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Conscious evolution
Does intelligence play a vital role in the evolution of an organism? In other words does an expansion of learning capacity, increase the odds of evolution for the particular biological entity?

Short answer: No, it doesn't. Evolution is a statistical process which is not influenced by any means of intelligence.

Why then is it that those who are intelligent develop skills, skills which would assisst them to adapt to the unfamiliar enviroment?

This will influence the procf selection, but not the evolution itself.

Selection is a crucial part of evolution. I disagree with you, Chris. Intelligence can actually be a favorable trait in some cases. This does not mean that evolution has an inherent drive to produce ever more intelligent organisms.

@Hav0k And it is not the other way round that being intelligent directs evolution in a certain way. Evolution can be seen a a two-step process: First a mutation occurs and then this mutation is selected for or against. We can influence the second step but not the first.

There is a disagreement between Chris and HavOk because of how the question is phrased I think. Yes, high(er) intelligence may be favorable (enhance fitness) and I am sure Chris would agree with that. When the OP is asking "Does intelligence play a vital role in evolution", (s)he dosesn't mean "does it influence fitness", (s)he means some kind of weird intelligent-driven evolution "I (because (s)he probably doesn't know evolution acts (mostly) on population) become what I think is better for me" or something like that. There is no way to answer yes or no as the question is too poorly phrased.

I hoped my long answer could help but I'm not totally sure. The OP should start understanding what is mutation, what is selection before going to the slightly more complicated details of my answer.

To whom it may concern: "Use comments to ask for more information or suggest improvements. Avoid answering questions in comments." Seems a reasonable question to me. If you have an answer, give an answer. If not, don't abuse the SE system.

First Comment
The questions in the OP's post (and his/her comments below the post) are very poorly phrased and let the reader think that the OP has few knowledge about evolution (no offense). This is a reason why I don't directly address my below answer in the terms of the question as it seems that the OP uses a unusual definition of the term "evolution". @Chris comment ("No, it doesn't. Evolution is a statistical process which is not influenced by any means of intelligence") probably sums up what the OP needed to read but I can't stand but giving a more complete answer about why is intelligence just a random trait and in the meantime arguing in a far-fetched text that intelligence still has actually some funny properties as it may yield to social help (social help does not necessarily needs intelligence) and eugenics programs (that might be argued that it doesn't need intelligence as well).
Summary of the answer

Intelligence (as many other traits) influences fitness
Intelligence (as many other traits) influence the environment that individuals are facing influencing then future evolution
Evolution is not dependent on the will of the individuals in the population.
Indirectly, intelligence may be of some particular interest as it yields to knowledge about physiology and evolution allowing Eugenic program and medicine which both influence future evolution.

Long answer
Fitness
Intelligence influence fitness (=reproductive success). So yes it plays a role in evolution just like any other trait that influence fitness.
Environment
Intelligence evolves and by its presence it will change future evolution as it changes the environment the individual faces. For example, if a bird is intelligent enough to bottle milk bottle, it might over the long term (and assuming that humans are not inventing some solutions to prevent birds from opening their bottles) evolve longer beak to seek for milk from the bottle. Also Intelligence shape culture (set of traditions). Theoretically, all traits does the exact same thing, so again there is nothing so exceptional about intelligence.
As a subset of the impact of intelligence on the environment the individual experience: Intelligence allow culture which changes through time and it is some kind of evolution called memetics. Again, culture changes the environment the individual faces and if culture changes often because of high intelligence, then the environment may change quickly as well.
General basic comment on evolution
It is very important to not think that intelligence will allow a population to "better evolve". Being intelligent does not yield to higher probability of adaptable evolution. It is not because you know what issue you're facing that you'll be consciously able to evolve to that. For adaptation to occur you have to select individuals that are more fit in the population. If individuals in the population know who are fit doesn't mean that those fit individuals will be more selected than otherwise.
Social help and eugenic programs
In addition to the previous paragraph I must point to some potential, indirect impacts of intelligence on the evolution of a population. A population of intelligent individuals may as a group decide on which individuals will reproduce. This is called eugenics and this is the kind of process by which intelligence influence future evolution in a particularly interesting and unique way. For example, we may decide that all people that carry a non-expressed disease gene are not allowed to reproduce in order to suppress this gene from the population. In the same order of idea the population learn how to treat people that have a given genetic disease, the selection against the gene variants (alleles) causing the disease will decrease, increasing then the frequency of the disease in the population. Therefore, some medical actions (and other kind of social help) cause less adaptable evolution while some eugenic program cause more adaptable evolution. I am not talking about ethics here and am not saying we SHOULD stop treating people with genetic disease. Note that other things like the evolution of trait architecture will yield to different ability to undergoes adaptive evolution.
Interpreting my answer
It is important for a starter in evolutionary theory to make sure to learn more about evolution before trying to interpret further this answer in an incorrect way. I want to avoid that someone with few knowledge in evolution starts to think that intelligence is some kind of magical trait or that evolution is a process answering to the conscious needs individuals may have. For the moment keep in mind that evolution has no foresight and is not the result of the will of the individuals in the population (except for eugenic program). Behind this answer there are (maybe hidden) slightly advanced topics such as the strength of selection, mutation-selection-drift equilibrium, the genetic load, trait architecture and evolvability.

Seems safe to assume that intelligence CAN influence fitness, depending on the selection pressures. As Hav0k mentioned, this won't necessarily be favorable, i.e. lead to more progeny. In the case of modern humans, even if a person got more mating opportunities by being, or just appearing to be very intelligent in some areas, it might not do much to affect the population if he/she chose to have fewer or no offspring. To the extent that intelligence was valued in a population, it could of course become very influential. Whether or not (potential) intelligence is something quantifiable that is vertically transferred is another discussion I guess.

Intelligence can have an impact on selection, but keep in mind that flexible intelligence (like the kind humans possess) is a high-cost/high-reward kind of adaptation.  Brains consume a lot of energy, so the resulting intelligent behavior needs to 'pay for itself' (in terms of survivability and ability to reliably gather the necessary food) if it's going to create a competitive advantage.


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The move from RNA to DNA and the necessity of reverse transcriptase
In this piece about giant viruses and the origin of life, in the context of the move from RNA world to DNA world, virologist Valerian Dolja states:

In order to move from RNA to DNA, you need an enzyme called reverse transcriptase

Is this true though? Don't many DNA polymerases work with both, ssDNA and ssRNA templates, i.e. they function as reverse transcriptases although they're not "true" reverse transcriptases. So, in order to move from RNA to DNA, a reverse transcriptase was not a necessity like ribonucleotide reductase was for RNA to Uracil-DNA and thymidylate synthase was for Uracil-DNA to DNA?

Yes, this is true. This flow of information is called the "Central dogma of Molecular Biology". It basically describes the flow of information from DNA to RNA to proteins. Since a virus needs to amplify its genetic information before it can take over the infected cell and make only viral proteins and its genetic information, it has two possible options.
DNA viruses can use the cells replication and transcription machinery to make copies and express proteins. RNA viruses either have to use a reverse transcriptase to make DNA from its RNA genome to go on like the DNA viruses. Or they have to have a special, RNA-dependent (works only on RNA templates) RNA-polymerase (our RNA polymerase are all DNA-dependent and work only on DNA templates) to make more copies of their genome. Our DNA polymerases are dependent on DNA, the same is true for our RNA polymerases. So if the virus is not encoding (and actually bringing a few molecules with it in the virus) of the RT-polymerase or the special RNA-dependent RNA polymerase it will not be able to spread.
Using ribonucleotide reductases would theoretically be possible, but it is not the way nature went. And since a cell contains huge amounts of RNA, I doubt this would be a feasible way, as the enzyme would reduce all RNA. And later on the new viruses also needs new (not reduced RNA) to be packaged into new viruses. This would also be problematic.

You're writing about protein synthesis while my question concerns the transformation from RNA World to DNA World.

Sorry, but this is absolute not clear from your question. Can you rephrase it?

Sorry about that, although I don't really see how it's possible to confuse the discussion of RNA to U-DNA and U-DNA to DNA transformations with protein synthesis. Anyway, I clarified the original post. For those not familiar with U-DNA, here's an article.. http://www.ncbi.nlm.nih.gov/pubmed/16164990

Could you give a reference for standard DNA polymerases using an RNA template?

@AlanBoyd Do you mean the original post by @5heikki?

@Chris yes, apologies for the ambiguity, OP asserts that standard DNA polymerase can use RNA template, but I would like to see the evidence for this.

@AlanBoyd Fine for me, I was just wondering. And yes, I would like to see evidence for it, too. Would be interesting.

Some top Google results for "DNA polymerase RNA template" (works even with Taq in vitro): https://norgenbiotek.com/display-resource.php?ID=82 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC389454/ http://www.pnas.org/content/71/4/1035.full.pdf From last paper: "It is clear from the results presented that E. coli DNA polymerase I is able to synthesize extensive, well-matched
complementary DNA copies from a variety of natural RNAs, provided that the molar ratio of enzyme to RNA template is above a critical level."

The PNAS paper is about the Rous Sarkoma Virus, which is a retro virus. I would expect a RNA dependent DNA polymerase (aka reverse transkriptase) there. The other ones are about DNA polymerase I from E.coli, which is interesting. However this paper (seems to be the original one on this topic) finds a much lower enzyme activity on RNA temples (between 0.1 - 0.4% of that on DNA templates) so the question is, how relevant this is. When there is DNA around this enzyme will most likely not use RNA as a template.

I imagine there wasn't much DNA around when RNA & protein to U-DNA & protein was happening (likely first in the viral realm) thanks to ribonucleotide reductase. The main point was that even present day DNA pols have at least some function in regard to polymerizing DNA from RNA templates and thus "true" reverse transcriptases were not a necessity to the transformation..

This argument seems to be very circular. In an RNA world there presumably wouldn't be any DNA polymerase at all - what we should be looking for is an enzyme that can make DNA using an RNA template - which is a reverse transcriptase. The key step in the evolution of such an enzyme would be switching from polymerising NTPs to polymerising dNTPs.

