is?

That is a woody compound umbel. A compound umbel is one with more than one set of pedicels between the peduncle and the flower. Hydrangeas also exhibit this type of inflorescence, although not necessarily woody.
In the picture below, I've marked all the levels where the pedicels branch.

End of peduncle, beginning of primary pedicels
Beginning of secondary pedicels
Beginning of tertiary pedicels
Beginning of quaternary pedicels, which bear flowers


text:
How does a woodpecker not give itself concussions?
How does a woodpecker go about smacking it's head into a tree without killing itself?

Physical perspective : The motion of a woodpecker's beak is a straight line motion. Researchers believe that concussion occurs in animals when the head is rapidly rotated around the neck (and brain stem), which is less likely in straight line motion.

This does look Quite painful. Ouch!

Various features of brain,skull and beak anatomy help to achieve protection.
A paper was published in PLoSOne in 2011 on this very topic:
Why do woodpeckers resist head impact injury: a biomechanical investigation
There is also a very readable summary on the BBC website. I advise that you read the whole article, but here is a quotation which lists the main findings:

The team's simulations showed that three factors were at work in sparing the birds injury.
Firstly, the hyoid bone's looping structure around the whole skull was found to act as a "safety belt", especially after the initial impact.
The team also found that the upper and lower halves of the birds' beaks were uneven, and as force was transmitted from the tip of the beak into the bone, this asymmetry lowered the load that made it as far as the brain.
Lastly, plate-like bones with a "spongy" structure at different points in the skull helped distribute the incoming force, thereby protecting the brain.
The team stresses that it is the combination of the three, rather than any one feature, that keeps woodpeckers pecking without injury.

Gibson (2006) identified three characteristics that help woodpeckers avoid brain injury:

their small size, which reduces the stress on the brain for a given acceleration
the short duration of the impact, which increases the tolerable acceleration
the orientation of the brain within the skull, which increases the area of contact between the brain and the skull.

Combined with Wang et al.'s findings, maybe that makes six features.
Gibson, LJ. 2006. Woodpecker pecking: how woodpeckers avoid brain injury. Journal of Zoology 270: 462-465


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Why do the brains of cocaine-users shrink faster than the brains of non-cocaine users?
http://news.sciencemag.org/sciencenow/2012/04/cocaine-may-age-the-brain.html?rss=1

Cocaine-dependent individuals showed a significantly greater-than-normal age-related decline in gray matter in prefrontal and temporal regions compared with healthy controls. By contrast, parts of the striatum appeared resistant to age-related volume decline in the cocaine-using group. Enlarged striatal volume has frequently been reported in stimulant-dependent individuals,5, 6 possibly reflecting a marker of reduced dopamine neurotransmission in this dopamine-rich brain region where drugs like cocaine work. Decline in striatal dopamine receptor density has been associated with normal age-related cognitive decline.7 The relative absence of age-related changes in the striatum of cocaine-dependent people may thus reflect another feature of an abnormal brain ageing process.

Could it be related to possible neurotoxicity, or to the long-term effects of dopamine receptor downregulation? Could the effects also be generalizable to those who take dopamine-based ADD medications?
A link to the Letter to the Editor appeared in Molecular Psychiatry to which the ScienceNow article refers:
Cocaine dependence: a fast-track for brain ageing?

Could it also not be related to non-cocaine lifestyle changes, such as diet?

