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What are the theoretical and actual (measured) minimum water potentials in plants?
I'm a plant physiology researcher, but water potentials are not really my thing, so I don't have a great grasp on the literature. I'm dealing with water potential data right now though, and it seems questionable to me. Some of the measured water potential (solute + metric potentials, after lysing cells to break turgor) are as low as -48 bars (most in -10 to -35 range).
That would, if my math is correct, translate to a solute concentration in the 2000 mOsmol range, which seems extremely high to me. Consequently, I'm trying to determine if there is an analytic issue with the data collection. I've run through the equipment chain, checked calibrations, and everything seems ok. I've also been combing plant physiology lit. for comparable data, and I find some in that range, but I can't find any theoretical work that would help set a 'ceiling' for what constitutes a reasonable solute + metric potential.
So, my questions are these:

What is the theoretical maximum capacity for dissolved ion concentration in water, and what pressure potential would that represent, compared to pure water.
Is anyone aware of plant physiology research that has attempted to establish a minimum in vivo water potential in plants (either total potential, or S+M if it's broken out)?

Sodium Chloride (which I am here assuming to be the major salt in your solution) has a solubility of 6 Moles/L this corresponds to 12000 mOsmol, so the 2000 mOsmol you are measuring is not entirely implausible. However normally plant cells should have an osmolarity on the order of 300-400 mOsmol. In order to judge if your value was calculated correctly, it would be necessary for you to tell us exactly how you calculated and how you measured.
I am not aware of such literature but I am not a plant physiologist myself.

Thanks. Measurements were taken two ways: tissue was measured in the field, with a 'pressure bomb' (https://en.wikipedia.org/wiki/Pressure_bomb) and additional measurement was done with both needle and woody tissue using chamber psychrometers  (a small sealed chamber that holds tissue and contains an electrode, the resistance of which changes depending on humidity, which changes based on the tissue's hydraulic status). The pressure bomb is pretty much foolproof, but the psychometry work depends on calibration, which i've checked, repeatedly, using lab standards.

Also, I'll add that your linked source for osmolarity isn't necessarily troubling for my result--osmolarity increases vertically with plant height (to pull water against gravity) so the lowest osmolarities would be seen in root tissue (tubers) and it would increase as you rise through stem, branches, and leaves. Hard to say though, since tubers aren't 'regular' roots, and plants deliberately manipulate solute concentration in 'storage' tissue, like tubers. I've done a similar teaching lab, and the variance between potato varieties is pretty huge.

Thanks for the clarifications. If you can exclude any other sources of water potential (capillary forces, air pressure, etc.) I guess the 2000 mOsmol are correct. However I must caution you again that I am a biophysicist, not an expert in plant physiology.


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Sheep vs. Furry animals

Why can't we take the fur of a fox without killing or skinning it just like the sheep , what's the biological or chemical structure or even the trait which is on a sheep's body that separates wool from its skin
Why can't we apply the bioclip technology on furry animals too ?

Not knowing anything about the fur trade, I would suspect it is mainly a matter of quantity of fur. Imagine taking only the fur (without the skin) of a fox. What could you want a do with it? The hairs are maybe 1cm long only. You need to take the skin to keep the hair together. With sheep, we are often not interested in the fur as we can process their massive amount of wool.

@Remi.b, see my answer. Quantity isn't a limiting factor, cow fur must be an abundant resource given the number of cows that get slaughtered. Also, sheep only have wool, no fur.

Sheep wool is like cutting long curly human hairs: they stick together due to the length and curliness.
For foxes, chita, rabbit, lions, etc, the hair are really short and parallel: it's like cutting your eyebrows: they won't stick together. That why you (used to) find them as carpet, kept with the skin.

@user27247 It does not seem very strategic to chose an answer that has received two down votes (and one up vote) and lack any sort of reference while Michael_A's answer has received 7 up votes and is much more complete.

May you allow the OP to make his own choice, without "politics" or "strategy" considerations, about what is the answer he found clear ? I'm scientist, but I also do science popularization. I agree  Michael_A's answer is detailed and very interesting... for readers having some scientific background. More importantly, how interesting it is, it doesn't answer the question (getting the hair without killing or skinning the animal).

@Fabrice NEYRET I'm not concerned by the OP exercising his/her voting right, even if I think it's a strange call. To be clear, I have answered the final question. Read the final sentence, you could shear a fox and produce a fabric but the fabric would likely be poor and there's no reason to do so. I have even provided, linked, evidence for my answer by giving a specific example where a fur is bioclipped/shorn and used like a wool.

Fur, wool, and hair are all made of keratins.
To the best of my knowledge wool and fur are separated arbitrarily, based on the properties of the fibres. This arbitrary division allows rabbits to have fur but selective breeding has produced angora rabbits, which have wool. The opposite should be possible, with time you could breed a sheep that has fur.
Length; Wool grows continuously and animals are clipped when the fibres are long. Fur often has a maximum length.
Structure: The structure of the keratin in the wool makes the fibres kinked (crimped). These kinks aid the production of fabrics. I believe the cuticular scales also aid in the production of fabrics.

Fur doesn't have kinks, so even if it's long enough to weave the fabric is likely to lack durability.
Some furs are used in textiles rather than pelts. Possum fur is 'plucked' and woven into fabrics with wool. The resulting fabric is slightly less durable. However, possum fur is hollow and smooth so possum fur fabrics are very soft and warm. The clothing is very good to to wear.
However, fur is generally inferior to wool for textiles and it took a couple of decades to develop techniques to produce textiles from possum fur. This happened because of odd ecological and economic drivers. Possums are are a major pest species in New Zealand where they contribute to the decline of native birds and insects. Millions of possums are killed every year in New Zealand. The market for possum skins is very small. This is why so much effort was put into producing a fabric from possum fur.
So you could shear a fox and produce a fabric but the fabric would likely be poor and there's no reason to do so.

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Does the term "fitness advantage" or "fitness disadvantage" make sense?
Same for the terms "selective advantage" and "selective disadvantage" which I intend to use synonymously.  There are usages of each on Google Scholar, but do evolutionary biologists understand what is meant?

What is unclear to you?
If you could highlight what is unclear to you, or what exactly are the semantic issues in your opinion, that would help to really address your misunderstanding. In absence of that, I will just give you a general explanation of their meaning.
What does 'fitness advantage' mean?
If a group of individuals has a fitness advantage, it means that this group of individuals has a higher fitness over some other group of individuals. The other group, then has a fitness disadvantage.
Natural selection
If we grouped these individuals based on genetics, then the genotypes having a fitness advantage will likely raise in frequency in the population. If we used phenotypic trait to group individuals and if the trait is heritable, then the frequency of these phenotypic traits is also likely to raise in frequency in the population.

Thank you.  That is about what I expected.  I just haven't seen that term frequently.  I just wasn't sure whether if a group has a fitness it, by definition, has an advantage.

What about the terms "less well-adapted individuals" or "less well-adapted natural enemies"?

The saying "les well-adapted" is less common the saying "fitness disadvantage". To me they sound very much the same. I would tend to think that we use the term "fitness disadvantage" when there is fitness variance in the population and we want to refer to it, while we could use "les well-adapted" to refer to the idea that the entire population has a lower mean fitness than some other hypothetical population (a load). In any, it really is the same concept but just eventually applied in slightly different context.

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Abilities used to survive against natural enemies: directional selection or frequency-dependent selection?
Regarding abilities used to survive predators and parasites, are they subjected more to directional selection or frequency-dependent selection?
It's usually that host-parasite coevolution is represented to be characterized by frequency-dependent selection, such that rare traits in hosts select for traits in parasites subject. That would make the phenomenon of female choice for "good genes" males surprising because one might instead expect healthy males to be more likely to yield sickly offspring or grandoffspring. Is this a simplification and are there some aspects of host immunity subject to directional selection? If so, which?
Same with anti-predator defense traits:  only frequency-dependent selection or some substantial percentage subjected to directional selection?
Thank you for your time.

Both. These are sometimes called "arms race" or "trench warfare" (directional) and "Red Queen" (freq-dependent).

Would you be able to offer more, such as what sorts of characteristics are selected on directional vs freq-dependent?

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How to determine the evolution of a dimension of fitness that has high variability of selection intensity?
How can one determine the evolution of a dimension of fitness that has high variability of selection intensity (low in some generations, high in others) compared to other dimensions of fitness?

Fitness is unidimensional (for an individual, it is a single point, not a matrix). Phenotype and environment are typically highly multidimensional.

The question is unclear to me. Are you talking about analysis of G-matrix (see Arnold et al. 2008 and this post)? Telling us what you've found for the moment would be helpful. Also, if you have a specific application in mind, you can let us know your end goal.

I mean, in a given generation, there may be stronger selection intensity upon an individual's ability to evade predators than upon an individual's ability to find territory.  In another generation, selection on each of these abilities may be more modest.  (I am referring to each of these abilities as a "dimension" of fitness.)  Does this make sense?

Oh ok. That makes sense. I don't think anyone ever referred to the covariance between a given phenotypic trait and fitness (as this is what you are describing I think) as a dimension of fitness. Roff's book, as I recall offers a good semantic on the subject but I don't fully remember it by heart.

I think that a case-study example in your post would be helpful to understanding exactly your goal (I am removing my close vote in the meantime).

This isn't my area of expertise, so excuse my ignorance if necessary, but I feel like your question might be more straightforward if you remove the "dimension of fitness" terminology unless this terminology is standard in the field. Perhaps your question is "How does variability of selection pressures between generations influence the evolution of relevant traits?" I am assuming you are looking for a semi-quantitative comparison of the rates of change in genotypes when selection pressures are variable vs. static across generations.

And it looks like Remi.b beat me to it - I would reiterate that a case study or explanation like in your comment would improve the question and help solicit quality answers.

Thank you, Remi.  Yes Bryan, but not just the selection pressure upon a whole genotype, the selection pressure upon individual traits.