The fact that present day DNA pols can work with RNA templates in my opinion hints that their main substrate might have once been NTPs. However, then thanks to ribonucleotide reductase you got these fancy new dNTPs and it turned out that they worked as a substrate too. Maybe the higher affinity was there from the start or perhaps it was all about some other advantages (e.g. evading host defenses). So then, over the next 3.7 billion years or so DNA pols further evolved to make use of dNTPs more efficiently, losing their affinity to NTPs almost completely.

..I think "true" reverse transcriptases are a much later evolutionary invention that happened after dsDNA genomes were already a thing. RTs were a new way to avoid them host defenses. Do any contemporary RTs work with U-DNA? I know arcaheal DNA pols generally don't..

..As far as I know, no retroviral genome has ThyA or ThyX for de novo dTTP synthesis. Many dsDNA phages (Caudovirales) have such genes though and these branch near to the root of the relevant trees..

You may be interested in the paper here:
http://www.jbc.org/content/275/33/25523.full.pdf . The authors find that single mutations in an RNA-directed RNA polymerase can reduce selectivity for an NTP substrate to the point that there is no significant preference for NTPs over dNTPs. However this comes at the cost of very much reduced rate of polymerisation.

also, do you think the OP is asking why viruses would ever use RNA instead of DNA?

I don't know if this is helpful in the context of moving from RNA to DNA world, but I do know that certain mutations to T7 RNA polymerase will allow that enzyme to use 2' deoxy nucleotides in addition to the normal ribonucleotides. These mutations were discovered by humans engineering the enzyme, but it's feasible that some transitional enzyme could have utilized both types of nucleotide. Then, those individuals with more DNA were favored because the DNA backbone is more stable than RNA backbone, eventually selecting for the modern DNA to RNA to Protein model.
Here is an article: http://www.sciencedirect.com/science/article/pii/S0168165613002940

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Promoter in the lac operon
Here is the question:
Suppose an experimenter becomes proficient with a technique that allows her to move DNA sequences within a prokaryotic genome. If she moves the promoter for the lac operon to the region between the beta galactosidas gene and the permease gene which of the following would be likely?
Here is the answer:
Beta galactosidase will be produced.
My question to you is: why is this so? I have no idea where this conclusion came from.
Thanks.

The question doesn't make any sense. Apparently before there is any manipulation there is already an intact lac operon present. Is it the lac operon or the lac operator that is being moved? And under what conditions is the production of beta-galactosidase being measured?

Unfortunately, I know nothing more about the question than you do. This is a test question that just doesn't make sense.

If you can, I would ask the test writer to explain.

Since @biogirl has given an answer, I'll add my opinion:
β-galactosidase would be expressed but the permease and transacetylase would not.
The operator lies adjacent to/slightly overlaps the promoter, upstream of the lacZ gene. Binding of the repressor to the operator blocks the promoter, and induction of theoperon involves the repressor leaving the operator unoccupied. If you precisely excised the operator and transplanted it between the lacZ and lacY genes then I think the promoter would be constitutively expressed leading to β-galactosidase synthesis, but the operator would block the polymerase from transcribing the permease gene. In this view the operator would be acting more like a terminator.
Then, if an inducer was added it would relieve the effect of the transplanted operator and the downstream genes would be transcribed. It's even possible that this experiment has been done sometime in the last three decades.
added later:
The OP has now edited the question in such a way as to make my answer, and the answer from @biogirl, nonsensical. The original wording referred to moving "the lac operon" not "the lac promoter", hence my question in a comment asking "operon" or "operator"?
I'll leave my answer here, but this question is now so compromised that I advise everyone to just forget about it.

I believe the answer should be that permease is expressed.

As you can see from the image, if the operator is moved between Z gene and Y gene, Y gene should be expressed and permease should be made.

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Examining milk for presence of harmful bacteria
I am not experienced in diagnostic bacteriology and am interested in understanding more about it in the context of analyzing food purity.
For example, imagine I have a supply of raw milk which might be, for example, a 20 gallon tank. I would like to ensure that listeria, e. coli and salmonella are not present in the milk.
Is it sufficient to take a single drop of the milk and examine it under a microscope or do I have to do more extensive sampling, for example, sampling every inch vertically or something like that?
What is the procedure to make sure my milk is free of the bacteria, or is that impossible?
I am not interested in procedures to kill the bacteria. I know those. I want to understand the diagnostic processes to tell if bacteria is there.

Starting on page 23 are outlined procedures and methods for sampling of milk as required by FDA standards. Of course, individual manufacturers will have internal QA procedures that ensure any state-level testing does not result in penalty to the manufacturer, but since I'm not in the industry, I can't give a more accurate answer. Also, Pasteurization is a method used to make sure microbial counts in the milk are low (not good) or zero (microbes are reintroduced as the milk is opened and used).

As @Kendall says, pasteurization (see here ) is what's generally used to kill pathogenic bacteria in milk. Looking at the milk under a microscope won't help. You'd have to do an ELISA-based assay or PCR... The easiest thing by far is properly carried out pasteurization procedure.

A simple way to know if milk contains any bacterial contaminations is to take ~5 ml of the milk and add a couple of drops of methylene blue to it. If the milk is sterile, it will stay blue. If any bacteria are present they tend to take up the dye, leaving the sample colourless after ~1 hour. A more extensive way would be to plate 3-5 dilutions of the milk sample on LB or nutrient agar.
You don't have to do much extensive sampling. Just make sure that you take a couple of well-stirred samples.

This would seem to only test for any bacteria, not just particular harmful bacteria.

Try to put some references!

@ImprisonedRhesus, if you need to test for particular harmful bacteria, PCR would be the preferrable option as it does not depend on the species and unlike biochemical tests, where you may have to spend more time and run more experiments

@TheMolecularBiologist Okay, if I use PCR I assume I would have to test for particular bacteria. Can I sample anywhere in a vat of milk? In other words does the bacteria spread out so it is present everywhere, or is there the possibility the bacteria would be in just one part of the milk and my sampling could miss it?


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Where can I find trees preserved for hundreds of years?
I assume there are climate conditions that cause trees to be preserved, since there are fossilized trees, however, it may be extremely rare to find a tree in a nascent state of fossilization.
Is it possible to easily find trees that have been preserved for 200-300 years? By a tree, I actually just mean a preserved stump.

Full trees will be hard to find, but a search for "petrified forest" might help you out.

Are you looking specifically for those in the wild? I'm sure there are museums and natural history collections that have specimens. There aren't going to be petrified/fossilized trees only a few hundred years old. Those processes take far longer.

swamps and bogs are a good place, anywhere the log will be perpetually submerged in oxygen poor water.

Yes, this occurs fairly regularly in Alaska and British Columbia (and probably other places with low-elevation glaciers that interact with forested zones) where climactic oscillations have led to rapid advance and recession of glacial extent.
In Glacier Bay, Alaska, for instance, there are a number of interglacial stumps (you can see a few sites marked on this map). These stumps represent a forest that was established in the ice-free interim period between the Last Glacial Maximum (10,000-15,000 ya) and the "Little Ice-Age" (~500 ya). Thus, these trees have been preserved under the ice for a few hundred years and have only been uncovered recently (<100 ya). Many of the glaciers in Southeast Alaska are receding, so new stumps are being exposed every day.

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Bird identification: song two low, two high, five short
This morning I heard a bird that had a song which was two low notes, two high notes, and five quick notes in succession. Location is New England.
Is there any way, short of asking an expert, that I can find out what a bird is from a description of its song or call?
Update - Bird Song Uploaded
I have been able to host a sound clip on Vocaroo:
Unknown bird, Massachusetts, forested suburban environment

@GerardoFurtado Nice website! Haven't heard of it before. I will add it to my repertoire of ID tools. Thanks! :D

Best guess is that the bird is a Song Sparrow, Melospiza melodia. Cornell Lab of Ornithology has a good website for basic facts about birds. Here is the account for Song Sparrow. There is a sample of typical song, but there can occasionally be some variety.
The song is kind of complex and the recording you linked to seems to garble or not capture some of the song, but the changes in phrases throughout the duration seem to match as does the pitch of most of the phrases.

+1 The first audio here is very close to OP's bird's song.


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Thyroid hormone metabolism and excretion
My understanding is that hormones generated by the thyroid gland, including, for example, T4, are excreted and recirculated in the body through the digestive tract. The reason for thinking this is that bile acid sequestrants such as cholestyramine cause a lowering of serum T4. In fact, patients who have hypothyroidism are explicitly warned not to use sequestrants for this exact reason. Here is a statement from a clinical trial discussing the effect:

The enterohepatic circulation of thyroid hormones is increased in
  thyrotoxicosis.Bile-salt sequestrants (ionic exchange resins) bind
  thyroid hormones in the intestine and thereby increase their fecal
  excretion. Based on these observations, the use of cholestyramine has
  been tried. The present study evaluates the effect of low doses of
  cholestyramine as an adjunctive therapy in the management of
  hyperthyroidism. -- clinical trial NCT00677469

Therefore, there would appear to be a metabolic pathway in which T4 is being excreted into the digestive tract and then is later re-absorbed in the lower intestine somehow.
What is this metabolic pathway? How exactly does this mechanism work? Does it have a name?
For more information on thyroid hormone sequestration see:
https://clinicaltrials.gov/ct2/show/NCT00677469
http://www.ncbi.nlm.nih.gov/pubmed/8435884

can you name a primary article that demonstrates that bile acid sequestrates lower circulating T4? Also, I'm not following why you state that T4 is excreted into the digestive tract (?) - can you clarify? T4 is a plasma hormone that acts on nuclear receptors in a wide array of tissues/organs and I've never heard that T4 is secreted into the GI tract and then reabsorbed... bile acids on the other hand are secreted into the GI tract and actively reabsorbed in the distal small intestine

@VanceLAlbaugh I have updated my question with further details.