The mechanism of action of cocaine is dependent on pre-existing dopamine production and secretion. Normally, secreted dopamine is cleared from the synapse via the dopamine transporter (DAT) located on presynaptic dopaminergic terminals. Cocaine inhibits
this reuptake of dopamine, increasing it's duration of action on post-synaptic dopamine receptors. Thus, cocaine's effect depends on neuronal dopamine production. Without intrinsic dopamine, cocaine would have no effect. This is actual not exactly true though because cocaine also inhibits serotonin and norepinepherine reuptake transporters as well but the same argument applies to those neurotransmitters as well.
The overall effect of cocaine on the nervous system is extremely complex as it prolongs the action of dopamine, serotonin and norepinephrine wherever those reuptake transporters are present. There is a particularly high density of DAT in the basal ganglia and nucleus accumbens. What these areas of the brain normally do is under intense study and debate. The accumbens may play a role in goal directed behavior and incentive salience, which is the attribution of value to various actions or objects in the environment. This is what naturally guides us to perform one action over another. The simplistic view is that cocaine "highjacks" this system such that cocaine itself acquires greater incentive salience than natural reinforcers such as food, sex, money etc.
Getting back to the original question regarding why cocaine causes brain atrophy. This appears to be a finding quoted from a paper by the original inquirer. It is not obvious to me what the mechanism of this atrophy would be. I suggest you look at the discussion section of the paper from which that abstract was quoted to see what the authors suggest. However, to my knowledge, such atrophy has not been widely discussed in the cocaine literature but I could be wrong.
For further information see Sulzer. 2011. How Addictive Drugs Disrupt Presynaptic Dopamine Neurotransmission.

To the poster talking about "brain shrinkage due to lack of fresh blood stimulation." This has no scientific basis.

Could you maybe add a reference to a good review article on the effects of cocaine to back up your answer?

Neuron. 2011 Feb 24;69(4):628-49. doi: 10.1016/j.neuron.2011.02.010.
How addictive drugs disrupt presynaptic dopamine neurotransmission.

Cocaine hits the brain with dopamine creating the desired high, which, the users seek. When used repeatedly, the brain begins to confuse it's own production with the user's introduction. Slowly, the brain begins to depend on the user's introduction and slows its own production to the point where it no longer produces it. This lack of production causes the part of the brain responsible for dopamine to shrink. It shrinks because it is tissue that is not being used and therefore doesn't get the proper blood flow to it and begins lose its health. Blood stimulation is lost, cell health is lost and size is thereby lost.
The brains of heavy cocaine users display little to no age-related brain shrinkage as compared to non-users because their brain has already shrunk to its limit. The shrink is due to lack of fresh blood stimulation. It is like a sponge that no longer is getting water and shrivels. After 2 days the sponge stops shrinking, it doesn't eventually shrink to a dust particle. It shrinks to its water-free size, the same way the cocaine user's brain shrinks to a blood-stimulation-free size. Age can't further shrink what's already maxed out in shrinkage.

Do you have any scientific sources to support your answer?

Nope.  "The loss of gray matter was most severe in prefrontal and temporal lobes, areas critical for executive function and memory."(ref)  Dopamine is produced in the substantia nigra and the ventral tegmental area.(ref)


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Why did the process of sleep evolve in many animals? What is its evolutionary advantage?
The process of sleep seems to be very disadvantageous to an organism as it is extremely vulnerable to predation for several hours at a time. Why is sleep necessary in so many animals? What advantage did it give the individuals that evolved to have it as an adaptation? When and how did it likely occur in the evolutionary path of animals?

e.g. dolphins can't afford to lose full consciousness when they rest, otherwise they would drown. So their mammalian brains have evolved in such way that only one half of the brain sleeps at a time.

Many migratory animals, like turtles and birds, have also developed this half-brain sleep.

According to one paper I have read, sleeping helps with learning process and many neural connections are reinforced in sleep.

There is the suggestion in the community (nothing published that I can find) that sleep evolved to stop animals venturing out when conditions weren't favorable for hunting (for example hunters of the day became hunted at night, or slow stealthy nocturnal animals becoming obvious in the sunshine). It's better if they just hunker down when their senses aren't attuned for the situations they may face.

Answering parts of your question is the aim of the book Why We Sleep by the sleep scientist Matthew Walker. The book is quite popular and up to date (2017).

This good non-scholarly article covers some of the usual advantages (rest/regeneration).
One of the research papers they mentioned (they linked to press release) was Conservation of Sleep: Insights from Non-Mammalian Model Systems by John E. Zimmerman, Ph.D.; Trends Neurosci. 2008 July; 31(7): 371–376. Published online 2008 June 5. doi:  10.1016/j.tins.2008.05.001; NIHMSID: NIHMS230885. To quote from the press release:

Because the time of lethargus coincides with a time in the round worms’ life cycle when synaptic changes occur in the nervous system, they propose that sleep is a state required for nervous system plasticity. In other words, in order for the nervous system to grow and change, there must be down time of active behavior. Other researchers at Penn have shown that, in mammals, synaptic changes occur during sleep and that deprivation of sleep results in a disruption of these synaptic changes.