I think a case study will be rather elaborate.  I'll work on it.  Thank you.

When I said genotypes what I really meant was allele frequencies that lead to particular distributions of genotypes in the population, sorry for the imprecise terminology - I think this fits what you are asking.

It's complicated. The classic answer is from Dempster 1955 Cold Spring Harb Symp Quant Biol 1955. 20: 25-32 (doi:10.1101/SQB.1955.020.01.005), which has a whole section on "Selection Intensity Varying With Time".  Summarizing:

An example from Kimura (1954) with a mean selective coefficient of zero: "the variation of selection facilitates the loss or near loss of alleles thus tending, if anything, to decrease rather than maintain genetic heterogeneity".
An example with haploid populations (approximately equal to the diploid case for weak selection) with a time-varying selection coefficient of $s_k$ shows that the behaviour of allele frequencies over time depends on the mean value of $m=\left\langle x_k \right\rangle= \left\langle\ln(1/(1-s_k) \right\rangle$, i.e. the geometric mean of the relative fitness; in general, the geometric mean is smaller than the arithmetic mean (i.e. variation in time would lower the fitness advantage of the more-fit allele). I believe the bottom line here (although it takes quite a bit of work to understand the whole story) is as given in the last sentence of the paper: "Selection pressures variable in space or time could act to maintain genetic variance of fitness ..."

On the other hand, Tănase-Nicola and Nemenman (2011), "Fitness in time-dependent environments includes a geometric phase contribution" (DOI: 10.1098/rsif.2011.0695) say it's still more complex:

the selection coefficient in infinitely slowly changing environments (we call this the adiabatic limit) is given by a time-average of static selection coefficients corresponding to each environment. This time-average is equivalent to the geometric mean result of Dempster [10]. It is independent of the order or the speed with which different environmental states are visited. However, for environments varying at a slow but finite rate, this time-average is not the whole story ...

All of the above is about the evolutionary dynamics of a single allele, not a comparison of the evolution multiple alleles/traits within the same genome.  Things could get (much) more complicated in that case, even in the absence of explicit pleiotropy, linkage, etc. (e.g the Hill-Robertson effect). I doubt there's a simple answer; I would suggest heuristic guesses based on independent dynamics of alleles based on the single-allele phenomena described above, followed by simulation ...

The question does not contain the term "time". Only in one comment did the OP said "in a given generation" and "In another generation" and I would suspect (s)he got lost in between several concepts in trying to clarify the question (but might be wrong). I am not sure the OP was interested about selection pressures varying through time.

fair enough, but what else would "low in some generations, high in others" mean?

I think it was a point where the OP got mixed up with two different concepts when writing his comment. But again, I might be wrong. It will be the OP's job to clarify it. (I am not saying the answer is bad, I just wanted to highlight the point that I find unclear in the post).

I also read the OP's original question to mean variability in time even if this wasn't mentioned explicitly (as opposed to variable pressure on different members of the species) - I think this is the more interesting question because variability across members of the species seems trivial.

Ben Bolker, I thank you very much for that answer.  Remi, this is the kind of analysis I was looking for.  Makes me wonder what you thought I was looking for.  Yes, I'm looking for selection pressures upon a trait varying from generation to generation (though not necessarily varying within a generation).  I've tried reading Dempster's article, but I'm stuck because I don't see how this answer was obtained:  "The change in p in one generation of selection is spq/(1--sq) in the haploid case and spq/(1--2sq) in the diploid."

I haven't looked at it carefully, but this is presumably what you get if you go through the algebraic steps of computing the expected number of each genotype (p^2, q^2, and 2pq in the diploid case or p and q in the haploid case), the relative number of offspring for each genotype, and then scaling by the total number of offspring - i.e. this should be found in any standard population genetics book ...

if this answers your question, you can click on the check-mark to accept it ...

Ben, I sincerely apologize. I did not get notification about your comments.  It actually appears that the formula given (spq/(1-sq)) is the same as the one Remi referenced in this post (http://biology.stackexchange.com/questions/15984/how-do-i-calculate-the-change-in-allele-frequency-in-a-haploid-population-under?rq=1). The derivation is there too. Now I understand it. I appreciate your helpful answer, but I don't feel it answers my question completely (maybe I have to better understand Kimura 1954). If I click the check mark, does it discourage future replies? Do you still get credit?

If you don't feel your question is adequately answered, there's no pressure to accept an answer. However, if you think you can edit your question to clarify what you don't understand, or otherwise try to improve the chances that I or someone else will be able to answer in the future, that would be useful.  You're also welcome to answer your own question, if and when you answer it to your own satisfaction ...


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Use numbers or algebra when introducing an evolutionary biology concept?
I'm working on an (approximately 20 pg) evolutionary biology paper for submission to a journal.  The paper introduces a couple of strategies (I use "strategies" loosely; they can be carried out by unconscious individuals).  I have described the strategies verbally.  However, I have also tried to offer additional clarity by putting the strategies into some numerical form.  I would imagine that there are many possible models that could be used to test these strategies.  I am using one model, with so many simplifying assumptions that even if I were to carry through an algebraic treatment under this model, it would be of little use in giving a general representation of when the strategies can be selected. My goal is to go through an example under the model in order to show how the strategies are supposed to work, not the conditions under which they can be selected.
Is it easier to follow an example with numbers or with algebra in place of those numbers?

It is easier if you use numbers and avoid symbolic calculation however, it is much more powerful if you can do symbolic calculations.

If you want to learn more about mathematical modelling in evolutionary biology, I recommend A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto an Day

I'm not asking whether it's easier to do.  I'm asking whether it's easier to follow.  Re powerful:  I am using one model, with so many simplifying assumptions that even if I were to carry through an algebraic treatment under this model, it would be of little use in giving a general representation of when the strategies can be selected.

to follow for the reader? IMO, symbolism always carry more intuition to the reader esp. if the number of variables is greater than say 3. You can always replace the symbols by realistic numbers in your end result to ensure the reader understands. ...I am not sure I'm answering your question though...

Yes, to follow for the reader.  What do you mean by symbolism?

Oh I just mean using letters instead of numbers. I guess I took that term from symbolic computation but it may not be the right term.


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How is "selection" best defined?
There is natural selection but there is also sexual selection which some regard as a category of natural selection.  There is also artificial selection (by humans).  The question is, what is a most appropriate for selection?  What criteria does a  force have to meet in order to be considered to have acted selectively?

if a trait is beneficial to the host, then the chances are that it would be chosen by natural selection.

Related: What is the relationship between sexual and natural selection? and What does fitness really mean?

see wiki evolution page. its a nuanced question like "can it ever be right to kill?"

@comprehensible I am not sure I understand the relationship between "can it ever be right to kill?" and "How is “selection” best defined?". IMO (see my answer), Wikipedia does not offer a good short format definition of natural selection. NS is, mathematically speaking, very accurately defined. There is left to phrase it correctly. I don't think there's much nuance. I am not sure what you mean by nuance though as your example depends only upon ones set of values (philosophy > value theory).

@Remi.b So what is NS's accurate mathematical definition?

@sterid All the standard Fisher's equations of natural selection. Have a look at any intro book to population genetics (Books on population or evolutionary genetics?)

@Remi.b Would you please put into a response what NS's accurate mathematical definition is?  My understanding is that Fisher's fundamental theorem of natural selection has been subjected to some controversy as a result of Price.

I don't think the so called Fisher's fundamental principle of NS is questioned by Price equation (but I might be wrong). Consider for example this simple equation for haploid selection $$p(t+1) = \frac{W_Ap(t)}{W_Ap(t) + W_aq(t)}$$ For more equations and explanations, please just have a look at an intro book to population genetics.

@Remi.b What do those terms represent?  Also, would you provide a citation please?

It really is a very standard equation. You'll find it in any good intro book to population genetics. It was published by Fisher at the beginning of the 20th century. I am a bit lazy to find the original paper but in any case, I would rather recommend to read an intro book than Fisher papers (Fisher is not really an easy to read author)!

I have a couple of intro books and I haven't seen that equation.  What do those variables mean?

Re my comment about Fisher, I was referring to what he wrote in this paper (DOI:  10.1111/j.1469-1809.1972.tb00764.x), "Fisher's fundamental theorem of natural selection is mathematically correct but less important than he thought it to be."

Consult a dictionary to see the meaning of the word, and then apply it to the context of interest, which you is not defined in the question, although I don't think it has anything to do with who is playing in a sporting event.

My favourite definition

Selection is a fitness differential associated to a genetic variance among individuals in a population.

You might want to have a look at What does fitness really mean?.
What I like about this definition
I personally went with this definition because it is short and clear cut and directly highlight the importance of mathematical statistics in the evolutionary biology literature.
What I don't like about this definition
This definition has the issue that it may be hard to be fully understood to a layman reader. Also, I think my definition lack a mention of the phenotype as being causal to the fitness differential. While such mention is not necessary, I think it would clarify in most minds what selection is really about.

Now, let's consider the definitions that we typically get when we google the question
Wikipedia
Here

Natural selection is the differential survival and reproduction of individuals due to differences in phenotype

I am quite unhappy with this definition. While I like that it highlights the fact that fitness difference is caused via phenotypic difference, it completely lack the idea that for a change in allele frequency to happen, this variation must be correlated to genetic variation.
I would note that the rest of the introduction on the wikipedia article clarify my criticisms. I only attack the short version (one sentence) version of the  definition.
Dictionnary.com
Here

the process by which forms of life having traits that better enable them to adapt to specific environmental pressures, as predators, changes in climate, or competition for food or mates, will tend to survive and reproduce in greater numbers than others of their kind, thus ensuring the perpetuation of those favorable traits in succeeding generations.