I have partially answered this question by discovering that the metabolic pathway is called enterohepatic circulation. In this interaction bile salts are absorbed and transported out of ileal mucosal cells by binding to albumin.
However, it is still unkown to me exactly how it is that thyroxine and other hormones are moderated in this process and how it works. Does the albumin collect thyroxine as well as bile salts? How is the process moderated? In other words, bile salts are allowed to be excreted according to some moderated control mechanism. What is this mechanism?

Since you're answering your question, googling "Clearing of Metabolic Waste via Enterohepatic Recirculation" might help. Actually, googling enterohepatic recirculation and anything to do with thyroid hormone(s) will help.

This is an interesting question, but, unfortunately, there is little exact information available. In 1990, de Herder wrote a dissertation on the topic, which is available from http://repub.eur.nl/pub/50862/900411_HERDER-Wouter-Willem-de.pdf . A second mechanism, by which bile acids act on metabolism of thyroid hormones is an endocrine effect, i.e. stimulation of type 2 deiodinase via the TGR5 receptor, see http://dx.doi.org/10.1038/nature04330 for details.


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How do mRNA vaccines work with respect to presentation of the antigen?
As I understand it, mRNA vaccines operate by taking a gene for some distinctive feature of the target virus and arranging for the cells of the vaccine recipient to manufacture the proteins that make up the distinctive feature and present them to the body of the host, which will then form an immune response to the feature.
My question is: how is this feature, assuming it has been manufactured, presented to the body? In other words, is the expectation that it would exist as a separate unit and that separate unit would exit the host cell somehow and be recognized?

Your cited example is the concept behind recombinant viral vaccines, like the ChAdOx1 by Astrazeneca. Nothing to do with mRNA one.

@Shred I edited the question to remove irrelevant comments about how the genomic material enters the cell.

I came here by accident looking for an answer on whether the cells contracting the mRNA get destroyed by the immune system. For instance, Dr. Mobeen Syed suggests that the material exits the cell only as: (1) exposed via MHC I, e.g. in case of a muscle cell, or (2) exposed via MHC II in case of antigen-presenting cell, or (3) debris when the cell self-destruction is triggered by a CD8 T cell. Such interpretation seems to be in conflict with the answers here suggesting that the spike material can exit an intact cell by itself. Video: https://youtu.be/9EfToFXwx98

@RomanRiabenko Well, you should read my comments below in the answers. Concerning cell destruction, when a cell undergoes apoptosis there is a protease cascade that destroys all the proteins in the cell before it disintegrates. Also, as I stated in my comments, a disembodied viral protein would not have the same folded shape by itself that it would have on an intact and complete virus, so it would be unlikely that a fragmentary viral protein would have a useful immunological pattern that could be acquired by a B cell.

@Shred: It's rather unclear, I admit, but I think the OP means SARS-CoV-2 by "vector virus". Still the Q could be edited for more clarity.

@Fizz No, Shred is right. I simply made the error of assuming that mRNA vaccines used a vector virus, which is not true. I removed that erroneous statement from my question already.

You still have a mention of "vector virus" in your Q: "2) is it expected that the vector virus would grow that feature on its own self and that new vector virions would emerge from the host cell with the distinctive feature sprouting from their outer shell?"

@Fizz I removed that part of the question.

@Fizz: I still haven't found out, maybe it goes without saying: a recombined vector virus - Adenovirus - does not only have the gene for the corona spike integrated into its genome (artificial recombination) but "comes as" modified virus, carrying the Corona Spike on its coat, next to its Adenovirus-Antigenes? Recombined Adeno-vector virus "is grown" in vitro? To recap my self-answer: manipulation of genome prevents translation for purpose of virus construction, however, "patentlike", this attenuation does not prevent translation for presentation of MHC by target cells.

@Imprisoned Rhesus "when a cell undergoes apoptosis there is a protease cascade that destroys all the proteins in the cell before it disintegrates." That does not imply that piecemeal fragments of "epitopes" exist as debris? This interests me as it doesn't seem very clear what B-cells are able to take up. B cells never take up whole virus - do they just "contact" antigen - no, as they coherently present on MHC 2 which means uptake of foreign antigen as such. Not whole virus?

MHC presentation of cleaved spike protein is only part of the picture; afterall, the immunity conferred by vaccines is largely owed to neutralizing antibodies produced by B-cells, which do not recognize MHC-bound peptides but rather intact antigen. While MHC presentation is important for T-cell (and ultimately B-cell) activation, the fact is that the spike protein encoded by these mRNA vaccines is presented on the surface of transfected cells for B-cell recognition.
Here is a great review that not only discusses the mRNA vaccines but, as far as I can tell, all of the other vaccine strategies as well. It should answer your question in more detail than I would presume to.
Heinz FX, Stiasny K. 2021. Distinguishing features of current COVID-19 vaccines: knowns and unknowns of antigen presentation and modes of action. NPJ Vaccines 6(1):104

In the course of cellular SARS-CoV-2 infection (Fig. 1a), the S protein is synthesized from one of the viral subgenomic mRNAs and co-translationally transported into the lumen of the endoplasmic reticulum (ER) by the use of a signal sequence at its N-terminus, comprising residues 1 to 13 of its total 1273 amino acids... After completion of translation, the protein remains attached to the ER membrane through a C-terminal membrane anchor... When S is synthesized as an isolated protein (Fig. 1b) (as in mRNA and adenovirus vector vaccines as well as for production of recombinant subunit vaccines), the pathway of biosynthesis is very similar.

Fig. 1: a Infected cells: Subgenomic mRNAs for viral structural proteins are translated in association with the ER (S, M, and E) or in the cytoplasm (N), and virus assembly takes place in the ERGIC. Virus particles are transported through the TGN and released from the cells probably via lysosomes. During transport, S is cleaved into S1 and S2 by the cellular protease furin in the TGN. Some spike molecules, not assembled into virions, are also transported to the plasma membrane despite the presence of an ER retention signal15. b Transfected cells: Biosynthesis of S occurs in the absence of interactions with other viral proteins. Proteolytic cleavage into S1 and S2 occurs in the TGN similar to that in infected cells, but some shedding of cleaved S1 and conversion of S2 into its post-fusion structure (S2*) may occur in the absence of stabilizing mutations. ER—endoplasmic reticulum; ERGIC—endoplasmic reticulum Golgi intermediate compartment; TGN—Trans Golgi Network; RNP—Ribonucleoprotein; Viral proteins: S—spike, M—membrane; E—envelope; N—nucleoprotein.

I think you may be misunderstanding the paper. The diagram you embed shows S1, a viral peptide pool, mounted on the exterior of plasma membrane. This can only be possible via presentation by MHC by my understanding. Also, the spike protein has something like 316 different peptides. I would expect these subunits to be presented, not the entire peptide pool all at once.  When a proteasome cleaves a protein I don't think it is predictable what subset of peptide sequences are created. If you are suggesting that the entire protein or one of the pools gets excreted directly by the TGN (continued)

I think that would be an unproven assertion, because I believe there are range of conditions a protein has to fulfill before it can be transported this way and viral proteins would not, I expect, fulfill these conditions. Furthermore, even a viral protein was execreted directly, it would not have immunological benefit because T-cells can only analyze peptides mounted on MHC, not free-floating molecules. B cells on the other hand bind to structures on complete and folded pathogens. (continued)

It would seem to be unlikely that a disembodied S protein would fold properly without the presence of the rest of the virion, and if the protein is not properly folded, that would seem to make it unlikely that a BCR would bind to it successfully.

S1 is not a "viral peptide pool", it is a domain of the spike protein. You can see the structure of the complete spike protein, including S1 and membrane-bound S2 domains in Fig 2 of the review. It is this complete, folded protein (or at least the S2 domain) that is displayed on the cell surface.

In concert with the cellular machinery, the spike protein has evolved to fold and enter the secretory pathway of infected cells naturally. It is not unreasonable to expect that it would follow the same pathway regardless of the absence of other viral proteins. Here is a paper which detects intact spike protein on the surface of HEK293T cells after transfection with either the wild-type spike protein mRNA or the mRNA of the Moderna vaccine.

That said, nobody is claiming that it's a perfect process and that the spike protein presented by transfected cells is identical to that on the virus. There are issues with spike protein produced from the vaccines adopting the unwanted postfusion conformation. This has been addressed by a double mutation in the vaccines to destabilize this conformation. It has also been observed that the vaccine and virus spike proteins show different glycosylation patterns which may affect immunogenicity.

@canadiener A "domain" of a viral gene is the same thing as a peptide pool. For example, see this paper where S1 and S2 are referred to as peptide pools: https://www.nature.com/articles/s41598-021-92521-4

@canadiener Molecules are not displayed by themselves on a "cell surface". That is an old pre-2000 idea and is a mistake. Material can only be displayed outside of the cell by specific molecules designed to do that, called "Major Histocompatibility Complexes". Both B memory cells and T cells only bind to peptides, not large folded proteins. MHCs display peptides, not large folded proteins.

SARS-CoV-2 enters the cell by its spike binding to Angiotensin-converting enzyme 2 (ACE2 receptor) on the surface of the cell, e.g. in lungs or blood vessels. Instead, to egress, it disrupts function and "hijacks" lysosomes of the host cell. The quote in the answer assumes that the folded spike protein may exit the same way. This makes this path specific to SARS-CoV-2 vaccine, may be not all mRNA vaccines.

@RomanRiabenko That’s a good point, thanks.  I might try and add it to the answer later.

Heinz...  "It is believed (...)that muscle cells, fibroblasts, endothelial cells, and/or immune cells such as dendritic cells contribute to the expression of S after intramuscular vaccination..." What does "contribute" mean? My guess: there is no need of non-dendritic cells presenting antigen on MHC for immunizaton to occur. What is contributed to by muscle cells?

Heinz et al. (linked to) " ... requires the interaction of B cells with the native protein, most likely by recognition of the spike anchored in the plasma membrane of S-expressing cells ..." Did this quote initiate the question answered? What exactly are "S-expressing cells?" If so wished I'll be able to refer to paper(s) that show that B cells are presented antigen on MHC by APC cells (dendritic cells) in lymph nodes - very exciting: there, it's not presenting only (as with Tc's) but it is a "handing over" of presented antigen for uptake  by B cells!
So, no need to "shed" (misfolding) prot.