This might explain why sleep deprivation affects heart rate.

This is a bit circular, in that sleep being "required for nervous system plasticity" simply means the dependence of nervous adaptation on sleep was never selected out. It doesn't answer why

This argument also fails to mention why there couldn't be a highly modular and redundant brain architecture with at least 2 modules for each neuroplastic subsystem that alternate sleep and wake cycles. Such technology already exists for large-scale server clusters and racks (called a rolling update) where a load balancer is used as a client-facing front end (routing requests to servers ready to accept them). When an update is deployed, servers are shut down, updated, and restarted in a "rolling" manner such that most servers are up at any time during the update.

I found this paper by Benington and Heller that expands on the previously mentioned theory of sleep as a mechanism to renew metabolism.  They hypothesise that sleep is necessary to replenish glycogen stores (mainly within astrocytes) in the brain.  These stores are normally used to supplement blood glucose due to the high energy demands of the brain.
It is suggested that this may also result in the manifestation of feeling sleepy as a consequence of the exhaustion of glycogen supplies in specific small areas of the brain.  Brief and localised depletion of glycogen stores mean that cells are operating with less energy than they normally have to work with.  This causes an increase in synthesis of adenosine from the breakdown of AMP.  The paper maintains that the increased levels of adenosine are detected by adenosine receptors which then triggers or increases (as seen on EEG scans) the feeling of the need for sleep:

In NREM sleep (which may lend some support to the theory as NREM sleep accounts for 80% of sleep and is most physiologically different to waking), this glycogen is most efficiently replaced.  During NREM sleep the release of glycogenolysis inducing neurotransmitters is reduced, allowing glycogen-synthase to predominate and glycogen levels to be restored.  However, these same neurotransmitters are key in the processing sensory stimuli (by tonically depolarising neurons in the sensory cortex).  Therefore glycogen replenishment will always be associated with a (strongly) reduced response to stimuli.
This leads to finally answering the question as to why sleep has an evolutionary advantage, which I will quote verbatim to maintain the authors momentum:

Glycogen replenishment during waking would be maladaptive because it would impair the organism's ability to to process and respond to sensory stimuli.  Sleep has therefore evolved as a state where animals retreat to a safe environment, behaviour is suppressed and glycogen stores are replenished.

So is it just a coincidence that the metabolic pathway of glycogen synthesis in brain evolved to be regulated by neurotransmitters? If it had evolved independently - we wouldn't need any sleep?

@MartaCz-C that's a really good point, and if I'm honest I've struggled to find an answer in literature for you.  However it could be said that as the glycogen reserves are in essence a backup power supply, even if neurotransmitters were not involved such a supply is not likely to be replenished without a greatly reduced energy demand (i.e. in sleep) as otherwise any glucose that arrived would be quickly used rather than stored in glycogenesis.  It could be an adaption rather than a co-incidence if this is the case - forcing an organism to take a period of rest to rebuild these supplies.

A sluggish response to stimuli is better than no response, so it still does not explain what sleep is for. animals don't need to be forced to retreat to safety by going unconscious the same behavior could evolve without going unconscious.

From what I've learned, there are two theories to answer that question:

Restoration - the body needs to rest in order to renew its metabolism (if an animal is active 24/7, it will constantly use up a lot energy and metabolism). It has been shown that mice that have gone a while without sleeping have a compromised immune system.
Preservation - sleep is assumed to confer a survival advantage. Night time is a dangerous time, so sleep sort of 'forces' an animal to lay low for a few hours.

Your point #2 says exactly the opposite of the question's premise. Would you care to expand a little bit (e.g. give some references)?