There are a few things I don't like about this definition
..traits that better enable them to adapt..
It sounds like they are talking about evolvability. I would just say traits that are better adapted.
..too much emphasis on the role of the environment..
Also, I don't like that it is presented as if all selection pressures where environmental (predators, climate, competition for food, etc...) and completely ignore a very important source of selection which are simply related to the functioning of the body. A mutation that causes an individual to fail copying DNA anymore will obviously be lethal and under very strong purifying selection. Such the "outside-of-the-body environment" is important but it is definitely not the only thing.
It is kind of a common misconception about evolution that selection occurs when there is a climate change and not so necessarily in other case in most people's mind.
..ensuring the perpetuation of those favorable traits in succeeding generations..
Well.. it does not "ensure" that these traits will be kept. First because it only increases the probability of certains allele to be kept or to reach fixation, it does not ensure it. Also, because depending on the genetic framework, once the underlying QTL have reached a given frequency, depending on the actual genetic mechanism (epistasis, dominance and others), traits that are being express might differ quite a bit from those that have been selected for.
Overall, I think the definition lack any notion to genetics.
Biology-online
Here

A process in nature in which organisms possessing certain genotypic characteristics that make them better adjusted to an environment tend to survive, reproduce, increase in number or frequency, and therefore, are able to transmit and perpetuate their essential genotypic qualities to succeeding generations

I like this definition. The only issues in my opinion are very similar to my above opinions

too much emphasis on the environment as done before
it seems that they define more the consequence of natural selection than what it actually really is.

What Google gave me when I entered 'what is natural selection?'

the process whereby organisms better adapted to their environment tend to survive and produce more offspring.

Again there is IMO, too much emphasis on the environment and no mention of thee actual mechanism (fitness - genetics correlation).

Potential confusion
Some people might use the term "selection" to refer to the existence of phenotype - fitness correlation and the "response to selection" as being the effect of such correlation of the population genetics whenever there is a non-zero association between phenotype and genotype. This nomenclature would typically be inspired by the terminology used in the Breeder's equation (see How to interpret the breeders equation?).
However, none of the definitions I could find clearly suggested that selection was nothing but a phenotype - fitness correlation as all of them implied that selection has a long term impact on the population phenotype which such phenotype - fitness correlation would not have in absence of a phenotype - genotype correlation.

Lewontin recipe
I am not sure a recipe count as a definition but Lewontin recipe is a good way to understand the what is natural selection

Individuals in a population varies in terms of a given trait
This trait has some heritability.
The fitness varies (not necessarily linearly) as the trait varies.

The recipe hides the complexities behind the term heritability. You can learn about the math of heritability at Why is a heritability coefficient not an index of how “genetic” something is? .

I find your preferred definition (at the top) too inclusive. Why does selection have to lead to changes in allele frequency, in the general case? It has to for the selection to lead to evolution, but you can have natural selection without evolution (if the selected traits do not have a genetic basis/no narrow sense heritability). In definitions, there are however often some confusion about whether they are defining natural selection or evolution by natural selection.

I'm also wondering why you only cite website/dictionary definitions instead of books/papers from evolutionary biology and/or philosophy of biology.

Yes, NS can be a process of evolution, but so can other factors as well. That doesn't however mean that NS has to lead to evolution. And I don't get your second point; ofcourse you can find argument on NS i peer reviewed literature (papers and books). Online encyclopedias are hardly an authoratative source. My answer contains a couple. Its a somewhat tricky topic though that sometimes bordets on semantics and the philosophy of biology. And I agree that there are probably conflicting views out there.

I think you're right. NS refers to the fitness - genotype association and not to the resulting change in allele frequency. I got confused due to the post The falsifiability of natural selection, edited my definition wrongly. I've edited it back to the original definition. I've removed my comment too. Thank you!

I seem to be missing something with your favorite definition of selection. When I think of selection, I think of a verb, and with that definition, am not seeing a verb. What am I missing?

Selection is defined as a process. It is a noun. Note that outside of biology the term selection can also be both a noun and a verb.

@Remi.b I think I now understand. I was misinterpreting the differential part to be before selection instead of after. So, the differential decreases as unfavorable/deleterious genetic variants get removed.

To be fair the word "is" was missing in the definition before. I edited after reading your comment $\ddot \smile$ That probably created your confusion.

@Remi.b Say the frequency of an allele has gone from 0.5 to 0.6 within a generation.  If you are given only this information, you do not know whether this is attributable to genetic drift or selection.  However, the fact that there is a change in frequency means there’s a positive correlation between the allele and fitness.  This does not mean there was selection.  This positive correlation could be attributable to luck/chance.  That is, it could be a change in frequency due to drift.  From my vantage, in order for there to be selection, there has to be an influence toward directional change.

Directional change, such that the population becomes better at managing the force of selection.

How selection is "best defined" is clearly subjective. However, even though it is a key process in evolution, the exact delimitation of (natural) selection is not clearcut, or rather, authors have defined it in slightly different ways in relation to the evolutionary process (see below, especially quote at bottom from Wade & Kalisz). A paper worth reading as a starting point, if you really want to dig deeper into the definitions of evolution and natural selection is Godfrey-Smith (2007) "Conditions for Evolution by Natural Selection". There, he goes through several attempts of verbally defining "evolution by natural selection" (among them two version of Lewontin's recipe that Remi.b mentions in his answer).
Many of the definitions take a similar form as this modified version of Lewontin's recipe (the 1980 version, page 491 in paper):

A sufficient mechanism for evolution by natural selection is contained in
   three propositions:
(LI) There is variation in morphological, physiological, or behavioral
   traits among members of a species (the principle of variation).
(L2) The variation is in part heritable, so that individuals resemble their
   relations more than they resemble unrelated individuals and, in particular, offspring resemble their parents (the principle of heredity).
(L3) Different variants leave different numbers of offspring either
   in immediate or remote generations (the principle of differential fitness.

The aim in this paper is however not only to define "natural selection" but "evolution by natural selection" (which is a bigger question). So from the definition above (or others in the paper), the issue is on how to draw the line between "natural selection" (as a condition) and "evolution by natural selection" (as a process). If this is at all possible. To me, it is natural to draw the line between "selection of phenotypes" and "transmission of phenotypes to the next generation" (through genetic variance/heritability), which sort of mimics the breeders equation. So to me, it is natural to see "natural selection" as the result of a fitness-phenotype correlation. In some ways, this mimics an the 1970 version of Lewontin's recipe (page 490 in paper):

Different individuals in the population have different morphologies,
  physiologies, and behaviors (phenotypic variation).
Different phenotypes have different rates of survival and reproduction in different environments (differential fitness).
There is a correlation between parents and offspring in the contribution of each to future generations (fitness is heritable)

Here, point 1-2 corresponds to my view of "natural selection", while the 3rd point is necessary for "evolution by natural selection". Note however that this definition has other problems if taken on its own, mentioned in the paper.
A similar view is expressed in Haldane (1957):

Natural selection is a statement of the fact that the fictitious parental population differs significantly from the population from which it was drawn. For exemple, with regard to any specific metrical character it may differ as regards the mean, variance and other moments. A difference in means is called a selection differential (Lush,1954).
Selection may be genotypic or phenotypic. Phenotypic selection may or may not lead to genotypic selection.

Here, (natural) selection is clearly seperated from the possible subsequent effects of selection (evolution).
Even more clearly put (also highlighting that there are different views on this topic), from Wade & Kalisz (1990, Evolution):

When we measure phenotypic selection in natural populations, we compare the phenotypic distribution at one time with the phenotypic distribution at some later time(s) within the same generation. It is from this comparison that we drawn our inferences regarding the operation of viability and fecundity selection. We deliberately avoid examining changes across generations because, when the process of transmission changes the phenotypic distribution, we would confound selection and transmission. We consider the clear separation of these two processes to be conceptually and practically important to the study of selection although we acknowledge that other authors prefer to include inheritance as part of the definition of natural selection (e.g. Endler, 1986).

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How do we find antibiotics?
So the last class of antibiotics were made in 1984 (I think), which makes it appear as though they are hard to find(/design maybe). How is it then they were discovered? Was it by chance? I know some where accidents, but how are the majority found, testing lots of chemicals on your target?
I imagine now we would have the capability to quickly identify structures and molecules unique to pathogens and be able to model them on a computer, and generate suitable proteins or other compounds that can interfere with their bonding/properties to damage the pathogen?
For something like a 70s ribosome in a pathogen, what is the process of being able to understand its structure, its shape, etc? How much effort does it take to model onto a computer? Or instead a single protein (as a 70s ribosome will be more complex), how long does it take to model a new protein?
Thanks for any help :)

You have lots of questions.  Which is the exact one you want answered?

Was it by chance?

Yes, sometimes, Penicillin was discovered by chance (and good observation), see http://www.nobelprize.org/nobel_prizes/medicine/laureates/1945/fleming-bio.html.

I know some where accidents, but how are the majority found, testing lots of chemicals on your target?

Other important classes, like tetracyclines, were discovered by screening of soil samples for antibacterial activity (The history of the tetracyclines
). At that time it was not known what is the target of tetracycline, it was only observed that it was able to inhibit bacterial growth.
A synthetic antibiotic, nalidixic acid, was discovered as an impurity in the synthesis of another pharmaceutical agent and later became the template for other important antibiotics like ciprofloxacin. (Origins of the Quinolone Class of Antibacterials)

I imagine now we would have the capability to quickly identify structures and molecules unique to pathogens and be able to model them on a computer, and generate suitable proteins or other compounds that can interfere with their bonding/properties to damage the pathogen?