Your assumption is wrong. A mRNA vaccine only contains a mRNA for the protein against which you want to vaccinate, encapsulated in a lipid membrane. These membrane vesicle  fuses with the membrane of the target cell and releases the mRNA into the cell. There free ribosomes can bind to the mRNA and translate it into a protein. Part of this protein is presented on the cell surface by the MHC complex and thus presented to the immune system. The mRNA is degraded after some time (although it has been modified to slow down this process), no further copies are made or integrated into the genome.
Speaking of virus based vaccines (like Sputnik V or Astra Zeneca) rely on a virus to deliver a piece of DNA into the cell which contains the information on the protein against which you want to vaccinate. This is transcribed into mRNA and eventually translated into protein. From the virus DNA usually the genes which are responsible for replication are removed so you get no new generation of viruses. Also the virus cannot do anything on its own, since it is not alive and needs a target cell and its machinery.
This resource gives a nice overview over the different vaccine types.

First of all, this does not answer the question. Secondly, your understanding is incorrect, if you actually read the link you put in your non-answer, you will see that in the section on mRNA vaccines, it explicitly shows a vector virus being used to insert the mRNA into the cell in steps 2 and 3.

@ImprisonedRhesus Chris's answer is correct. You are reading the wrong section of the link, the part about viral vector vaccines rather than the mRNA vaccine (the top row in the image is the mRNA vaccine; no viral vector there). The part of this answer that specifically addresses your title question is "Part of this protein is presented on the cell surface by the MHC complex and thus presented to the immune system" while the rest addresses other misconceptions in the question.

@BryanKrause Huh, ok, so I stand corrected, but it is more or less irrelevant to the question how mRNA gets into the cell. I am asking about the presentation afterwards, so focusing on a minor and irrelevant part of my question that happens to be wrong seems like a comment, not an answer.

@ImprisonedRhesus The vast majority of the text in your question is centered around misconceptions of how things work and imagined solutions based on those misconceptions. I think an answer that failed to address those would be incomplete.

@BryanKrause The question is about how the antigenic material is presented. How the antigenic material gets into the cell is irrelevant to the question. In any case I have eventually figured out the answer to the question (with no help from this community), so I will post an answer.

@ImThen you should clarify the question.

@Chris I edited the question to remove irrelevant comments about how the genomic material enters the cell. You know this community would be a lot more useful if it spent more time answering questions and less time obsessing about minor errors in the question. The people who ask questions are typically those who don't understand the subject very well to begin with. If I was a PhD in immunology I would never have asked the question in the first place.

@ImprisonedRhesus You are still mixing vaccine types. A mRNA virus does neither contain virions nor does is replicate. It is simply translated.

I'd like to kno, about  manufactured adenovirus carrying the corona-spike on its coat? Aas a vaccine producer, how do I replicate the vaccine virus after recombining its (in case of Adenovirus) DNA? I have heard of some kind of helper cells to replikate attenuated "dead" virus in vitra, manufacturing vector virus. Does this technique lead to recombined adenovirus carrying the spike or not?

@PeterBernhard Please make this into a new question.

How do mRNA vaccines work with respect to presentation of the antigen?

According to a DynaMed article, the egress mechanisms expected to play a role are 3:

(Note that this image may be somewhat misleading, in that [skeletal] muscle fibers [which are very long lived, multi-nucleated cells] don't normally express MHC-I according to a (peer-reviewed) article. I'm unsure if satellite stem cells in the muscle, which serve to repair the multi-nucleated fiber cells by supplying nuclei, have MHC-I.)
As you self-answered, in muscle cells, the MHC-I pathway exposes peptide fragments to "killer T-cells" (CD8)... but there's also release of proteins into extra-cellular space from where they are picked up by B cells, which produce antibodies.
Further MHC-II is engaged in APCs present in muscle and lymph nodes; we know at least from the reported side effects of mRNA vaccines that lymphadenopathy (swelling of lymph nodes) does happen often enough following mRNA vaccine administration.
I think however that the relative ratios of spike protein (following mRNA vaccine administration) reaching these 3 routes haven't been
exactly quantified. (I've search a fair bit, but I could not find any papers on exactly that issue.)
Ultimately, both memory B cells and memory T cells (hopefully) give long-term immune memory against that kind of infection, which at least give the host a head-start in a race against a new infection.
It's worth noting that mRNA vaccines don't produce the same ratios of neutralizing to binding antibodies (to the spike) as a real SARS-CoV-2 infection.

vaccinees generate more non-neutralizing antibodies than COVID-19 survivors resulting in a lower ratio of neutralizing to binding antibodies. These data were already apparent in the early phase clinical trials but remained unrecognized at the time (Walter, 2020).
[...] the burning question of whether the abundant non-neutralizing antibodies do have a protective effect in vivo will need to be elucidated by follow-up studies

mRNA vaccines also produce a lot more (spike) neutralizing antibodies than a real infection (same paper), at least initially--there's apparently a fair bit of decay over time though. Both of these suggest that spikes produced by mRNA vaccines get a lot of B cell attention, which might indicate a lot of them spikes produced by mRNA vaccines egress into extra-cellular space.

As I commented to a different answer, I don't really believe the "extra cellular protein" stuff, unless you give me much more specific info. First of all, B cells only recognize FOLDED and intact pathogens, like a complete virus. The idea that a B cell would successfully memoize a disembodied protein fragment seems unlikely to me. Also, the shape of this fragment would be different than what it would be on a complete virus, so even if it did so, there would be no immunological benefit. (continued)

Secondly, you have not shown how a disembodied viral protein can exit a human cell. Viruses use a complex envelopment mechanism to get out of cells which is only available to a complete virus, not viral fragments. Genuine cell self-product proteins only can leave the cell through the Golgi apparatus which requires specialized carriers that human-generated proteins are designed attach to. There is no evidence I know of that a viral fragment would be able to adopt these carriers and use the Golgi apparatus to escape the cell.

"The idea that a B cell would successfully memoize a disembodied protein fragment seems unlikely to me." Please ask that separately as it's a simpler issue to answer on that level, not related to mRNA vaccines. You could even ask it on Skeptics SE. The 2nd issue (protein egress) is more interesting/challenging to prove directly, I admit, but again it's better suited for a separate question. You've basically used this Q of yours to ask two different ones, related to your disbeliefs. (Your counter-theory that only MHC-I works still doesn't explain anti-bodies, I'll note, though.)

"B cells only recognize FOLDED and intact pathogens" That is completely untrue. B cells will recognize foreign sequences or structures however they're presented to them, whether it's a protein fragment or an intact virion.

S.Seneff, G.Nigh suggested that muscle cell also presents MHC II. "Muscle cells do express MHC class II proteins (Cifuentes-Diaz et al., 1992). As contrasted with class I, class II MHC proteins specialize in transporting intact proteins to the surface as opposed to small peptide sequences derived from the partial breakdown of the proteins (Jiang et al., 2013)." https://dpbh.nv.gov/uploadedFiles/dpbhnvgov/content/Boards/BOH/Meetings/2021/SENEFF~1.PDF

@Fizz First view first  "figure" up above: seems like there are muscle cells expressing at least some - i.e. not zero - MHCI. As I read from you, just yesterday, muscle cells "overexpressing" MHC are subjet to myositis. Muscle cells do express MHC, correct? Compare picture above.

@PeterBernhard: Apparently that page with the pretty image is somewhat less reliable than I thought. The article is signed off by two MDs, but they work for DynaMed. I'm not sure why I wrote it was the Canadian Medical Association. I probably had a different page opened as well and confused the two. Looking at their bios, one of the authors [Iacoviello] looks like a fairly reputable academic in infectious diseases, but maybe that immunology detailed slipped them. Or it might be controversial whether muscle cells have MHC-I, but I've not seen the claim of MHC-I outside that image, TBH.

@PeterBernhard: On the other hand, there's a peer-reviewed article that says the opposite, so that seems more plausible to me. I would not be surprised if other cells in the muscle like stem cells (which produce nuclei that serve as replacements for those in muscle fibers) have MHC-I, but I'd have to check that.

@Fizz (removed to chat all right by me). The "article" you cite, I read, that's the one. Again, how did you google it? This is awesome as it beats basic textbook wisdom. Even found articles like "MHC2 - two - they shouldn't do! - on myocytes. Just one simple logic: it's undebated that muscle fibers are able to express MHC1 (they go the genes), so in case of infection (re question I found your statement, different question..) the very infection may induce expression. Anyway, why are muscle cells not autoimmunically killed for "misssing self"?

@Fizz How about setting up question(s) on non-APC cells expressing MHC1- and -2. Could you cite any basic textbook for MHC2 on non-APCs and - inversely - for non-APCs, nucleated -"aha", cells Not expressing MHC1. Aha: you did mention "nuclear production", ... "Do muscle cells "denucleate"...? Thanks for answering at all, even having received your message I haven't managed to scroll down and read your text. I was stunned by the picture. I will soon delete this comment as chat, except for not on "nuclei". My note on simpleminded infection inducing expression might be left undeleted.

The way the antigenic material is presented is via a peptide MHC complex which appear on the surface of the cell. The various proteins present in a given cytoplasm are randomly selected and automatically chopped up by proteosomes and the resulting short peptide chains are then channeled through a special kind of cellular structure called a major histocompatibility complex and mounted on its surface exterior to the cell. If the target antigen protein is indeed being successfully manufactured inside the cell, then we can it expect that these products will be periodically cut up in the manner described and be exposed. The exposed peptide then serves as an example both for helper T-cells to stimulate immune response (such as antibody class switching), and also serves as the epitope to cytotoxic T-cells which can kill the infected cell. Below is a diagram illustrating the mechanism:

Downvotes with no comments.

This isn't incorrect, but it's incomplete in a major way to the point of being misleading; the vast majority of mRNA vaccine studies measure (neutralizing) antibodies, but how do you get [any] spike antibodies from this "cytotoxic T-cell"?