Point 1 seems to be a circular argument (or flat out wrong): if the animal weren’t sleeping it could hunt / forage for food. Even in sleep, we expend some energy so this calculation will always come out favourably on the side of staying awake.

@KonradRudolph - the body always expends some energy, but the energy the body uses while sleeping is a fraction of the energy it takes to stay awake/hunt/etc.

@nico - I found an excerpt from a book- here

@Innab It’s irrelevant that the energy expense is only a fraction. The important thing is that there is any at all. Do the math, it will never be beneficial to rest instead spending the same time hunting, because the net energy balance of hunting is positive (i.e. energy take-in rather than expense), so in sum, resting will always spend more energy than hunting.

@KonradRudolph surely that is only the case if the hunt is successful - therefore sleeping can be less disadvantageous in terms of energy expenditure if the odds are heavily stacked against successful predation at a certain time of day.

#2 also doesn't apply to nocturnal animals; especially animals that are active at different times of the day specifically to avoid predators.

Why sleep persists is fairly easy, why it is needed is an unknown.
Sleep appears to be necessary in any organism with a brain, that is anything with any kind of concentration of neurons. That is when denied it said organisms die. So all that has to happen is that the benefits of a brain outweighs the cost of sleep.
The length of sleep needed correlates with brain size, at least the REM part of sleep other parts correlate with metabolic rates. Now this can be seemingly confounded in larger complex brains (birds and mammals especially) when organisms start folding the brain to increase neuron density without increasing overall size. In this case these organisms are increasing hte "size" of the brain without making the brain larger, by increasing density.  Worse some organisms "sleep" for long periods, but only a short portion of that time involves the neural activity associated with sleep (like REM), sleep in more complex animals (those with very large complex brains) contains many functions.
In organisms with tiny brains and slow metabolisms (aka the earliest things with brains) sleep does not take very long so the cost is minimal, the benefits of a brain (and thus learning) can be high. Later as brains get larger the cost goes up but so does the benefit, if it was possible for a brain to be retained without the need for sleep it should have been selected for at this stage. So in all likelihood the need for sleep is something fundamental to how neurons function and can't be changed without seriously disruptioin their function. It is not uncommon for unfavorable things to get locked in evolutionarily in this way, the cost to change them (in this case the loss of brain function) is far larger than the cost of sleep so selection keeps it around.
Now the complexity of sleep makes sense, if you already have this required period of downtime, it makes sense evolutionarily to tack on anything else that would be best done during said time. Better to use the triggers and time for existing downtime activities for any others that get added then have even more downtime. So now we have a slew of confounding factors that muddy studies and make it hard to tell what parts are essential.
We don't know why sleep is necessary, there are many ideas but not a lot of evidence. Given the complexity of sleep this is not surprising, teasing out which functions are fundamental is not easy. There is a current leaning towards it being necessary to clear out metabolites that disrupt neural function, it appears this process is highly disruptive to the brain if the brain is awake, to the point simply shutting down brain activity (movement in particular) is far safer for the organism. But as with all research this is very preliminary and sleep is poorly understood so acceptance is and should be very tentative.


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Is there a cheap and easy way to check for potentially unsafe UV exposure?
My lab has an older large Fotodyne tabletop UV transilluminator for visualizing gels.  It has a UV blocking cover that hopefully reduces UV that passes through, but I've always been suspcious as to how effective it is.  Obviously this part can be replaced with a new one, but short of guessing on the recommended 50 hr lifetime, how would one know the level of UV passsing through?  I considered simply placing a gel on top, but that is far from quantitative.  I am really just curious if there is an easy to make and/or obtain sensor that could be used to know when UV expose could be considered dangerous.

Is there a more appropriate tag than DNA?

Agreed, I'm still below the threshold for creating tags.  Safety or visualization would have been remotely closer.

I'm not sure this is on topic in its present state.  It's more about safety procedures than the formulating or running of gels.

@jonsca safety procedures should surely be included within experimental design?

@bobtheowl2 sorry about that, didn't even consider your rep!

@RoryM This seems more of an laboratory equipment maintenance issue rather than something directly involved with the process of experimental biology.  Perhaps a meta post is in order.