In theory, yes, but from computer simulation to a drug there is a long, bumpy road. Most bacteria have a cell wall (with either one or two membranes, see here for a detailed discussion), so drugs need to penetrate this barrier before reaching their target. Even if they do so, they must also preferably inhibit bacterial enzymes but leave human enzymes active. This is especially complicated for targets, like DNA replication, protein synthesis, etc. which evolved early in evolution and are common to bacteria and humans. Some antibacterial drugs target tiny differences between humans bacteria, for some like Gentamicin it works well, for others like Chloramphenicol the side effects are dose-limiting. Here is a good blog entry on this topic: Antibiotics not as easy as theysay, look at the blog for other excellent comments on drug discovery and antibiotics).
For something like a 70s ribosome in a pathogen, what is the process of being able to understand its structure, its shape, etc? How much effort does it take to model onto a computer? Or instead a single protein (as a 70s ribosome will be more complex), how long does it take to model a new protein?
To quote Wikipedia:

"Prokaryotes have 70S ribosomes, each consisting of a small (30S) and a large (50S) subunit. [..] The large subunit is composed of a 5S RNA subunit (120 nucleotides), a 23S RNA subunit (2900 nucleotides) and 31 proteins."

To get a computer model of the structure for a single protein where a similar protein is known, it takes a few hours. But to validate this model, i.e. showing that the hypothetical structures matches the real structure, it takes months of human work. You can imagine how much work it is for 31 proteins. In addition tiny deviations in the model, may cause your predictions to give false positive or negative hits (i.e. your computer model predicts that inactive compounds bind to the target or real inhibitors don't do anything to the target).
The traditional approach, finding compounds which kill bacteria or inhibit their growth, is much more promising since one might discover novel targets in bacteria and microorganisms came up with dozens of ways of killing their competition. One new approach is to cultivate bacteria which cannot be cultivated with traditional methods and screen them for antibacterial compounds, e.g. as described in this summary of this research article
Some more good reads on this topic:

The role of serendipity in drug discovery
A Brief History of the Antibiotic Era: Lessons Learned and Challenges for the Future

I don't think that computer modeling will be the way new antibiotics in the near future are discovered. Besides all the issues with modeling itself as mentioned above, it's also really easy to find something that kills bacteria (semi-relevant XKCD: https://xkcd.com/1217/), but you really need something that's also mostly harmless to human cells. So you'd need to model not only the ribosome (and who says that's the only / best target) but also the whole of the human proteome to see if a compound doesn't to anything bad there.
For the near future I don't think we have anything better than just screening: throwing everything we have at bacteria and human cells, and seeing which compounds specifically kill bacteria. An example of a big project in this field: http://www.nature.com/nature/journal/v533/n7602_supp/full/533S65a.html
To make your hit-rate a bit bigger you can always make a big selection of "antibiotic-like" molecules and test those: http://www.nature.com/nature/journal/v533/n7603/full/nature17967.html


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How is Coenzyme A Transported to the Matrix?
So, I've been researching cellular respiration on my own, and trying to keep track of most of the major processes. However, I do have one question left: I can't seem to find any sort of information about how Coenzyme A (I think it's made in the cytosol) is transferred to the matrix (the inside of the mitochondria, inside the inner membrane). Is it transported with a shuttle like for NAD+/NADH, a translocase like for ATP/ADP, or something else? Thank you for your time.

Good question, to which I cannot find the answer. I doubt whether it is a shuttle, because the nature of shuttles is that they don't transport the difficult bits. There is a carnitine shuttle for transporting acylCoA across the inner mitochondrial membrane, but it transports the acyl-carnitine, not the CoA. The mammalian enzymes for CoA synthesis were only identified this century, so I don't think it's text book stuff.

I noticed that PANK2 (a mitochondrial pantothenate kinase) seems to be essential for normal mitochondrial function.  1 2 Is the CoA being made in place?

I think this can clear your doubt...As it shows how the transport is done between the matrix and cytosol..
And it also explains the presence of coenzyme A ie CoA SH at both the sites.

It would be great to source this answer... as it stands, it doesn't have any authoritative references.  Thanks!


text:
What is the exact percentage of spectral changes that human pinnae introduces into the acoustic input signal?
I read somewhere that amount of spectral changes that human auricula introduces into the input signal is 6%.
Now I cannot find that literature.
Does anyone know a source that might confirm this, or may confirm this him/her self? Well or contradict it if necessary.

%of what? dB per frequency band? It depends on various factors, including the acoustic frequency. Could you specify your question?

Even that is OK info. I am looking for any spectral change introduced by pinnae. Someone just put out, I guess a summarized percentage for all changes caused by pinnae. Intensity/freq ratios i.e. power spectral density changes are fine, if you know where to find the info.

I can have a look for a decent paper. Please give me 24h. Perhaps adapt your question accordingly as it is quite vague. It may help me and others to formulate an answer. And what do you mean with even that is OK? What is it that you want to know? Be specific. It's a cool topic though. Happy to spend my time on this :)


text:
What's the best way to measure/calculate the size of a light beam at the sample of a microscope?
I am using a microscope with an LED derived light through the epi-fluorescent port of a microscope.  I know that the "field of view" for a given objective is equal to the field number/magnification but I don't know that this is the actual area of illumination on the sample.  In my case, I am using a 40x objective with field number 26.5.
Secondly, if I were to use a pinhole filter between the light source and the back of the objective would this limit the area of illumination so long as the pinhole was smaller than the f.o.v. dimension?
I would be grateful for any answers, most of the information I can find on beam size at sample is related to spot size calculations of resolution.

Well you can always use a piece of white circular paper and draw the outline of the light onto it since it should be visible. This is a quick and dirty method that can be improved by taking a photo of the light with a camera if you have one and then comparing the distance of the edge of the paper measured with a ruler to that of the circle of light.


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Is pork poisonous?
Besides religious prohibition, there are several non-religious arguments against eating pork. A few of which are:

Pigs and swine are so poisonous that you can hardly kill them with strychnine or other poisons.
Swine and pigs have over a dozen parasites within them, eg tapeworms, flukes, worms, and trichinae. There is no safe temperature at which pork can be cooked to ensure that they will be killed
The swine carries about 30 diseases which can be easily passed to humans

I would like to hear some scholarly verification regarding these points. Simple Yes-No-Yes will be enough, elaboration is welcome, though.
Thank You

These "non-religious" arguments all seem to be found in religious contexts.
The whole "pigs are immune to poison" thing may have stemmed from the fact that pigs can successfully kill and eat poisonous snakes. But so can people.

Pigs and swine are so poisonous that you can hardly kill them with strychnine or other poisons.

This is a non-sequitur. An animal being poisonous does not imply that it resists to poison, nor the reverse is true.
In any case, to the extent of my knowledge pigs do not produce any specific poison. Obviously, if you could provide a more specific claim, this could be tested a bit more in depth.
The second part, instead, is plain false. You can definitely kill a pig with strychnine.
Both the Merk veterinary manual and Diseases of swine, 9th edition report an oral lethal dose of 0.5-1 mg/kg.
For comparison, the CDC reports a probable lethal oral dose of 1.5-2 mg/kg for humans.

Swine and pigs have over a dozen parasites within them, eg tapeworms, flukes, worms, and trichinae.

Sure, pigs do have parasites. Chapter 55 of Diseases of swine is specifically on parasitic infections.
Now, do ALL pigs have them? The answer is no, some parasites are more common than other, and the amount of parasites depends on the health status of the farm.
For instance:
Northern Europe (Roepstorff et al. 1998)

In Denmark (DK), Finland (FIN), Iceland (I), Norway (N), and Sweden (S), 516 swine herds were randomly selected in 1986-1988. Individual faecal analyses (mean: 27.9 per herd) from eight age categories of swine showed that Ascaris suum, Oesophagostomum spp., Isospora suis, and Eimeria spp. were common, while Trichuris suis and Strongyloides ransomi-like eggs occurred sporadically. Large fatteners and gilts were most frequently infected with A. suum with maximum prevalences of 25-35% in DK, N and S, 13% in I and 5% in FIN. With the exception of the remarkably low A. suum prevalence rates in FIN, no clear national differences were observed. Oesophagostomum spp. were most prevalent in adult pigs in the southern regions (21-43% in DK and southern S), less common in the northern regions (4-17% adult pigs infected), and not recorded in I. I. suis was common in piglets in DK, I, and S (20-32%), while < 1% and 5% were infected in N and FIN, respectively. Eimeria spp. had the highest prevalences in adult pigs (max. 9%) without clear geographical differences. I. suis and Eimeria spp. were recorded for the first time in I, and I. suis for the first time in N.

USA (Gamble et al. 1999)

To determine Trichinella infection in a selected group of farm raised pigs, 4078 pigs from 156 farms in New England and New Jersey, employing various management styles, were selected based on feed type (grain, regulated waste, non-regulated waste).
[...]
A total of 15 seropositive pigs on 10 farms were identified, representing a prevalence rate of 0.37% and a herd prevalence rate of 6.4%. A total of nine seropositive pigs and one suspect pig from six farms were tested by digestion; four pigs (representing three farms) harbored Trichinella larvae at densities of 0.003-0.021 larvae per gram (LPG) of tissue; no larvae were found in six pigs.

China (Weng et al. 2005):

The prevalence of intestinal parasites was investigated in intensive pig farms in Guangdong Province, China between July 2000 and July 2002. Faecal samples from 3636 pigs (both sexes and five age groups) from 38 representative intensive pig farms employing different parasite control strategies were examined for the presence of helminth ova and protozoan oocysts, cysts and/or trophozoites using standard techniques. Of the 3636 pigs sampled, 209 (5.7%) were infected with Trichuris suis, 189 (5.2%) with Ascaris, 91 (2.5%) with Oesophagostomum spp., 905 (24.9%) with coccidia (Eimeria spp. and/or Isospora suis) and 1716 (47.2%) with Balantidium coli. These infected pigs were mainly from farms without a strategic anti-parasite treatment regime.

However, note that Boes et al. 2000 reports higher percentages.