@Fizz Helper T-cells (CD4+) can attach to MHC just the same way that cytotoxic T-cells (CD8+) attach. However, CD4+ cells stimulate an immune response that includes antibody signalling. I added a statement to that effect in my answer.

You're still missing direct B cell activation, which is a major part of the immune reaction. B cell receptors bind directly to antigen and cause B cell activation, which is then enhanced by $T_H$ cells, but not initiated by them. The MHC-I pathway is only part of the system. You're also completely missing the MHC-II pathway (which CD4s recognize, CD8s only do MHC-I)  and the effect of professional APCs.

@MattDMo Let me know if this comment of mine got go be removed, as maybe it refers to some other question, which might exist at Stackexchange.
Re "B cell receptors bind directly to antigen and cause B cell activation" . That should work without any uptake of antigen? Do B cells uptake whole virus? Or do they uptake "debris", see above, nothing left after "clean apoptosis"? And, what's more, if presentation on MHC2 needs incorporation, may contact and let go suffice in a situation of activation of memory B cells?

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


text:
How are viruses isolated?
I read several different articles about virology, including the Wikipedia article on viruses and none of them explain how a virus is isolated. Some talk of injecting a virus into a chicken egg, but this does not isolate the virus, it just reproduces it.
If a researcher filters the particles in a serum to get those of a particular size, it proves nothing, because every creature has many thousands of different viruses in their blood, so any sample filtered by size will potentially have hundreds of different viruses in it, all the same size range. How can they possibly be separated?

Fairly relevant publication.

I eventually figured out the answer to this question after reading some introductory textbooks on virology.
Though, as another answer states, there are many different possible techniques to isolate a virus, there is one basic approach that can be considered the standard method.
The key pre-condition is that you must know or suspect the type of cell which the virus uses to reproduce. Most viruses use only a single cell, or perhaps two different kinds of cells at most, to reproduce. There are about 200 different kinds of cells in the human body.
Once you know (or suspect) the cell type, the next step is to obtain a culture of that cell so that you can grow that cell type indefinitely, an immortal culture.
Next, the researcher samples a subject thought to harbor the virus (or viruses) of interest in the area where there might be infected cells. The sample is purified by filtration and/or centrifuge to remove bacteria, cells and other organisms so that only viruses remain. The sample is then diluted to various degrees and each stage of the dilution is used to innoculate a different cell culture. If successful, then a plaque will appear on or in one or more of the cultures after a number of days where the virus is multiplying. That section of the culture can then be taken out and the plaque will hopefully contain a single virus of a single genetic type, which is called an isolate. The isolate can then be further studied.

This answer is misleading as concerns cell types for culture. Rather than choosing the differentiated cell type the virus infects and attempt to immortalise it — a lengthy and specialist process — you see if you can infect established immortalized cell lines — not necessarily human (remember they initially used eggs). Your remarks about tissue specificity reflect a misunderstanding. Tissue specificity reflects the mode of delivery of the virus. For infection in vitro this has been circumvented and all that is required is the receptors the virus uses, which will be present on many cell types.

Apologia
This answer was prepared in response to a previous question about Measles virus, but the question was removed for reasons I am not party to but which I can guess. As I spent some time on it I thought I’d post it in reply to this question. It is specific for measles virus, although there are obviously aspects that apply to other viruses, and deals with characterization as well as isolation. I am not a virologist (although I have done some biochemical work on pig herpes virus) so the it was is based solely on my reading of the papers cited and of Field’s Virology. I welcome suggestions for corrections or additions. It may seem to some that the question does not justify an answer of this detail. However it may also be of interest to young contemporary students and researchers who may have difficulty in envisaging the technological limitations of post-war experimental science.
Original Isolation and Characterization
The Edmonston strain of measles virus was isolated in 1954 by Enders and Peebles from the blood of a child with measles, David Edmonston. Before this scientists had found that an agent which was small enough to pass through filters that retained bacteria (i.e. possibly a virus) could cause measles when inoculated into monkeys and could be passaged in eggs containing developing chick embryos — the best method available until then. What Enders and Peebles managed to do was to maintain the virus in cells growing in tissue culture (a far more convenient host experimentally) — initially primary human kidney cells, and then monolayer cultures of chick embryo cells.
They used light microscopy to detect the changes in the cells that demonstrated that they were infected (the original paper contains many photographs of the cytopathogenic effects on infected cells). They could passage the virus by inoculating uninfected cells with infected cells, and they also isolated some virus from the cells by breaking open the cells and using the technique of centrifugation to separate the (larger) virus particles from the soluble cell contents and debris. (Subsequently much improved purification procedures were developed, resulting in preparations suitable for electron microscopy.)
One of the main techniques for characterizing viruses at this time was immunology. Thus, they found that the tissue culture fluid reacted with the antibodies in serum from measles patients by the complement fixation test, showing that it contained measles antigen. Previously they had showed that the cytopathogenicity of their preparations was neutralized by such antibody-containing serum.
Their paper ends with a summary of the evidence that what they isolated was the viral agent responsible for measles, and the further evidence needed for conclusive proof.
Subsequent characterization
The subsequent 60 years saw a steady improvement in analytical method, so that characterization did not rely solely on observation of cell pathology and immunology (the methodological repertoire of which also developed immeasurably). Electron microscopy in the 60s allowed cellular infection to be followed in greater detail and, after improvements in purification, the structure of the virus itself to be observed. The nucleic acid, protein and lipid envelope components could also be analysed with such purified virus.
The emerging techniques included gel electrophoresis of proteins (to determine their size and relative abundance, and to effect small-scale preparations). Larger scale purification of the virus proteins was possible with purified preparations, allowing  amino acid sequencing, especially of the most abundant proteins (e.g. the nucleocapsid protein, N),  and cDNA cloning and sequencing technology led to the sequencing of the whole Edmonston virus genome by Bellini et al. in 1985. This latter resulted in a much greater understanding of the gene expression of the virus, and provided tools such as specific oligonucleotide probes for various genes and antibody reagents to detect specific proteins.
Comment on Poster’s specific questions
The crux of the argument in the question would seem to be:

“If a researcher filters the particles in a serum…any sample filtered by size will potentially have hundreds of different viruses in it, all the same size range…”

The above addresses this only implicitly. To be explicit:

Using either the serum from patients infected with a specific virus, virus passaged in eggs or viruses grown in cell culture one is massively increasing the proportion of that virus to any contaminants.
It is not easy to grow viruses in cell culture. Therefore when conditions are found for one virus they are unlikely to be optimal for other (low-level) contaminants. Thus the actual passage in culture removes viral contaminants. The purification problem becomes one of separation from cell debris.

Modern Methods of Purifying Measles Virus
Below is a summary flow chart taken from the article Manufacture of Measles Viruses by Langfield et al..

One of the key methods in this proces, Tangential Flow Filtration, is also known as Cross-Flow Filtration and is described in this Wikipedia article.

There are many ways. In many cases especially traditionally viruses of interest were either the only virus present, or overwhelmingly more abundant than other types, so simple dilution will end up with a single virus type. Differential growth can help; many viruses have very specific growth requirements and if you only offer a particular cell type (or an egg -- most viruses do not grow in eggs!) it's not unlikely that only a single virus will grow out. Those are probably the most common and simple approaches -- dilution, or attempted growth with many different cell types/conditions followed by dilution. If they don't work, it becomes a lot tricker. Complexities in Isolation and Purification of Multiple Viruses from Mixed Viral Infections: Viral Interference, Persistence and Exclusion (pointed out by @CMosychuk in comments) reviews some approaches.


text:
Do brain cells regenerate in the adult brain?
I know that most cells in the body regenerate, dying and being replaced with new cells. For example, in bone special enzymes move radially outward from the marrow in a narrow tunnel, destroying the old bone as they go and replacing it with new bone cells. In this way, our bones are slowly regrowing and being replaced constantly.
Is a similar process at work in the adult brain? Do neurons in the adult brain die and become replaced with new neurons? If so, how are the connections re-established? Each neuron is connected to other neurons by a complex network. If cells are regenerated, how do they re-connect to existing cells?

Short answer
Neural regeneration in the adult brain is confined to two localized hot spots, namely the hippocampus and the anterior lateral ventricular wall. Establishing connectivity between new cells and existing neurons is mediated, at least in part, by the growth cones present on axonal tips of newly formed cells. The growth cone responds to various stimuli and guides the axon towards it new target.
Background
As to your first question: Also adults can regenerate brain cells, albeit in a few restricted, specific regions of the brain. A continuous level of neural regeneration occurs throughout adult life in at least two locations. The first is the subgranular zone of the dentate gyrus of the hippocampus, the region of the brain involved in learning and memory. The other is located in and near the anterior lateral ventricular wall of the cerebral cortex. While neurogenesis in the adult hippocampus is relatively limited, the subventricular zone is thought to continuously replace interneurons in the olfactory bulb (Clarke, 2003).
Studies have shown that neurogenesis folloing neuronal cell loss due to injuries occurs only within the germinal structures mentined above, and not in cortical or striatal structures. Even when neurogenesis in the striatum (but not cortex) has been reported following ischemic injury, the resulting neurons survive only a short time. Hence, under normal circumstances structural or functional recovery in non-neurogenic brain regions is limited (Hallbergson, 2003).
Re-establishing connectivity between new cells and the existing tangle of neurons in the neurogenic regions of the brain is complicated. An important structure in this regard is the growth cone (Fig. 1); it is present in developing axons that are not yet synaptically connected. They are motile structures present on the tip of the growing axon and guide axons to their synaptic targets. They control the cytoskeleton and determine the course and rate of axonal outgrowth. Neurons and growth cones can detect a variety of external signals to establish neuronal migration and neurite outgrowth. A key in this process is chemotaxis. Several classes of molecules, e.g., secreted factors, adhesion molecules and cues from the surrounding extracellular matrix and adjacent cells are involved in the process of neuronal pathfinding and growth. To advance over larger distances however, gradients are insufficient and neurons use mechanical cues (durotaxis). For instance, neurite outgrowth has been shown to be affected by the mechanical stiffness of the substrate. Glial cells have been shown to be softer than their environemnt and neurons preferentially seem seek out glia to grow to (Lu et al (2006); Park (2002); Pawlizak (2009)).