@jonsca sure sounds like a plan =)

The instrument you are looking for is probably an UV-meter.

That does seem obvious after looking at products available in a google search.  Maybe one the reusable ~6 level color changing sensors would be adequate or even one of the ~$30 handheld digital models. Spending several hundred dollars is out of the question though. I was just hoping someone would say, oh yea all labs in the world use this cheap x sensor to warn us of excessive exposure (analogous to radiation badges).

@bobtheowl2 I did try and find a radiation badge style dosimeter for you but it seems the only ones they have at present are for 24/7 exposure studies and tend to be quantitative rather than a qualitative red light approach


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Is fat distributed proportionally around the body?
One guide I have been using to tell me if I really am gaining a lot of weight is a ring around my 2nd last finger on my right hand, if I can slip it on and off without any resistance then I'm fine, however I've been basing this from the notion that if I gain weight it's proportionally distributed around my body, as such, if I get fatter so do my fingers
So I am wondering, is fat distributed proportionally around the body (ie. if your waist gets bigger then your fingers will get bigger along with it)?

What about simply using scales to track your weight? However, this is of course separate from the fat distribution question (to which I suspect the answer is no), but it would save you some trouble.

@fileunderwater's suggestion to use a scale is probably the best answer you could get, but looking at this broadly, the answer is no.  The oft-referenced apple and pear shapes are indeed very real and have medical consequences.  One of the issues is that there are sex differences in fat distribution.  There is no evidence I can find that finger fat is a good correlate of overall body fat, although admittedly yours could be.  It is also likely a function of how much overweight you were when you began the "experiment" i.e. the relationship probably isn't linear.
That being said, in men the ratio of the length of the second and fourth digits are otherwise meaningful.


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Can humans be printed?
Is it possible to spray stem cells on fully grown skeleton to get fully grown humans?
Currently, just read about recent advances, and wondered if something like this is possible.

No.
Very early in the development of an organism, it is just a clump of cells.  Then those cells communicate, and determine where they are in the clump, which determines their eventual fate in the full organism.  In mammals, for instance, cells split into three different layers, and the skin and nerve cells develop from cells in the outermost layer...etc.
You can't just dump a bunch of stem cells somewhere and expect them to know where they are and what they should be developing into.

I am tempted to downvote such a strong opinion... what if you replicated the exact configuration of elementary particles of a person?

A skeleton is itself very complicated.  It's not just apatite in the shape of a skeleton.  The bones have structure, and many have bone marrow.  Tiny cells navigate through the bone matrix, keeping it sound.  Those cells, and the ones in the marrow, need a blood supply to keep them alive.  Plus, what swbarnes2 said.

And through these cells our bones are actually alive. The osteoclasts and osteoblasts are in a constant process of building up and breaking down bone mass.

See spryaing stem cells is not that easy as it sounds.The main difficulty working with stem cell is keeping their stem cell characteristics intact till the development actually begins.Stem cell can be amny types such as pluripotent,totipotent,multipotent etc.As you asked bone,bone is also a result of stemcell.So point is first you have to generate bone and bone generation is a massive and intricate process.You need many growth factors for this process and these growth factors are developmental time specific it means it is expressed at only a certain point of time.So I think it's difficult


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Metabolic efficiency for fats and sugars
I am making an exercise for physics students about the first law of thermodynamics, burning heat and evaporation heat. So my idea is to use cycler which runs on fats and sugars where proportion determined by respiration quotient. The amount of evaporated sweats would be determined from inefficiency of using the fuel. Unfortunately I am unable to find efficiency data to form the exercise.
So what are typical efficiencies to run skeletal muscles on either fat or sugar molecules?
EDIT
Assuming respiratory quotient measured at the time of cycling is 0.7 so all energy is obtained from oxidizing fats:
$$ C_{16}H_{32}O_2 + 23 O_2 -> 16CO_2 + 16 H_2O + \Delta G$$
what part of the $\Delta G$ can do mechanical work $A$ or simply what is typical value of efficiency coefficient:
$$\mu = \frac{A}{\Delta G}$$

A quick google on "muscle efficiency" turns up a number of articles.  Wikipedia gives an estimate of 18--26% efficiency, https://en.wikipedia.org/wiki/Muscle

Muscles first transform those compounds to ATP.