The prevalence of helminths in pigs was investigated in five rural communities situated on the embankment of Dongting Lake in Zhiyang County, Hunan Province, People's Republic of China, in an area known to be endemic for Schistosoma japonicum. The helminth prevalences identified on the basis of faecal egg count analysis were: Oesophagostomum spp. (86.7%), Ascaris suum (36.7%), Metastrongylus spp. (25.8%), Strongyloides spp. (25.8%), Trichuris suis (15.8%), Globocephalus spp. (6.7%), Gnathostoma spp. (4.2%), Schistosoma japonicum (5.0%) and Fasciola spp. (1.3%).

Kenya (Nganga et al. 2008):

A total of 115 gastrointestinal tracts (GIT) from 61 growers and 54 adult pigs were examined between February 2005 and January 2006. Seventy eight (67.8%) had one or more helminth parasites, of which thirty six (31.3%) were mixed infection. Ten types of helminth parasites encountered in descending order of prevalence were, Oesophagostomum dentatum (39.1%), Trichuris suis (32.2%), Ascaris suum (28.7%), Oesophagostomum quadrispinulatum (14.8%), Trichostrongylus colubriformis (10.4%), Trichostrongylus axei (4.3%), Strongyloides ransomi (4.3%), Hyostrongylus rubidus (1.7%), Ascarops strongylina (1.7%) and Physocephalus sexalutus (0.9%).

There is no safe temperature at which pork can be cooked to ensure that they will be killed

False. Proper cooking, as well as freezing (but see below) are effective in killing worms.
The CDC suggest:

The best way to prevent trichinellosis is to cook meat to safe temperatures. A food thermometer should be used to measure the internal temperature of cooked meat. Do not sample meat until it is cooked. USDA recommends the following for meat preparation.
For Whole Cuts of Meat (excluding poultry and wild game)
Cook to at least 145° F (63° C) as measured with a food thermometer placed in the thickest part of the meat, then allow the meat to rest for three minutes before carving or consuming.
For Ground Meat (excluding poultry and wild game)
Cook to at least 160° F (71° C); ground meats do not require a rest time.

Also

Curing (salting), drying, smoking, or microwaving meat alone does not consistently kill infective worms; homemade jerky and sausage were the cause of many cases of trichinellosis reported to CDC in recent years.
Freeze pork less than 6 inches thick for 20 days at 5°F (-15°C) to kill any worms.
Freezing wild game meats, unlike freezing pork products, may not effectively kill all worms because some worm species that infect wild game animals are freeze-resistant.
Clean meat grinders thoroughly after each use.

The swine carries about 30 diseases which can be easily passed to humans

Again, sure pigs can carry diseases that can be passed to humans, but proper storing and cooking of meat is effective in getting rid of the great majority of bacteria.
Finally in 2012 Public health England reported food poisoning caused by red meat as accounting for 17% of all food poisoning incidents, with pork accounting for 3%. By comparison, poultry accounted for 29% of food poisoning events (although people eat more poultry than red meat).
Similarly, the CDC report on the Attribution of Foodborn Illness (1998-2008) puts red meat accounting for 12%, pork as accounting for 5.4% and poultry 9.8%.

Just a summarizing note: The primary reason to be careful with pork is for tapeworm- Taenia solium. Most pathological form of the disease is neurocysticercosis (mostly because it is difficult to cure compared to gut infection).

@WYSIWYG: good point. Taenia can be quite problematic especially in poor countries where it is more prevalent.

@nico ... thanks. you may find more here. as you said: if you could provide a more specific claim...  i would like to add: Farmers will often pen up pigs within a rattlesnake nest because the pigs will eat the snakes, and if bitten they will not be harmed by the venom

First: There is no biological reason to not eat pork. These bans (Jewish and Islamic) are based on religious rules, so this is more a cultural, not so much a biological answer.
The reasoning that pork meat would deteriorate pretty fast in warm climates is true, but it is also true for all other sorts of meat (like cattle, goat or sheep). Besides cultural reasons (think of India, where cows are holy) there is another reason according to the antrologist Marvin Harris.
In his book "The Sacred Crow and the Abominable Pigs" (you can find a chapter on pigs here and another interesting article on that topic here) he says that feeding habits are important, too. While goats, cows and sheep can be fed a grass only diet, this is not possible for pigs. They need a grain-based diet (where they compete with the humans for the food) or at least rich woods to survive. As these were depleted by the humans in the middle east, pigs couldn't be held sustainable.

Joseph Campbell also points out that pigs are across many cultures very strongly associated with mother deities.  So it would make sense that the Jews, with their strong rejection of female deities, would deem the animals most closely associated with them to be off-limits.  Also remember Cain and Abel.  The God of the Bible just doesn't much like farmers, he prefers herders.  Farmers keep pigs, not herders.


text:
Does the source of caffeine affect the biological impact?
I've recently decided to give up my morning coffee in lieu of a caffeine pill. Both are around 200mg (my Tim Horton's XL 4x4 was 240 mg of caffeine) of caffeine. We were talking about the various impacts this has on my body (for example, I now need a different source of the whopping 680 calories the beverage used to give me) and one thing that came up was that the caffeine pill would be more damaging to my liver.
I was resistant to their claims, since they were simply basing it off what they heard in college from various health advisers, but three people from different backgrounds all concurred that the pills would be more harmful to my liver in spite of the the fact that there's a decreased quantity.
The points to their argument were:

The concentration of caffeine pills is greater than that of the coffee.
The caffeine in the pill is synthetic, and thus harder for the liver to process.

My counter to those points were that the tablet takes longer to dissolve than the coffee which I'd expect go straight into my bloodstream. (And in fact, I notice it takes longer to get the kick from the pill, and it lasts longer, which would be consistent with my counterpoint). As far as synthetic, I was under the impression a chemical is a chemical, that's what's so great about chemicals.
I understand that changing from coffee to pills will have some sideeffects (less antioxidants, a need to replace the sugars I had before, etc). But my question isn't around those - it's specifically around whether the effects on the organs (emphasis on the liver) are different when caffeine in similar dosages is delivered via a pill as opposed to a brewed liquid. Other comments (as opposed to answers) are welcome, as I would not blindly ignore wise consul, but I would appreciate if answers focused on the question.

For your body it makes no difference where the caffeine comes from. It works in the usual way.

The caffeine in the pill is synthetic, and thus harder for the liver to process: caffeine is caffeine, so that myth can be dropped from the question. The thing here is pharmacokinetics. Perhaps the pill takes longer, or shorter to be absorbed, that may, or may not affect liver function.


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Periods of Heavy Speciation
I have a set of microRNA ages with corresponding labels suggesting which clade they first emerged from. For instance, for hsa-mir-1, let's say, it would have an age of Eutheria. I have several peaks in the distributions of my age. One idea I had was to check to see if these peaks correspond to periods of intense specialization. For instance, the Eutheria clade saw a vast diversification of species relative to other clades. I'd like to determine this from a more computational perspective rather than Googling each clade.

Can you clarify what exactly your question is? You want to phylogenetically classify using microRNAs??

My guess (as your question need heavy editing!!) would be MiRdup.

MiRdup Goals:

Validation of pre-miRNAs predictions
Prediction of mature miRNA

Abstract: MicroRNAs (miRNAs) are short RNA species derived from hairpin-forming miRNA precursors (pre-miRNA)
  and acting as key post-transcriptional regulators. Most computational
  tools labeled as miRNA predictors are in fact pre-miRNA predictors and
  provide no information about the putative miRNA location within the
  pre-miRNA. Sequence and structural features that determine the
  location of the miRNA, and the extent to which these properties vary
  from species to species, are poorly understood. We have developed
  miRdup, a computational predictor for the identification of the most
  likely miRNA location within a given pre-miRNA or the validation of a
  candidate miRNA. MiRdup is based on a random forest classifier trained
  with experimentally validated miRNAs from miRbase, with features that
  characterize the miRNA-miRNA* duplex


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Where in the world does blue eyed whites originate from?
I know that there were no blue eyed people until ~6000 years ago due to a mutation and all blue eyed people have a single common anchestor.
But where in the world does it originate? I assume it originates from somewhere in Europe but is it known more specifically where like Scandinavia, Eastern Europe, and so on or is it impossible to know?

Wikipedia has your answer already !

@Dexter Exactly where is the answer to the "Where in the world..." question?

@fileunderwater Reference no 46

@Dexter How about elaborating on that instead of posting an uninformative link to a wikipedia page. I also dont see how the finding of a blue eyed human in Spain from 5000BC is answering the question of the origin of blue eyes. Are there other 5000BC hunter-gatherers from other parts of Europe with sequenced genomes (where the allele wasn't found) used as comparisons? Otherwise it is only showing that the allele is more than 7000y old and occuring in Spain at that time.

@fileunderwater I agree I didn't elaborate. Sorry about that. However that doesn't mean I posted uninformative link. Link suggests 7000 y old skeleton with homozygous HERC2–OCA2 locus which is strongly associated with blue eyes.  In fact first link from google search gave me origin of blue eyes in Black Sea region (and guess which gene was correlated ? OCA2.

@Dexter Sorry about the wording "uninformative link" - I meant that the link text was uninformative, not necessarily the content. Your last link is the first one that seems to provide an answer to the question though. You should post it as an actual answer instead.


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Evolution of spider webs?
Web making seems like a fairly complex behavior built from a pretty strong material.  So how exactly did it evolve? Do we have any clues about what kind of features/behaviors preceded web making and made it possible? Are there any examples of convergent evolution?

All actually very interesting questions!

Some creator gods were involved. Spiders aren't creative enough to come up with this idea.

One of the comment to David's answer (which covers the history and reasons for spiderwebs in its two links) mentions a comparison between web patterns and molecular phylogeny. Not precisely that, but I found this article which opens up some interesting possibilities (I can delete this or turn it into a comment if you consider it too unrelated, please let me know).

Fernández, Hormiga & Giribet. 2014. Phylogenomic Analysis of Spiders Reveals Nonmonophyly of Orb Weavers. Current Biology.