Fig. 1. Fluorescently labeled growth cone on the tip of an axon. source: wikipedia
References
- Clarke, Bone Marrow Transplantation (2003); 32: S13–S17
- Halbergson, J Clin Invest. 2003 Oct 15; 112(8): 1128–1133
- Lu et  al., PNAS (2006); 103(47): 17759-64
- Park, et al., Bioessays (2002); 24(9): 821-7
- Pawlizak, Thesis, University of Leipzig (2009)

So when you write that neural regeneration is confined to particular places, are you implying that most of the cells in the brain do not regenerate? They form once and never die, the neuron lives for decades and is not replaced?

@ImprisonedRhesus - correct. Some small-scale migration may take place, out of the zones where neurogenesis takes place, but that is negligible.

Ok, so that means that many of the neurons in a person's brain are 30, 40, 50 years old, or however old the person is? I thought that cells had fixed lifespans that were short, not lasting years. From what you are saying there are cells that can live for decades?

I'd be a little careful with the word "regeneration" - it might be appropriate to the subventricular zone replacement of olfactory neurons, but I think "neurogenesis" is a better term for the other types of adult processes that form new neurons. Regeneration implies that they are directly replacing neurons that have degenerated, and I don't think there is good evidence for that.

@ImprisonedRhesus Cell lifespans vary greatly among tissue types. In the adult mammalian nervous system, almost all of the cells come from fairly early in development. Even the growth that AliceD is talking about is in some very small areas and contributes even a small fraction of the cells to those areas. Indeed, most brain cells are around for decades. There is definitely no broad-scale replacement of neurons like you have for blood, skin, etc.

@BryanKrause That is very interesting that some cells like blood cells should only last for a few months, but brain cells last for a lifetime.


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Role of drift in evolution of sexually dimorphic traits
Is there a model for predicting how drift can affect the evolution of a sexually dimorphic (SD) trait? I've been trying wrap my mind around this paradoxical question; sexually dimorphic traits evolve due to sex-specific selection. So how can drift affect SD traits?
I've found the quantitative genetic equations (eq 1) in Lande 1980 very helpful for thinking about the parameters and how sexual dimorphism evolves.
Can this model be applied to a population bottleneck? Or comparing the degree of SD in a trait of two divergent populations (assuming s, Ne and other parameters remains constant).
$$
\begin {pmatrix}
\Delta z\\
\Delta y\\
\end{pmatrix}
= {1 \over 2}
\begin{pmatrix}
G_m B \\
B^{T} G_f\\
\end{pmatrix}
\begin{pmatrix}
P_m^{-1} s_m\\
P_f^{-1} s_f\\
\end{pmatrix}
$$
Edit: I've added the equation from Lande 1980, which models the phenotypic response for sexually dimorphic traits. I'm wondering how aspects of drift (Ne and fixation probabilities) can be merged with an equation such as this. From my understanding drift may affect the G, B and P matrices (that is the Genotype variance covariance, intersex (B) variance covariance and Phenotype matrices. One of the assumptions of this equation is that these matrices remain constant.

I don't understand; where is your paradox?

Note that it is a good habit to always link your references. I can't check right now, but I am pretty sure that Russell Lande has many publications in 1980 making it hard to know what equations you are referring to.

I added the link to the Lande paper, I've only recently been allowed to link sources. Maybe a better way to rephrase my question is 'can drift overcome sexual selection in the evolution of sexually dimorphic traits?'

[C]an drift overcome sexual selection in the evolution of sexually dimorphic traits?

Short answer
Yes
Long answer
There are many ways to consider the effect of genetic drift. Here is one: One can approximate the probability of fixation of new mutations (using diffusion equations) with
$$P_{fix}≈\frac{1-e^{-4Ns} }{1-e^{-4s}}$$
, where $s$ is the selection coefficient and $N$ is the populations size. As you can see, a larger population size (the lowest is the genetic drift) corresponds to a higher probability of fixation of a beneficial mutation (to reach frequency of 1 in the population). If you don't have a good intuition of why genetic drift is inversely proportional to the population size, please have a look at this post. The most important point to keep in mind about the effect of drift is that when drift is high, every mutation pretty much behaves like neutral mutations.
This approximation is accurate under some assumption, for instance that the population is panmictic (=random mating). This equation holds true regardless of the reasons why a mutation affects fitness. The mutation may affect the activity level of an enzyme or it may influence how attractive an individual is to the other sex. So yes, in any case, a beneficial mutation may fix although it is deleterious (because of drift), or it may not fix although it is beneficial (because of drift).
A mutation might be beneficial in both sexes, detrimental in both sexes or beneficial in one sex and not in the other. In such cases, I suppose it is possible that the above equation must take a slightly different form. In any case where the mutation has a different impact on the fitness in each gender, I don't know how the above formulation would solve to but I'd think that you could simply replace $s$, by $\frac{s_m+s_f}{2}$, that is the average of the effect in both sexes (where $s_m$ and $s_f$ are the selection coefficients in males and females respectively). Intuitively, I think this should hold true as long as the sex-ratio is 1:1. The exact calculation of the probability of fixation doesn't matter to your question though. Note that mutations having the opposite effect on fitness in each gender often end up being on sexual chromosomes (if any) or at least being expressed in one sex but not in the other. In such case, a fixed mutation often end up being beneficial in one sex while neutral in the other. In any case, genetic drift will obviously affect the evolution of sexually dimorphic traits.
EDIT

could you clarify "As you can see the highest is the population size (the lowest is the genetic drift),"?

The impact of genetic drift can be measured in terms of how it affects probability of fixation or how it affects the rate at which heterozygosity at a neutral site is lost. An intuitive explanation for why $N$ and genetic drift are inversely proportional can be found here.

Are you referring to the positive correlation with P fixation and Ne?

Yes. I could have referred to that as to something else though. Note that the correlation between $P$ ans $N_e$ is perfect ($r^2=1$) because $N_e$ is defined on the concept of genetic drift.
Definition of $N_e$
Let's WR (stands for Wright-Fisher) be a population of size $N_{WR}$ where mating is random and there is no variance in fitness.
Consider now the population A. Let's its size be $N$. A experiences a given level of genetic drift based on its mating system, population structure, variance in fitness, etc.. the effective population size $N_e$ of A is (by definition) the size of the WR population ($N_{WR}$) that experiences the exact same level of drift, that is the same probability of fixation for a new mutation and the same rate of heterozygosity lose at a neutral site.

Thanks for the answer, I think I see where you're going but could you clarify "As you can see the highest is the population size (the lowest is the genetic drift),"? Are you referring to the positive correlation with P fixation and Ne?

Thanks. That is a good review for me on the parameters of drift. However for this question I'm trying to understand how drift (stoichastic sampling of alleles) can affect the cross-sex genetic covariances for a trait (B). Reading more of the literature this week has led me to conclude that this question is likely more complicated than I initially thought.

I wrote my question asking about the relationship of drift in the evolution of SD (sexual dimorphism), but after reading up more on the subject I've determined there are at least two parameters to consider when thinking about the evolution of SD.

Population structure and demographic history (Ne and drift outlined nicely by @Remi.b )
Intersexual correlation of the genetic architecture of the trait(s) evolving SD (how much genetic variation is shared between the homologous male and female traits?)

The intersexual genetic correlation between the sexes will constrain evolution in the sexes if selective forces are distinct for the sexes. This degree of correlation can be represented as rMF for single traits (Lynch and Walsh 1998 chapter 24) or the B matrix when examining the relationship between multiple traits (Lande 1980).
Two recent papers by Connallon and Clark (1 and 2) outline their adaptation to Fisher’s geometric fitness model which to predict mutation affects on traits given distinct phenotype-fitness spaces for the 2 sexes. The mean phenotype of each sex is a certain distance and angle away from the fitness optima (this vector represents the magnitude and direction of directional selection). The angle of these vectors represent the difference in selective forces for male and female traits. The current phenotypes are moved along the landscape by the addition of novel genetic variation (mutations).
 Mutations shift the trajectory of the current phenotype towards the optima. As in the selection vectors, the difference between the mutation vectors is quantified by the angle between the sex specific vectors, and can either move both sexes towards their respective optima or move only one sex towards their optima (sexually antagonistic selection).

While this model doesn’t directly take into account Ne for predictions on drift, it does emphasize that distinct fitness landscapes eventually cause antagonistic selection due to decoupled fitness effects for female and male traits due to random mutations.

“Evolution of sexual antagonism occurs whether or not selection favors phenotypic divergence between the sexes.” 1

This wasn't a direct answer, but it provided insight into how selective forces and pleiotropy of traits can shape the evolution of SD.


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About molecules and their shape
When a molecule is being used in some biochemical process it has a certain 3-d structure. Is this maintained throughout it's usage or can one specific molecule change it's 3-d shape while it is being 'used' in the process. Can a specific molecule in all it's interactions in a cell say , take on 4 or 5 distinct 3-d shapes??

It's too broad. But as per enzymes and basically proteins it happens.

All molecules have a 3D shape. This is referred to as it's conformation. Most molecules have certain degrees of flexibility. For example, single bonds usually allow free rotation, while double bonds don't. Cyclic structures have less freedom, but can still twist into several shapes. This can be important because some molecules bend into a certain conformation and then fit into protein binding sites they normally couldn't fit into. And it's not just small molecules, proteins, RNA, and DNA fold into specific shapes, and often must be unfolded, twisted, or bent in order to carry out their function. Protein dynamics is an active field of study. A great example is the ATP synthetase, which has a large rotating portion and acts a lot like a motor.


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About animal ecology and one view of this in science fiction
In the movie the Matrix Agent Smith said something like, 'all animals strive to find a natural 'equilibrium' with there environment ,... a harmonious existence with their ecosystem', ( forgive misquoting). Is this true that each animal 'does' a lot of activity whether by instinct or an ad-hoc form of 'simple' planning to 'cooperate' with it's environment ,or exist 'harmoniously with it?