This is a very complicated question. You need to rephrase your question to be more specific.
Efficiencies of energy utilization from glucose in the presence of O2 (aerobic respiration) are considered to be in the 40% range. Quite good when you consider that an automobile combustion engine is in the 20-25% range.
There is some evidence that betahydroxybutarate (B-OHB) actually provides more available energy for work than does glucose.  See Paper Here.
However, what is often overlooked is the energy needed to generate B-OHB from fat during ketosis, which results in a net loss in efficiency compared to glucose.
One of my favorite blogs is Peter Attia's "The Eating Academy."  He has a Post that goes into this subject somewhat.
I know this isn't a complete answer to your question, but again, you need to be more specific.
Respiration with or without O2.  Efficiencies in generating ATP from source material or only net efficiencies after the ATP -> ADP.

I made second part more specific. In your language I want efficiency of energy utilization from fats in the presence of O2.

If its needed you can also assume that fats are taken only from tissues

Ok I got right source http://www.ncbi.nlm.nih.gov/pmc/articles/PMC543577/pdf/1743-7075-1-15.pdf the lipids have the same efficiency of generating ATP specificly 40%

Excellent. If my answer was useful, please do indicate so.


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parallels or replicates?
I am writing an article where I describe real-time PCR experiments. My collaborator, after reviewing the article, consistently replaced the word "parallels" with "replicates". Are they not synonymous?
I prefer the word parallel, because, in the context of PCR, it implies that these three identical experiments were performed in the same real-time PCR run (and not consecutively).

Can you give a couple of examples of the text in question?

Replicates is certainly more common usage in general. If you wish to emphasise that these replicates were performed in the way that you describe perhaps say "replicates run in parallel".

Parallels is not as good a word imho - you can run several concurrent experiments and call them run in parallel. replicates are the same experiment.

In any case, parallels won't work, you want experiments run in parallel which is not the same thing. Parallels cannot be used that way.

The explanation I got when learning how to do qPCR was that you need run both replicate experiments and parallel experiments to get publishable data.
Replicates (or biological replicates) would be qPCR runs on independently collected samples. That does not count your control vs your experimental groups. So for my work I had to collect 3 sets of control tissue and 3 sets of experimental tissue from independent sets of animals (in my case 3 generations but for mammalian work I think three different animals would be ok).
Parallel does imply that you ran the the samples together in the qPCR machine. I think the standard is that for each sample in a particular replicate you need to run three qPCR reactions in parallel. So in total you need to run 9 wells of qPCR reactions for each test group.

Technical replicates show that the technical integrity (pipetting, master mixes, detection) is consistent, which biological replicates show that the effect you are measuring is genuine and happens not by chance. Usually you do three technical replicates per run and sample and repeat an experiment three times independently.


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Measurement of glucose concentration in the human brain
If I want to measure the exact glucose concentration in a human brain then how can I proceed to do that? Is there any technique or assay to do that?

It is possible by using 13C NMR Spectroscopy.
It has been done after infusing enriched D-[1-13C]glucose in six healthy children. The results showed that at euglycemia glucose concentration is about 1 micromol/ml.

Source: Gruetter R, Novotny EJ, Boulware SD, Rothman DL, Mason GF, Shulman GI, Shulman RG, Tamborlane WV. Direct measurement of brain glucose concentrations in humans by 13C NMR spectroscopy. Proc. Natl. Acad. Sci. U.S.A. 1992 Feb 1;89(3):1109-12. PubMed PMID: 1736294.


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Does inhaling glue (glue sniffing) reduce appetite?
I have heard from many homeless people that they sniff glue just to reduce appetite, as it comes cheap and is more affordable than actual food.
Is this true, and if yes, why? This is totally opposite to the effects of marijuana where people feel hungry.

GLUE SNIFFING : Involves inhaling the fumes from domestic and
  industrial products (glue etc.).