Chopped summary:

Spiders constitute one of the most successful clades of terrestrial
  predators. Their extraordinary diversity, paralleled only by some
  insects and mites, is often attributed to the use of silk, and, in
  one of the largest lineages, to stereotyped behaviors for building
  foraging webs of remarkable biomechanical properties. (...) Prior molecular efforts have
  focused on a handful of genes but have provided little
  resolution to key questions such as the origin of the orb weavers.
  We apply a next-generation sequencing approach to resolve spider
  phylogeny, examining the relationships among its major lineages. (...)
  These results imply independent origins for the two types of orb webs
  (cribellate and ecribellate) or a much more ancestral origin of the
  orb web with subsequent loss in the so-called RTA clade.

When comparing molecular family trees, orb weaving araeonoids and deinopoids seem to be more distantly related than thought.
That discovery leaves two possible explanations for the evolution of the spider web: It either emerged much earlier than previously expected and was later abandoned by some species (most believe so). Or, web-spinning and the capacity to spin silk evolved multiple times. Both theories are viable, they just need to catch more spider families to prove which one fits better.

Maybe this answer to another post is helpful for you as well https://mathoverflow.net/a/372105/161287 . It gives interesting perspective on the various roles and purposes of spider webs (with interesting links), and it looks at spider webs from a conceptual point of view.


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Is it easy to test human Flicker Fusion Threshold?
How would you go about testing human flicker fusion threshold? Is the testable rate consistent in humans over time or volatile?

Flicker-fusion rates are very easy to test in humans: you provide a flickering light-source, set it to flicker at different speeds, and get the people to tell you whether the light is flickering or constant. This paper (from 1952) achieved a flickering light by putting a rotating disc with holes in it in front of a projected light source. A more modern testing unit is demonstrated here.
The human flicker-fusion rate does not appear to be a constant. In addition to being influenced by attributes of the light source (such as its wavelength, how much the brightness changes, etc), it also appears to be influenced by factors such as stress and fatigue (pdf).

Great - thanks for the information. I'm mainly curious on how human flicker-fusion rate in athletes might correlate to size and/or performance. As in some players (possibly smaller) 'see' the game faster. But this seems tough to test in a non-biased way. It seems like testing reflexes/reaction times would be more appropriate.


text:
What happens when you take a deciduous tree and place it in a climate controlled greenhouse?
The greenhouse would have stable level of light, (matched with day/night wavelength brightness changes like outside the greenhouse), humidity and temperature.
Do certain processes in the tree not trigger?
Does this harm the organism, and are there changes in life expectancy?

Transplantation success rates vary between species. Do you have a particular deciduous tree in mind? Or are you imagining creating a greenhouse around the tree?

Are you asking whether the tree would drop its leaves in the fall, or if it would just keep on growing as outdoor trees do in the summer?

I dont really know to what extent this has been researched/tried, but I want to know what happens to trees that have evolved to lose their leaves (and other adaptations ofc) when winter stops and the weather doesnt fluctuate annually.

It harms the trees, seasonal chemistry in the plant is reduced and weakened they have tried growing apples and decidious fruit trees at the equator and they have to treat them chemically to help them stay stronger:
http://www.actahort.org/books/49/49_14.htm
the tropics have seasonal queues, and in a greenhouse with no temp and light change, the plant would be very disoriented, the critical glucose and leaf cycling would be very degraded, because plants have most of their queues from temps, water and sun.
http://www.madsci.org/posts/archives/2001-02/981072513.Bt.r.html
more infos

My understanding (as a gardener) is that a lot of temperate-zone fruits actually require a certain number of chilling hours - that is, time spent below some temperature - to trigger fruit production the next season.  (Something similar applies to some bulb & seeds - they don't sprout unless they've experienced some chilling.)  I don't know whether that applies to things other than fruit production, though.

@jamesqf My understanding from living by the Mediterranean, where winters without any chilling night aren't uncommon but most European fruit trees grow and produce fruit, is that chilling days are not critical. Daytime length is probably more important as regulator.

@Pere Dec. The meditteranean evokes citrus grapes and almonds, I just checked this info for apples: Most apple varieties need 500 to 1,000 chill hours or temps below 45 degrees F.... some northern plants require some time in the freezer to sprout, and they do have deciduous biochemistry, where some seasonal change is essential.


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Electroporation vs gene guns

What are the pros and cons of using electroporators (left) and gene guns (right) for transformation in terms of:

Price
Target organism
Efficacy
Ease of use
Maintenance

I am not an expert on gene guns but I will try to give my answer on this question anyway.
Price-wise they are both relatively cheap. The electroporators consumables are only the cuvettes, they cost 5-10 dollar/each. The gene guns use microbeads as bullets and depending on the material they cost between 200 and 300 dollars per microgram, 10-50 dollars per shot, a bit more expensive than electroporation.
About the organisms, guns are used mostly for plant-cells and few other "hard to electroporate" organisms. I don'd have a proper list of them but roughly, if you work with bacteria, yeasts and mammalian cells, then go for an electroporator.
If you need to work with tissues or entire organisms like worm/insects/plants then go for a gun, you definitely cannot electroporate a leaf. But in general, check the literature on what is currently the best method to transfect your system of choice.
Efficacy, also in this case it depends form the cells you are working with. Electroporation reach 10^9/10^10 transform ants per microgram of DNA in case of E.coli and this is the best efficiency you can get nowadays. All other cells will be transfected at lower efficiency, how much lower? It depends from the cells!
Easy of use. They are both very easy to use, it is matter of pressing a button. For the electroporation you need to prepare electrocompetent cells, but the procedure is very easy. For the gene guns you need to coat the beads with DNA, also very easy.
Maintenance. The electroporator do not need any maintenance at all while the gun may need some care in the long run since it has pumps and pressurised chambers, this stuff usually need some attention but nothing special.
Some references:
bio-rad.com/LifeScience/pdf/Bulletin_9541.pdf
bio-rad.com/webroot/web/pdf/lsr/literature/4006174B.pdf
bio-rad.com/webroot/web/pdf/lsr/literature/4006217A.pdf

Would you have any references to add to support your claims?

I bet instruction manuals from bio-rad should be ok as reference. Here they are: http://www.bio-rad.com/LifeScience/pdf/Bulletin_9541.pdf ; http://www.bio-rad.com/webroot/web/pdf/lsr/literature/4006174B.pdf ; http://www.bio-rad.com/webroot/web/pdf/lsr/literature/4006217A.pdf

Great. Please add them to your answer. +1

We use both devices routinely in our lab and I have to say that I prefer electroporation over biolistic any day. The former is cheaper and faster as the only consumable is the cuvet while you have stopping screens, macrocarriers, rupture disks and helium as consumables while electroporators only need cuvettes. Cell preparation times are usually faster for electroporation as well. That being said, you often don't have a choice...

Price
Looking through Google shopping and visiting s few websites, it seems that electroporation is 3000 - 8000 dollars depending on what features you want.On the other hand, gene guns are much more expensive. The most common gene gun, the Helios model from Bio-Rad, is about $17000, including all the necessary parts. As you can see, a gene gun can be more expensive.
Also, the gene gun needs bullets, which are microbeads (or microcarriers, as Bio-Rad calls them), and those cost around 600 dollars. The electroporation cuvettes each are $90. However, they can be cleaned and reused.
Target organism
According to Wikipedia, gene guns are used for mainly for transforming plant tissues, but is also used for animal tissues. According to Bio-Rad, it is good for mainly plant systems and animal systems, but can be used for algae, bacteria, and more.
Electroporation seems to be used more for bacteria. They have used it for yeast also. It has been also used for animal tissues, but it isn't the most suitable target organism. It seems better for in vitro systems since for most electroporation systems need the tissues or cells to be transfected in a cuvette.
Efficacy
For gene guns, the efficiency depends on the environment and the type of cells being used. The transfection efficiency varies for various cell types. I can't find many estimates for the efficiency of gene guns. But some of them are 10-20% of the DNA. Electroporation is agreed to have a very high efficiency. According to Wikipedia:

Normal preparation of compentent cells can yield transformation efficiency ranging from 106 to 108 cfu/μg DNA. Protocols for chemical method however exist for making supercompetent cells that may yield a transformation efficiency of over 1 x 109.[6] Electroporation method in general has better transformation efficiency than chemical methods with over 1 x 1010 cfu/μg DNA possible, and it allows large plasmids of 200 kb in size to be transformed.

Ease of use
Both are very easy to use. They only require the press of a few buttons. However, if you want to find out how to use, you should read the manuals and protocols. The Helios gene gun system manual is available here. The MicroPulser electroporation system also from Bio-Radd has the manual here.
Maintenance
Maintenance for a gene gun is pretty simple. For example, Bio-Rad's handheld gene gun has a simple maintenance (from here):

The improved modified barrel is low in maintenance. It can be cleaned
  easily, using 70% ethanol. The tip of the barrel contains a circular
  nylon mesh, which should be replaced regularly to retain optimum
  performance. To change the mesh, simply unscrew the tip, remove
  the spent mesh and insert a new one over the O-ring. Once the tip is
  screwed back in-place, the hand-held gene gun is operational.