The answer to the question as stated is, certainly: No. Neither on a conscious level, nor at the level of instinct does an animal have the goal of keeping the ecological balance of its environment intact. Quite the opposite: it is constantly trying to overturn that balance, attempting to change the system and bring it to a new situation, one in which it (the animal) and its children have a higher survival and procreation chance than the current one. Whether the new situation will be stable (= a balance) or not is not a criterion, and cannot be predicted by any animal acting on the environment (including the humans).
To use an example: As the news outlets have been warning us in recent years, if all bees were to die, our whole ecosystem could collapse. Yet no bee is pollinating flowers because it somehow feels that this will prevent the collapse of the current ecosystem. It gathers pollen because its swarm is hungry.
There is also nothing "natural" about the equilibrium our ecosystem is in, at least not in the sense implying that "this is how it should be, and everything else is so bad that it goes against the very laws of nature". It is just one random equilibrium of many possible states of our planet, some including an ecosystem in equilibrium, others including self-destruction of the ecosystem. All of these states are equally natural, and the planet has passed through several of them before establishing the current one (which isn't about to stay here forever either).

By the way I didn't say animals were 'doing' things to be in a state of better 'equilibrium' with their environment ,I just took this as a paraphrase from the movie the MATRIX. I , myself was wondering if the statement FROM THE MOVIE had any truth. I didn't say I believe it.

There is a purely philosophical issue behind your question. What does trying mean? Does trying doing A means that an individual is aware of how to achieve A and will behave so to achieve it?
The likely correct answer (it really depends on you definition) is "No" (with some eventual exception among those that have high cognitive abilities such as humans). No, animals don't try to create a nice ecosystem. Animals (just like any living things) just evolve in response to their environment and this ends up creating ecosystems. The ecosystemic balance is just the result of the non-cooperative actions of the different species at play in the ecosystem. For example, animals reject nitrogen not in order to help plants to grow but only because nitrogen is a waste and is toxic for them. You may want to make you understand how evolution works.
For those who have a good enough knowledge in evolutionary biology, I have to admit that the above answer might be slightly wrong if we consider some special kinds of selection such as kin selection, species selection or even ecosystem selection. I think the answer to the question remains "no" given the "conscious" side of the definition of trying that the OP was probably using.
Update
Cooperation is easy to explain, real altruism is more complicated. Real altruism is when one individual makes an action that benefits to the others lifespan reproductive success but decreases the lifetime reproductive success of the one producing the action.
Within population real altruism can be explained by kin selection. see this post for more info.
Between species real altruism is much more complicated to explain. It would need to use concepts such as species selection. But does between species real altruism even exist (beside some behaviour from species with high cognitive abilities)? I don't think so.
What you are interested in is inter/species cooperation. Very often the individual that offers something to the other also directly gain something. For example, the animal excrete nitrogen because it is toxic and the plant take advantage of this. But sometimes an individual (actor) pay a cost for producing something to the benefit of the other individual (recipient). In return, the actor will receive something back from the recipient. For example, in the lichen, the algae offers energy while the fungi offers shelter. If one stops the other will die and both will lose. There are known cases also where individual A stops offering goods t individual B if individual B stops offering goods to individual A. This kind of traits are best studies with the tools of game theory.

I agree that the question is formulated very badly, has a strong philosophical bent, and could be interpreted in different ways. But there is a surprisingly simple answer: all interpretations I can think of are false. Animals do not strive towards maintaining environmental balance, neither consciously or unconsciously. The existing balance is a byproduct of the sum of their independent non-cooperative actions.

I didn't dare being so radical because it keeps kin selection, ecosystem selection and species selection aside. But I updated my question now to clarify my point using your comment. Please let me know if you have other suggestions.

There is some cooperation in nature; like a 'social order' in a group of animals , or symbiosis. How can these things develope if all animals are exerting their independent non-cooperating actions?

see update in my answer.

No
There are many, many examples of species in their native environment accidentally destroying their ecosystem when external factors constraining their ability to reproduce are removed. For example when wolves and other large predators were removed from most of the American west ungulates like deer and elk nearly stripped the environment bare, to the point that riparian lowlands were completely stripped of vegetation and native willow populations were severely effected.
Similarly, invasive species, when introduced, aren't intentionally trying to drive other species to extinction, it's just that their adaptations are so mismatched the invasive species succeeds disproportionately often allowing for a population boom. For example, sea lamprey weren't trying to wipe out lake whitefish and lake trout when they got into the Great Lakes, they were just too good at what they did.
Even in humans "living in balance with ones environment" is a rare idea, and generally only occurs in populations that have the resources to spare and don't have to worry about their own survival.


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building intelligent structure with random evolution requires series of non useful steps
In order to build an intelligent design such as a bridge or a mechanical watch, you need a series of non useful steps.
As far as I understand, in random evolution theory, the "intelligence" involved is the process of natural selection.
The problem with this is that natural selection requires that each step be advantageous right away. If I want to build a bridge, I need many steps which would be disadvantageous until the final product which would be advantageous. This would be like trying to write a computer program where each line of code must be advantageous to the program. An intelligent design just cannot be done like this.
How does modern biology deal with this problem? To say it all happened at once, is not possible since the probabilities against this are simply outside the capabilities of a random system. Furthermore even if by some freak monumental event it happened, it would need to happen again many times since there is a huge diversity of intelligent designs in life forms such as lungs in birds vs gills in fish, or sexless reproduction in bacteria versus male/female reproduction in animals (which are fundamentally different).
(Also, as side question has there been ANY experiment demonstrating that such a thing is even possible? I mean for example, to have a computer simulation of random self-replicating molecules, then having an intelligent human being picking out the best version and eliminating the others, then repeating, etc. until you have an intelligent design.)

The key idea you're missing is that evolution is not random. Read up on "selective pressure".

@MattDMo it is random in the sense that there is no intelligence involved. my question is that you cannot build an intelligent design like a mechanical clock without a series of non-advantageous steps. try writing a computer program where each line of code is advantageous to the program. it just doesn't work like that.

Unfortunately, evolution is not like writing a computer program, which has a very strict syntax, type checking, etc. Please read through the comments and answers to this recent question for a more in-depth discussion. This response in particular addresses the computer analogy. "Advantageous" is a tricky word. There are plenty of instances of DNA changes ("mutations" if you like) that may be negative in the short run, but prove protective otherwise. Sickle-cell anemia is one of those.

@user813801 There are already a great number of  answers online to debunk these standard naive intelligence design flaws. Have you had a look at them? It would probably be more helpful to you if you address your potential misunderstanding to these explanations rather than re-asking a question that has already been answered thousands of times.

You probably want to follow an introductory course to evolutionary biology such as the free online course by UC Berkeley Understanding Evolution.

What you say is true, but the answer as to how modern evolutionary theory understand this considers other ideas about living things which seem to allow so called 'neutral traits'.
Neutral traits being those phenotypes which seem to have no particular relationship to fitness. Toungue rolling is an often mentioned example.  Some folks argue that there is only adaptive changes and phenotype, others like Gould and Lewontin argue that some traits can be the result of pleiotropy.
So first of all this sort of discussion can tell us that the question is argued both ways in a convincing enough way that it is not resolved in biology - some argue quite confidently that all traits are selected for and things like flagellar motors and upright ambulation and eyeballs evolve because of and experiencing constant evolutionary pressure.  Others argue that these genes that produce these things are doing something else useful while they are becoming these later more useful traits.
The common twist here is plieotropy.  That the genes that are producing the phenotype one is observing is also participating in one or more other biological traits that may is being positively selected for.
A more interesting example of how this works is the domesticated silver fox experiment. Foxes which have had domestication bred into them (just to show that it can be done by selection) lose their red color and their ears are softer and fuzzier.  Nobody tried to select for these traits, but they come associated with each fox that is domesticated.  Are these traits plieotropic or only very tightly linked?  So far they have not been exhibited separately.  In any case I think its fair to say that the experiment didn't care about the color of the fox - only its meekness towards people.  These traits come along for the ride.
So it might be with any other desirable genetic trait.  If a gene becomes closer to producing a lung from a gill, if that gene is sticking around it must be because there is positive selection for that trait, even if the lung like gill is not particularly useful for that fish.
Sorry but I actually disagree that it is obvious that non-useful steps must be had for any such complicated trait.  If that were true then you would have a point, but not every biologist would give that to you.
It might be a bit surprising that such discussions are and continue to be matters of faith in science, but I hope you don't dismiss it because of this either.  All sciences do assume some things that make their view of the world make more sense.  But there are also other components of these theories which are consistently observed and understood that demand them... until they don't.
I don't give really any credence whatsoever when someone says 'this is a widely accepted theory by the scientific community'.  This in itself is not a scientific statement, but more the hope that someone else has one somewhere.  But a refutation must also take under consideration what is being refuted.

is there any evidence whatsoever that it is possible to build an intelligent design with this method such as a computer simulation as i wrote in the question. thanks

traits which arise spontaneously without natural selection cannot explain this, since that would be even worse since then there is no pseudo-intelligence involved. could also be that the foxes change spontaenously as part of their genetic code to adapt to the environment.

there is a lively conversation going on right here. http://biology.stackexchange.com/questions/16106/how-does-the-creative-process-of-biological-evolution-work/16108#16108   In my opinion none of this rules out intelligent design - but on the other hand I don't think one can prove there is a Maker by looking at evolution either.  that's been consistent with my life experience too...  :)

"This would be like trying to write a computer program where each line
  of code must be advantageous to the program. An intelligent design
  just cannot be done like this."