I think the reason why they sniff glue is the same as why they sniff petrol; they seek an escape route out of their misery and boredom. Being cheap intoxicants they suffice their demands. It has little, if anything to do with reducing appetite if you ask me.

@AliceD yes, agreed ! But I have told by many that it reduces their apetite

I have tried that enough number of times to say that it doesn't reduce appetite. It gives hallucinations though.

I searched for credible material and you seem to be right!

Short answer
Various inhalants, most notably organic solvents including those used in paint and glue suppress appetite.
Background
From the Division of Alcohol and Drug Abuse I learned the following:

Initial effects [of various inhalants] include nausea [...], and a loss of appetite.

And the Humanitarian Irin News reports the following on Nepali street youths:

The adhesive glue contains toluene, [an] intoxicating hydrocarbon [...]. The solvent [...] causes hallucinations as well as dampening hunger pangs [...].

Indeed, acute exposure to organic solvents has been associated with a loss of appetite (Gregerson, 1998), and chronic exposure to toluene in the industrial workforce has also been linked to appetite suppression (Kishi et al., 1993).
References
- Gregerson, Am J Industr Med (1998); 14(6): 681–701
- Kishi et al., Environmental Res (1993); 62(2): 303–13

This may not be absolute. For example not everyone would feel nausea (in fact one may have the feeling of being lively) or loss of appetite. Only thing that I can say surely about glue sniffing is that it irritates the mucosa.

@WYSIWYG - I added scholarly references including a meta study. The anecdotal material cited supports this view. Your experience against the literature :)

I can bring all my friends and accomplices in the crime for testimony :P There may be chronic effects but not in the sense that OP is asking.

@WYSIWYG - I double checked my references and I conclude the effects of sniffing have obscured your memory :) The Gregerson study specifically mentions acute effects on appetite, which is confirmed by OP, the news report and the Drug Abuse website.

Or perhaps I am quite voracious inherently :D


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Why do some people find vegetables so repellent when evolutionarily they should find them an attractive and thus tasty food?
Why do certain people (especially kids) find vegetables so "repellent" when evolutionarily they should find them an attractive and thus tasty food?
I ask this question because if Darwin's theory of evolution is true then foods like vegetables that us human beings have been eating and attaining better health from eating for millions of years should have a taste that accordingly attracts us to them.

Your view of "so repellent" may be cultural or a result of growing up in the western world

I "tuned down" a little bit the question. Saying that "people find vegetables repellent" is a gross exaggeration. Some people may do, but I would not say that they are the majority (unless you have proof otherwise).

It would be nice to see some actual numbers (peer-reviewed papers anyone?) showing food preferences in different countries... that may tell a lot.

I tend to think this is a conditioned response, not entirely an evolved one.  People who don't eat meat habitually cannot stand it.  same is true for large amounts of sugar.

Evolution is not that simple. There is no selective pressure for a feature if it does not ultimately in some way benefit reproduction or the offspring. Vegetables are healthy for us now because we live much longer than we used to in an environment not dominated by us, and they contain many nutrients which help to sustain a healthy body beyond, say, 50.
However, if you imagine an average life span of around 30, it becomes clearer why evolution would favour foods high in energy over foods containing high amounts of micronutrients. Over such a time span, the long-term effects of a diet rich in fat and sugar do not develop significantly, but the energy supply is exactly what is needed to sustain bare life to the reproductive age.

A healthy diet is also more likely to result in us being more healthy and thus looking more attractive to potential mates so it still seems odd that the foods that are among the richest in said vitamins are so repugnant to us.

Attractiveness is a cultural value - it wasn't long ago (only a few hundred years) that the ideal figure was actually everything else than slim. Have a look at depictions of beautiful women and men in art throughout the centuries (e.g. in the antique god/esses of beauty, or paintings of literary figures which are supposed to be beautiful). Healthiness also depends on context. As I said, today what we consider healthy are things that sustain a healthy body for a long life. Not long ago, what was healthy were things that sustain life at all.