Electroporation needs almost no maintenance as well.


text:
What is the necessary criterion for the maintenance of signaling honesty?
Zahavi's (1975, Journal of Theoretical Biology) handicap principle held that the cost associated with a signal is integral to ensuring that signal is accurate, since dishonest signals would be too costly to bear.  Grafen (1990, Journal of Theoretical Biology) held that in order for signal honesty to be maintained, the signal must be differentially costly, such that it is more expensive for lower-quality individuals.  Getty (2006, Trends in Ecology and Evolution) disputed this:  "Here, I show that (Grafen's) most well known and
influential result (‘the marginal cost of advertising.
should be greater for worse males’) [6], which is widely
interpreted as a proof of the handicap principle, is based
on a simplifying assumption that does not generalize to
signalling in sexual selection. I show that the general
criterion for reliable signalling can be interpreted to mean
that higher quality signallers must be more efficient at
converting signals into fitness and that, in sexually
selected signalling, higher quality signallers can be more
efficient in spite of higher marginal costs."
Nevertheless, Biernaskie, Grafen & Perry (2014, Proceedings of the Royal Society) wrote, "It has long been a challenge to test for the relevant costs of
animal signals [2,17,18,25,42]. This is because, as stressed
above, the modern view of costly signalling theory does not
necessarily imply that observed signals will be costly;
instead, the key prediction is that a given signal size will be
differentially costly for low-quality individuals [2,13,17,31]."  The criterion of differential costliness continues to be invoked despite Getty's critique of it.  So, my question is, what is the criterion necessary for the maintenance of signal honesty?
Note:  This question asks about the maintenance of costly signals that could theoretically be faked, not so-called index signals that cannot be faked.


text:
What is Hamilton's rule for multiple generations?
What is Hamilton's rule as it applies to multiple generations?  Is it that the lineage success given up by the actor must be exceeded by the lineage success acquired times the relatedness between actor and acquirers?  How is this represented?


text:
Is the suicide of a moribund individual to be considered group selection?
When a moribund individual commits suicide (e.g., Refardt, Bergmiller & Kummerli, 2013; http://rspb.royalsocietypublishing.org/content/royprsb/280/1759/20123035.full.pdf), is this to be considered group selection?  It could be considered costly to the individual, since the individual commits suicide and, therefore, loses reproductive opportunity.  And it occurs to the benefit of the group, by saving resources for the group and sparing it susceptibility to infection.  Is this group selection or does group selection require an intentional formation of a group?  If not, what else is necessary for this to be an example of group selection?  (Thank you.)

this seems a subjective answer

@ina What answer are you talking about?

It depends on what form of group selection you are talking about.
Group selection carries a lot of baggage and can refer to two very distinct concepts.  Concepts of group selection comes in two forms type 1, selection occurring on the group level, and type 2 selection on the group level that produces adaptations in said group or organism. The latter is the traditional usage of "group selection" the first(type 1) is now commonly (and confusingly) referred to as multi-level selection. (type 1 and type 2 are my terms I am using them to keep the two concepts identifiable)
Type 2 aka multi-level selection
Group selection (type 2) is simply selective pressures that occur above the individual level, kin selection could be seen as a form of this or it could not. It is still producing advantages and disadvantages to the genes and genes are still acting as the basic unit of evolution. Selection is occurring between groups with the differences between the groups being a product of the genes of the individuals within those groups. The genes are still favored or unfavored there is just many levels on which that the genes products can manifest. This models of group selection are basically just another form of gene based selection and adaptation it just adds another layer in which selection can occur.
Now few argue this form of group selection could not occur just that it would be swamped by normal gene based selection in most instances. There are genes known that are horribly detrimental to the individual and population in return for greatly favoring their own spread, the famous R2D2 gene in mice is an example.
Bacteria can be problematic in this as relatedness may not be a good measure of whether they share the same genes, and kin selection only requires shared genes. Could the behavior in bacteria be group selection in this case, yes, of course it could also be kin selection, the relatedness (Hamilton's original description) description of kin selection is really only useful in animals. In organisms with more lateral gene transfer they only need to share the gene in question, they could be completely unrelated in any other way. Indeed the paper even proposes this low but non-zero relatedness.
Now the big problem type 1
Type 1 is the traditional and first usage of the term group selection, but also the one only rarely proposed today, making it a very confusing term.
the big difference between kin selection and group selection (type 1) is that kin selection (or any form of selection including type 2) is about the selective advantage to the gene, an already well established principle, while many forms of group selection (type 1) propose a new "thing" on which selection occurs. what this thing is is never well defined but then neither were genes when natural selection was discovered.
To prove this form group selection and not kin selection you would have to show no selective advantage (or disadvantage) to the gene, basically you have to eliminate kin selection and other phenotypical expressions as a possibility. Proposed forms of group selection (type 2) can be shown to be products of normal gene based selection so you have to show this is not occurring. (thanks to Remi for this source). Intentional group formation in intelligent organisms (humans) is so far the only proposed mechanism in which this could work, and this would fall under memetics, which means it is occurring when related genetic differences are minor or non-existent.
Your paper does not show this form of selection, it does not even attempt to.
for a further breakdown of the diffrent forms of group selection I recommend this paper, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4850877/

Yes, group selection could have been selecting for suicidal behaviour.

[D]oes group selection require an intentional formation of a group?

There is clearly no need for intention or consciousness for group selection to occurs (e.g. Aviles 1986).
The majority of people working in social evolution agree that kin selection and group selection are the same thing (Lehmann et al. 2007; Abbot et al. 2013). However, people's intuition often fail when talking about group selection while it is not too bad when talking about kin selection (H. Kokko during a speech and L. Lehmann personal communication).

A comment when down voting would be welcome

By "intentional," I was not asking about consciousness.  I meant, does group selection require the selection of processes that would be oriented toward the formation of a group?  But I believe the answer is no because it doesn't even require the formation of a group.
In my understanding, kin selection and group selection are not the same thing, but they have the common property of selection of cooperative behavior (put broadly) via genetic similarity to the recipient.  But the attribution of this genetic similarity is different:  In kin selection, it occurs by descent.


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Overall, for the most part, which is more important--capturing prey or surviving predators or parasites?
For animals in nature, does selection intensity tend to be stronger upon abilities used against parasites or predators or abilities used against prey?  Any empirical reports would be appreciated.
I understand that it would depend somewhat upon the species and the time, but I'm asking about a typical generation in most species.

By strength of selection, I am assuming you mean what it typically means, that is the fitness variance in the population, right? Or do you mean something else like "number of deaths caused by ..."?

@Remi.b I mean that if you were to assign separate numerical values to  an individual's ability to capture prey and to an individual's ability to evade predators or parasites and you were to model that individual's fitness, would the coefficient in front of the ability to capture prey be higher or lower than the coefficient in front of the ability to evade predators or parasites?

The coefficients would depend upon the range of values your metric would take. But the fraction of variance explained by each trait is not. This is the definition I expected. It is likely hard to find such estimates but it is very interesting and it would great to have that. +1


text:
In which direction plants' root grow in weightlessness?
As far as I know, roots of plants grow to the direction of Earth's gravity - this is called gravitropism.
But what happens if plants are in space? Are they able to perceive gravity in state of weightlessness? Either way, where do they grow their roots in those circumstances?
Note: this question may fit better either to Space.SE or to Astronomy.SE, but I was not sure about it.

@TheLastWord I couldn't use Stack Exchange for a very long time because of various reasons.

Astronomers on the International space station have done exactly that and grown Arabidopsis Thaliana in space. You can read the whole article here.
Plant roots apparently grow away from the seed exactly like on earth seeking out nutrients.

either you or me should remove the answer because both are exactly the same.. I am removing mine but take care not to post an answer that is exactly same as a previous one.

but wasn't mine listed before yours..

well.. the listing it seems is not chronological. When I posted there was no answer. Nevermind. The objective is achieved. Mission accomplished :)

It is actually. When I started typing, there was no answer listed.. You started answering after me but submitted before me.. But yes Mission accomplished.. :)

Roots are negatively phototropic in addition to being positively gravitropic. Both growth patterns are mediated by the same hormone, auxin. Removing one factor or the other will not prevent roots from growing "down."


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Are there parasitoids of mosquitoes ? (other than nematodes)
Outside of nematodes, are there any examples of organisms that are parasitoids of mosquitoes ?
I could not find any example in literature so far. I'm notably interested to know if the most known mosquito genera (Aedes, Anopheles, Culex...) have already been described to be parasitized by other insects (e. g. parasitoid wasps), and if this is a common phenomenon in nature.

It happens I just found an answer to my question in a recent review book by George Heimpel and Nicolas Mills. It appears that for now we do not know any  parasitoid of mosquitoes.
Quoting chapter 1 :

"Most insect herbivore species are attacked by
  one or more parasitoid species, but some major
  arthropod pest groups appear to be entirely free
  of parasitoid attack. For instance, we know of no
  parasitoids that attack mosquitoes or other biting
  flies with aquatic larval stages, and no parasitoids
  that attack phytophagous mites or adelgids."

Source:
Heimpel, G., & Mills, N. (2017). Definitions and Interactions. In Biological Control: Ecology and Applications (pp. 1-18). Cambridge: Cambridge University Press. doi:10.1017/9781139029117.003


text:
How does 2-mercaptoethanol lead to shift of the band to a higher molecular weight?
I have a project to isolate a protein with biological properties from a plant. The purified protein forms four bands with similar molecular weight on SDS-PAGE (30–35 kDa) in the presence of 5 % 2-mercaptoethanol, and two bands with lower MW (27–30 kDa) when 2-mercaptoethanol is omitted.
How can these results be explained? What is the easiest and lowest cost method to separate closely related proteins (if that’s what these are, and not just subunits of a single protein)?

I have made edits to try and make this question more readable. Please check my edits to ensure I have not changed your intended meaning.

What do you mean by "purified protein"? Are you asking if your protein is actually purified, or are you confident that it is pure and want to know how to handle next steps?

2-mercaptoethanol (2ME) reduces the disulphide bonds in proteins. If disulphide bonds are connecting two polypeptide chains ("intermolecular") then 2ME would cause them to separate and therefore instead of a higher molecular weight (MW) band you would get one or more lower MW bands.
However, if there are disulphide bonds in the same polypeptide chain, they may cause the chain to fold up. This results in the polypeptide chain to effectively have a smaller hydrodynamic radius compared to the fully denatured chain. In such cases reducing the disulphide bonds using 2ME would cause the band to shift to a higher MW.

What is the easiest and lowest cost method to separate closely related proteins

This is a different question altogether and there are several techniques depending on how "dissimilar" or "similar" the closely related proteins are. 2D PAGE (with isoelectric focussing) is one technique that can offer higher resolution compared to a normal SDS-PAGE. There are many other chromatographic methods.