On the contrary, this is precisely how most successful programs are developed nowadays: using incremental test-driven design. You start off with a blank program and a test (typically "does it compile") which the blank program fails but which it can be made to pass by a trivial amendment (such as adding a function called "main"). With that success under your belt you move on to another test - e.g. "does it produce output", which might be satisfied by the addition of a "print 'dddagcahx'" statement.
Suppose we've decided that the purpose of our shiny new program is to take a year and tell us whether or not it is a leap year. Then our next four tests, expressed in the sort of language commonly used for such tests, might be

    Assert.That(Year.IsLeap(1996), Is.True);
    Assert.That(Year.IsLeap(1997), Is.False);
    Assert.That(Year.IsLeap(1900), Is.False);
    Assert.That(Year.IsLeap(2400), Is.True);

Now it might seem that the next step would involve a "big bang" conversion of our "print random nonsense" program into a fully fledged leap year calculator,  but in fact we can pass two of the new tests simply by always outputting "True" (or alternatively always outputting "False") regardless of what input we are given. So we change "print 'dddagcahx'" to "print 'True'" (or print "False") and already we're passing four out of six tests. Even a stopped clock is right twice a day.
And so on. Even the largest program can be developed incrementally in this manner. Every small addition to the program is "advantageous" in that it enables the program to pass tests which it previously failed.
It used to be that programs were not developed in this way. Back in the 80's, say, the prevailing philosophy was "Big Design Up Front". Not a line of code would be written until after months or even years of meticulous design had taken place. The big problem was that this typically didn't work. Millions would be spent on software projects which then had to be scrapped because of design flaws which only became apparent during implementation - or, worse, only when the program was in the hands of customers. This could have been averted if there had been a partially-functioning system at every stage of the development process.
So the message of software development is that an intelligent design CAN be done like this, i.e. incrementally and "where each line of code must be advantageous to the program"; and it is the alternative "it all happens at once" approach which is problematic for reasons which you yourself have pointed out.
(See e.g. exercism.io for an excellent hands-on introduction to test-driven development.)


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Odds of Fusion of Chromosome #2
There is strong evidence that chromosome 2 in humans is a fusion of two chimp chromosomes (i.e. common ancestor of chimps and humans) as explained at wikipedia here
The question is what are the odds of a similar event occuring at random in newborns?
I have read conflicting reports, some say these things happen in about 1 out of a 1000 live births, while others placed the odds at somewhere around 1 in 7 billion.

Its not the fusion of two chimp chromosomes. To be more precisely - its the fusion of two chromosomes in common ancestor (chimp & human).

Do those "conflicting reports" write about same field: fusion chromosomes in newborns or rearrangements in cancer, or in between species?

@Pgibas they were estimating the odds of the chromosome 2 fusion happening the way it did in newborns today.

Robertsonian translocations occur with a frequency of approximately 1 in 1100..

Would be good to add the references for the conflicting reports.

@Remi.b couple of articles on line by biologists. not creationists. offhand cant remember the sites.


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Is the "endo-" prefix in "endotherm" inconsistent/opposite to its use in "endothermic reaction"?
It seems to me that the "endo-" in the biology term "endotherm" is opposite to the "endo-" in the chemistry term "endothermic reaction." Is that the case?
As I understand it:

an exothermic reaction is one that releases energy into the environment
an endothermic reaction is one that draws energy from its
environment.

Given that, I would have expected that:

an exotherm "ectotherm" would be an organism that releases energy into its environment (i.e. warm-blooded)
and  that an "endotherm" is one that draws energy from its environment (i.e. cold-blooded)

As Wikipedia puts it (emphasis mine):

An endotherm is an organism that maintains its body at a metabolically favorable temperature, largely by the use of heat released by its internal bodily functions instead of relying almost purely on ambient heat.

That really does seem to better match the "exo-" prefix.
Is there a real inconsistency here, or do I just understand this incorrectly?

See the section “Distinction between endothermic and endotherm” on this wiki page: https://en.wikipedia.org/wiki/Endothermic_process

Endothermic = "inside + temp", as in their source of heat is from within.

The prefix "endo" comes from the Greek "endon" meaning "inner". "Therm" comes likewise from the Greek "therme" meaning heat.
Thus Endo = inner, Therm = heat, heat from inside!
The confusion applies in chemistry, not in that someone has it wrong, but that molecular reactions sometimes release heat - this is obviously to the outside so it must be "exo". The Greek opposite of exo is endo, so the converse reaction (absorbing heat) must be endothermic.
Note also that in the case of an endothermic reaction, the heat supplied for the reaction to work comes from within the materials of the reaction, it's just that in the process of the reaction occurring the heat is "used up" so the reaction vessel feels cold. Because the heat is coming from inside the reaction "endo" makes sense here too.
I did my basic chemistry too long ago for me to remember for endothermic reactions if environmental heat is needed for the reaction to proceed, but I suspect that at any temp above 0 K, the answer is generally no; the heat comes from breaking of intra-molecular bonds.

"Because the heat is coming from inside the reaction "endo" makes sense here too." Bingo, that makes it make sense and consistent, thanks!


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What is the difference between nucleotide polymorphism (θ) and nucleotide diversity (π)?
In my population genetics book (see reference at bottom) they define them as:

Nucleotide polymorphism (θ): proportion of nucleotide sites that are expected to be polymorphic in any sample of size 5 from this region. Of the genome. $\hat{θ}$ equals the proportion of nucleotide polymorphism observes in the sample (S) divided by $a_1 = \sum_{i=1}^{n-1} \frac{1}{I}$. If n= 5, $a_1 = \frac{1}{1}+ \frac{1}{2}+ \frac{1}{3}+ \frac{1}{4}+ \frac{1}{5}=2.083$
Nucleotide diversity is the average proportion of nucleotide differences between all possible pairs of sequences in the sample. In R, I came up with that code which is in accordance with what is in the book.
   data # Only polymorphisms
   total.snp # This is the total number of sites that were looked (e.g. 16 might be polymorphic over the 500 sites that we've looked at. So 484 sites are monomorphic)

   n = nrow(data) # Number of samples
   pwcomp = n*(n-1)/2 # Number of pairwise comparisons
   for(i in 1:n.col){ # Compute the number of differences in the samples that are polymorphic
     t.v = as.vector(table(data[,i]))
     z = outer(t.v,t.v,'*')
     temp= c(temp,sum(z[lower.tri(z)]))
   }

   pi.hat = sum(temp)/(pwcomp*total.snp) # Nb of different pairwise comparison/(nb all pairwise comparison * total nb of loci (polymorphic or not))

In the book, they say

On the other hand, there is a theoretical relation between θ and π that is expected under simplifying assumption that the alleles are invisible to natural selection.

In summary θ = π with this assumption and large sample sizes.

So what is the difference in the
Why are we calculating both
(what could they tell us)?

Hartl, D. L., & Clark, A. G. (1997). Principles of Population Genetics (3rd ed.). Sinauer Associates Incorporated.

You are also confusing definition of these terms with their expected values (typically computed from coalescent theory). Let's look at an example.
Consider a haploid population of 6 individuals. We will represent these individuals with 5 sites that can take values 0 or 1.
00000
00001
00000
00010
00010
00000

Polymorphism
In this population there are $S=2$ polymorphic sites. In other words, there are two sites for which different individuals take different values in the population. Over these 5 sites, the fraction of polymorphic sites is $\frac{2}{5}$. You use $\theta$ for this quantity but to me, $\theta$ is typically used as a short hand for $2 N \mu$ (or $4 N \mu$ for diploid populations).
Under an infinite allele model, in a single panmictic haploid population (without selection and other assumptions), $E[S] = 2 N \mu a$, where $a = \sum_{i=1}^{k-1} \frac{1}{i}$, where $k$ is the sample size.
Genetic diversity
Genetic diversity is also known as expected heterozygosity. While it is most often called $\pi$, I will call it $H$ to avoid confusion. Imagine, you randomly sample two individuals in the population, what is the probability that there have different alleles at a given locus?

At locus 1, $H = 0$
At locus 2, $H = 0$
At locus 3, $H = 0$
At locus 4, $H = 2 \frac{2}{5} \frac{3}{5} = \frac{12}{25}$
At locus 5, $H = 2 \frac{1}{5} \frac{4}{5} = \frac{8}{25}$

You can average over all loci if you want.
The expected heterozygosity in panmictic population (without selection and other assumptions), $E[H] = \frac{4 N \mu}{1 + 4 N \mu}$. You should notice a relationship between $H$ and $F_{ST}$ here!
Nucleotide diversity
The nucleotide diversity is the equivalent of $D$ from Nei and Li (1979) and is highly related to $D_{XY}$ (Nei, 1987). Once you've managed to demonstrate that the expected coalesence time is $N$ (I won't do the demonstration here), then under an infinite site model, the number of mismatch between two individuals is logically $E[D] = 2 N \mu$ (it is the number of mutations that has happened in both lineages since the the coalescence event). For diploid population, multiply everything by 2.
Relatedness between $D$ and $S$
Under a neutral model $\frac{S}{a} = D$. Actually the standardize difference between $\frac{S}{a}$ and $D$ is what is used in Tajima's $D$ tests.
Source of information
Hartl and Clarck is good IMO but I would also like to recommend reading Population Genetics: A Concise Guide by Gillespie who explain all of that wonderfully.

Thanks! Actually, $S = nb.polymorphic.sites / total.nb.loci $. In my example θ = $S/a_1$. This is what you say is $S/a =D$. So in this case, it's not exactly $4Nμ$. And I guess here $μ$ is the mutation rate. Thanks for the book! I'm going to read this carefully.


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Human body control?
What can we consciously control in our bodies besides our muscles and brain (thought, memory, etc.)? Is the notion Bio Feedback related to this matter?
EDIT: I mean I can move my muscles at will but I can't order my liver to "work" since it's not managed consciously by the human mind. I heard about having some sort of control over temperature, heartbeat, sweating, etc. using techniques like breathing in martial arts or what they teach at the military to fool the lie detector. So my question is : What CAN we control?

Can you expand your question? At the moment I am not really sure in which direction you are thinking.

Is it still unclear?

Please define more clearly exactly what you mean with "conscious control". You can e.g. increase your pulse by hyperventilating, but this is quite different from deciding to raise your left arm. Do you consider both to be examples of body functions we can consciously control?