While I'm flattered that you accepted my answer already, I would suggest that you leave it open for a bit longer to encourage other people to give their answers. My answer was not a very good answer in the sense that it's only reasoning and not drawing upon any reliable sources :)

OK I appreciate your honesty, for that I will leave it open and unaccept your answer, but I will also upvote your answer.

@Armatus body fat is a special case, and not that related to micronutrient deficiencies. I do not believe there are any cultures anywhere in which rickets, pockmarked skin, missing teeth, and other signs of vitamin deficiency are valued.

@octern Thanks for your comment! Could you clarify how micronutrient deficiencies relate to the question, answer or my comment earlier?

In the comments, Brenton Horne said that a healthy diet increases attractiveness, and you responded that "attractiveness is a cultural value". I was pointing out that while preferences for body fatness have changed, most of the ways in which micronutrient-rich vegetables can contribute to appearance have been consistently favorable.

Let me also say that I am shocked, shocked that you did not immediately pick up the context for a two year old conversation that was abruptly resumed.

I must humbly apologise for this most intolerable shortcoming of mine, I shall endeavour to re-read every word I write on the internet at least every six months! [I actually did re-read the whole thread earlier, but failed to make the connection] On topic, I would expect overweight to be indeed related to micronutrient deficiencies - in that overconsumption of food (particularly the kinds of foods available in such cultures where overweight was considered attractive) would simultaneously at least prevent deficiency.

Though in retrospect, I'm not sure anything about attractiveness, i.e. sexual selection, is very relevant to evolution of taste - at the very least considering that overcoming our sense of taste is a pretty easy thing to do in order to increase attractiveness (which is very evident today).

Vegetables provide calories and don't kill you. For a hunter-gatherer, that's reason enough to eat them even if you don't like the flavor a lot. Finding nourishing foods "repellent" is a modern luxury.
Additionally, the bitter flavors in vegetables may be less noticeable to people who were not raised from infancy with hyperpalatable, sugar-sweetened food.

I would suspect there are many reasons from behavioral to genetics to anthropological. I think the answer you are looking for (as you have posted it here) is sensitivity to phenylthiocarbamide or PTC. PTC is an organosulpher thiourea. It has a very bitter taste and the ability to taste PTC is determined by ones genetics. It I s a dominant trait and about 2/3 of the population can taste it. Although it is not found in food there is a large body of evidence linking the ability to taste other thiourea compounds with dietary habits. For example, smokers and coffee nuts are more likely able to taste PTC. They also more often dislike certain vegetables. If you ever want to find out if you have the ability to taste it you can try tasting test strips that contain PTC.

To a certain extent how much people like various foods is a relative thing. Vegetables are indeed more desirable as food over, say, rocks, but often less desirable than, say, cake. Our bodies get more energy from sugar than vegetable matter, so evolutionarily we prefer the taste of sugar.
This is complicated by the fact that our tastes are often learned/environmental. Like, I love clams but I know many people hate clams; there isn't some biological reason for this, it just comes down to I grew up near the coast and they grew up inland.

Can you please add some references?


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For emphysema, which of the respiratory volumes is affected?

It could be the tidal volume because it affects how a person inhales and exhales normally.
It could be the residual volume and functional residual volume, because it increases its amount. Because it traps air.
On the other hand it also affects the Forced vital capacity because it decreases the amount of air that can be forcibly exhaled immediately after one inhalation.

To learn obstructive/restrictive lung diseases, I find it easiest to think in extremes at first, with vivid descriptions of why.  So in obstructive lung diseases, like COPD/emphysema:
Total volume increases because so many of the walls of the alveoli have been destroyed, they are like giant floppy bags instead of nice firm bubbles.  There's more empty space, and total volume is therefore increased.
Reserve Volume and End Respiration Volume increase because these alveoli are large and stretched and floppy and can't push as much air out, even when you try.  (Decreased elastic recoil.)  They also flop shut often before the air is expelled - trapping air in.
Tidal volume may not change at all, but it takes longer to exhale than with normal lungs.  That is why FEV1 and FVC are lower, for the same reason.
Residual volume