@R.Rasoulpour iayork's comment is under the question. Anyway, if you think this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.

this is the right answer


text:
What metric(s) is a good proxy for relatedness?
In attempting to seed a simulation, where an individual foregoes resources that go r to same-type individuals and (1-r) to all members (including same-type individuals).  What commonly used metrics are a good proxy for r in this sense?  In other words, if I am seeing a simulation to replicate the parameters of the mean population for, for example, a zebra finch or a human or a house mouse, and I am looking in empirical reports of these species and r does not appear, are there other metrics that are convertible?

I'm not sure to understand what you are looking for. Are you seeking for a way to calculate genetic relatedness? If ris a value for giving food to same-type individuals how do you define same-type? Is it from genetic relatedness or other way?

Thank you for the reply.  No I'm not looking for a way to calculate genetic relatedness.  I have written a simulation and am looking to feed it realistic values for relatedness.  Emphasis upon populations of the zebra finch, human, house mouse, and also populations of trees.  But r is not reported commonly and other metrics are reported more typically, such as FST.  I don't know whether they are substitutable or convertible into r.

This article by Harpending would suggest that but I'm not seeing it in a textbook and am not familiar enough with these measures. Harpending, Henry (2002-11-01). "Kinship and Population Subdivision" (PDF). Population & Environment. 24 (2): 141–147. @Untitpoi

It would seem from the article, unless I am wrong, that 2*Fst is a good proxy for the Hamiltonian r (if benefits can be confined to within subpopulation).  Am I wrong?  @Remi.b


text:
Is it appropriate to say "selection of" or "selection for" an allele that evolves by genetic hitchhiking?
In terms of Sober's selection of/selection for distinction, is it appropriate to say that there was selection of or selection for an allele that evolved by hitchhiking?  I am inclined to say selection of.  Is that correct?

I never remember which is which in Sober's terms and I have a hard time finding a reference that would clarify that for me as they are behind paywalls. Would you mind quoting the definitions of "selection for" and "selection of" in your post?

That's a good question and I don't know the answer because they are discussed in Sober's 1984 book, The Nature of Selection, but I do not have access at the moment.

So, your primary question is not so much about hitchhiking but rather about the terminology of Sober.

I suppose so.  Hitchhiking in terms of the terminology of Sober.

The expressions "selection for" and "selection of", their definitions and their usage have been subject to a number of semantic issues throughout the literature. Good and Griffith (1995) is a good read on the subject.
I would argue that neither "selection for" or "selection of" is appropriate to use in the context of genetic hitchhiking because, in this context, by definition, the increase in frequency of an allele is only due to a different locus nearby that is under selection. So an allele that evolves due to hitchhiking is not directly under selection and only changes frequency indirectly due to nearby selection on a linked site.

Could you please clearly define the terms "selection of" and "selection for" so that we can understand why you consider these terms poorly apply to the case of genetic hitchhiking (or of linked selection to be more general).

Yes, sorry! This paper is helpful. I think my disagreement is with the level of selection we are talking about. But I am happy to be corrected! From this reading, Sober's usage seems that "selection for" would be for the trait that improves fitness, while "selection of" would be some trait that necessarily is brought along (e.g. p9 discusses the polar bear). For an allele, I would only say linked selection in order to prevent any misinterpretation of how selection acts at the genome level.

Good and Griffith (1995) that you pointed out was a very helpful read for me. I edited (adding this paper into it among other things). Please feel free to roll back (or re-edit) if you don't like my edit. By the way... Welcome to Biology.SE!


text:
Is it trivial to assume a version of Hamilton's rule that applies for numerous generations?
Is it trivial to assume that a version of Hamilton's rule that applies to numerous generations is:
C > rB
C = lineage fitness lost by an actor,
B = lineage fitness gained from the act, and
r = relatedness between actor and those that gained lineage fitness?
Or does this rely upon a particular derivation of Hamilton's rule?  If so, does anyone know of a citation in which this derivation is made?
Thank you very much.

I am not sure what you mean by "applies to numerous generations". If the following does not help, can you please clarify what you meant?
Hamilton's rule expresses the condition for which, under a prisoner's dilemna game (see game theory), the stable equilibrium that will be reached is the one where everyone is cooperating. Hamilton's rule is, therefore, a condition to determine the directionality of a dynamic system (the system is dynamic because the state of the system varies over generations).
EDIT

what if the values of B and C differ depending on [the generation]

In other words, you are asking

What if the (social or not) environment is changing over time?

Well, under such circumstance, of course, the simplistic rule that consider B and C as constant won't hold.
You could not simply replace B and C by the the arithmetic mean (or by the geometric or harmonic or any other mean) as the system as two stable equilibriums and upon reaching one there would be no way to get out of it (at least as long as the game remains a prisoner's dilemna).

Hamilton's rule states (according to Wikipedia, for one):  A gene responsible for an altruistic act should increase in frequency if rB > C, where:
B = additional reproductive benefit gained by a recipient
C = reproductive cost to the actor
r = the genetic relatedness of the actor and recipient
My question is, what if the values of B and C differ depending on how many generations have elapsed since the act because of a disparity in the number of, for example, grandoffspring or greatgrandoffspring?

For example, what if after 1 generation, B is F offspring and C is H offspring and after 5 generations, B is G descendants and C is J descendants?  And what if H > rF but J < rG? Is it trivial to assume the act will gain frequency after a long number of (> 5) generations because J < rG?  Is it still Hamilton's rule even if it deals with C and B in the form of descendants rather than offspring?

@sterid Thanks for clarification. Please see edit.

I am not asking about the environment changing.  Here's an example.  Consider Jim relinquishes resources and they go 10% to Bob and 90% equally to all individuals (so, r = .1).  Consider that Jim would have 2 offspring from the resources and Bob would get 9 offspring from them.  But after 5 gen, Jim would have 8 descendants from the resources and Bob would get 100 descendants from them.
2 > .19 but 8 < .1100
Then after 1 gen, there is less of the variant responsible for the act than at gen 0, but after 5 gen, there is more of the variant than at gen 0 (the variant has evolved).


text:
Is there a map of the individual motor axons in the limbs?
As of right now, I can only find a map of nerve fibers, but not necessarily the individual neuron axons.
For example, here's a map of the nerves in the arm and hand.
http://www.innerbody.com/anatomy/nervous/arm-hand

Maybe, sort of; can you clarify why you want this information or what type of map you are looking for?

Nerves are somewhat variable (the image on your link shows an idealized version). Axons are even more variable than nerves. Consider that nerves are growing out from the CNS to muscles that are developing from a completely different germ layer. The actual axons reaching individual parts of muscles are not at all conserved.

@BryanKrause Yes. I'm trying to learn more about how biological neurons could be connected directly to computers instead of indirectly through EEG. If that were possible, I could definitely see full motor and sensory capabilities being implemented in bionic arms.

No it is not possible to map axons at that fine of a scale between individuals.
You mention a possible use for controlling bionic arms. There are a bunch of problems with that approach.

Like @kmm says, at the fine level there is a ton of variation.
I think you are failing to appreciate just how many axons there are, even going to a particular muscle; while each muscle fiber only gets input from one axon, there are thousands of fibers in a single muscle.
The EEG-based approaches to prosthetic control are most relevant when there is a problem with spinal function, for example caused by an injury. In this case, there is no connection between the motor neurons and the brain.
Axons often degrade if their targets are damaged. Therefore, if a hand is lost in an accident, for example, the neurons projecting to the muscles of the hand will atrophy.
If the axons themselves are in place, there are already prosthetics that operate based on muscle contractions in existing muscles. It takes some time to train users to use these devices, but most movements you make involve all sorts of muscles you may not realize are involved, and it is quite possible for brain plasticity to allow muscles in, for example, the shoulder, to control a bionic hand after an amputation.

If for some reason the issues I raised don't apply, there is another alternative: mapping. You don't need to know which axons you want information from, you only need to be able to record their activity (which you will need anyways to operate the prosthetic). Record the activity while the patient tries to move their finger, for example: now you know the signal you should transduce into a finger movement. The technical challenge, then, is being able to isolate that signal from all the other signals from all the other axons in the same nerve. This challenge is related to, though not precisely the same as, the challenge of isolating a signal in the EEG.

With diffusion tensor imaging I they're pretty close on mapping fibers, at least in the brain.

@AliceD Source? DTI is worlds away from mapping individual axons, unless some massive new technological leap has totally escaped my notice. It would certainly be possible to use DTI to map the statistical connectivity of different brain regions but that is nothing like what the OP is suggesting. DTI resolution is on the order of mm, axons can be closer to 1 micron.

aha gotcha.  +1 and thanks for clearing that up for me. Perhaps adding your sources may help you get some more up votes.

@AliceD Yes indeed, I'll try to track some down where possible. Possibly of interest to you I did some research on DTI methods and it seems there are some recent works that get the resolution down to 100um and below, but these are with high-strength 7T+ scanners that are sized only for rodents.


text:
Why women have high Erythrocyte sedimentation rate?
Why ESR (Erythrocyte sedimentation rate)
1. higher in women
2. increases with age
3. increases in pregnancy, infection, malignancies
what I thought so far : since women are menstruating so there shall be some blood loss and this might be related to that.
For age I have no clue and in pregnancy might be related to fact the mass of rbc increases during pregnancy.
But is that right ? and what about  2 and 3 ?

I have already shown an attempt at the question


text:
Would this be called a complex?
When an intermediate is formed between a substrate and an enzyme, this is called an enzyme-substrate complex.
When a molecule is bound to its respective transfer protein, (the molecule being transported is unchanged when released from the protein at the destination) would this be called a complex? If not, what would this be called?

Yes, it's a complex. Anything bound to anything else in biochemistry is a complex, especially when you're talking about proteins. The bonds need not be covalent, either.