text:
Can DNA act as a translation substrate?
I get conflicting answers.  One would think if it was true, it would be rather seminal and widely known.
There are papers from Khorana[1], Holland[2], and Bretscher[3] (late 60s) that suggest that it is quite easy in the presence of antibiotics like neomycin.
But more recent papers like this one[4] still openly ask the question, and that the only thing we know is that the initial ribosome binding step is similar between RNA and DNA.
I can't reconcile these papers.

Morgan AR, Wells RD, Khorana HG. 1967. Studies on polynucleotides. LXXIV. Direct translation in vitro of single-stranded DNA-like polymers with repeating nucleotide sequences in the presence of neomycin B. Journal of Molecular Biology, 26(3):477-497, doi:1016.10/0022-2836(67)90316-6.
McCarthy BJ, Holland JJ. 1965. Denatured DNA as a direct template for in vitro protein synthesis. Proceedings of the National Academy of Sciences USA, 54(3):880-886.
Bretscher MS. 1969. Ribosome Initiation and the Mode of Action of Neomycin in the Direct Translation of Single-Stranded fd DNA. Cold Spring Harbor Symposia on Quantitative Biology, 34:653-651, doi:10.1101/SQB.1969.034.01.075.
Damiana L, Marty-Detravesa C, Winterhalterc M, Fourniera D, Paquereaua L. 2009. Single-strand DNA translation initiation step analyzed by Isothermal Titration Calorimetry. Biochemical and Biophysical Research Communications, 385(3): 296-301, doi:10.1016/j.bbrc.2009.05.044.

As far as I can tell from the paper you linked to (Damiana et al) it is possible but inefficient:

Naturally, we tried to translate ssDNA, but as previously described
  elsewhere, direct DNA translation was not really efficient in absence
  of antibiotics such as neomycin [5] and [6]. It seemed that the
  elongation phase was the limiting step in the direct translation of
  single-stranded DNA. Whether direct participation of DNA in protein
  synthesis could play any role in vivo must be excluded, although such
  a role could be attractive for modelling the evolution of the earliest
  forms of life.

Yet Damiana et al. still say:
"Is single-strand DNA translatable?"
"With these experiments, our purpose was not to test whether or not ssDNA could be used as a translational template in cells but..."
By "not really efficient", they mean they could not detect their intended peptide product, which seems more like "no, it doesn't work".
"All previous work had tested if ssDNA allowed direct translation, but results obtained were not really convincing and the possibility that only some steps could be restrictive was not checked."


text:
Is DNA mutation locally energetically stabilizing the DNA molecule
I am no biologist, but as a physicist, a spontaneous mutation (seen as a chemical transformation) should lower the energy of the system, at least locally. So I wonder if any research has been done along these lines for the DNA.

Not all reactions lower the chemical potential energy of all of their products - consider any endothermic reaction, in which heat energy becomes chemical potential energy. Reactions actually happen to increase the entropy of the universe, not the stability of it - looking at potentials is an approximation only.

Even if you just want to approximate the truth by considering energy potentials, why shouldn't your understanding equally predispose you to the expectation that the other reaction product would become lower energy?

@Mason: Physical systems always spontaneously evolve to lower energy state.

@hanuman, I'm with Masonk. DNA mutations are more a result of entropy than any enthalpic driving force. Plus, what system are we talking about, DNA? Cell? Life?

I am a physicist: thermodynamics entropy is a macroscopic parameter (as T) which is only defined for systems made of a large number of particles like a gas. There is no thermodynamics for a single molecule...You just have QM, energy and momemtum conservation for a single molecule.

@Hanuman, from a stat thermo point of view, the polymer isn't merely a single molecule but rather beads on a string. From what I understand, you should be able to quantify entropy by comparing the number of states W. Furthermore, in the problem that you are providing, you are not looking at a single DNA molecule but external factors like mutagens and enzymes. Those molecules will act in concert to increase the entropy of the system.

a spontaneous mutation (seen as a chemical transformation) should lower the energy of the system

Why do you think that? Because it’s an endothermic reaction?
Consider that mutations don’t happen “just like that” (at least to my knowledge) –they are triggered by external energy influx from things like reactive oxygen species or ionising radiation. So yes, they cost energy but that energy doesn’t come energetically unstable chemical bonds; it is supplemented from external sources.
So it’s not necessarily true that mutations produce lower-energy chemical bonds.

The reaction kinetics of DNA mutations are complicated by the fact that the DNA doesn't exist in isolation, and in fact is actively processed and maintained by the cellular machinery.
For example, as Alan Boyd notes, the most common spontaneous mutation is the deamination of cytosine to uracil: Cyt + H2O → NH3 + Ura.  On its own, the reverse of this reaction, i.e. spontaneous amination of uracil to cytosine, would be very unlikely, if only because the low concentration of ammonia compared to water in cellular fluid.
However, in a living cell, there are DNA repair enzymes that actively look for uracil in DNA and remove it, allowing other enzymes to come along and replace it with the original cytosine.  This keeps the effective Cyt → Ura mutation rate far below what it would be in the absence of active repair.

I'm going to attempt an answer to this at the level of undergraduate biochemistry: apologies in advance if this is not sufficiently sophisticated.
The most frequent spontaneous mutation is deamination of cytosine to uracil (hydrolysis with loss of ammonia). Strictly in terms of the double helical structure of the DNA molecule this, it seems to me, would be destabilizing because of the change from a GC base pair (3 hydrogen bonds) to a GU base pair (2 hydrogen bonds).

Thanks for your answer. If the DNA molecule is locally destabilized by a spontaneous mutation, the odds for an other spontaneous mutation to restore the stability locally are greater and that should slow evolution to a standstill if only spontaneous mutation were to be considered.

source: Stack Exchange

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Why isn't there any repulsive force between Na+ and K+ disrupting thier roles in transmembrane voltage/ action potentials
Pretty self explanatory question. I have a basic grasp on the "How" and "Why" of Reversal/Action Potential in and between neurons, but this question lingers.

I’m not sure the question is quite clear: the repulsive force of the ions is necessary for their role (otherwise you wouldn’t get an electrochemical gradient across the membrane).

The electrochemical gradients are estabished from movement and difference of each ion internal and external concentrations - K+intracell/K+extracell -, NOT between differing ions ie not between Na+ and K+.

Actually a fair point.

I agree with rwst's response below, and just wanted to add that it's not the individual ion species that matter, but the fact that there are several ions, each with ion channels of varying permeabilities. Both sides of the membrane are electrically neutral, but the chemical potentials differ due to the channels. More specifically, the resting membrane potential exists because of the higher permeability of the K+ channels.

The carriers of the charge are ions and they get repelled from each other well enough. Other than their charge there is only the size in which they differ (for all practical purposes). This means, as long as we are talking about membrane potential, the actors are just a mix of 1+ ions which don't come near each other. When size matters, for example in an ion channel, we are talking about single particles, so there is no action of a repulsive force between K+ and Na+.
From another angle: The charge is a force that emerges from a sea of particles, regardless if they are all of one kind or mixed K+/Na+. If you talk about a force between K+ and Na+ then you would have to separate all 10^15 or so K+ ions from 10^15 or so Na+ ions which is simply impossible, as they are mixed up.
http://en.wikipedia.org/wiki/Brownian_motion
http://en.wikipedia.org/wiki/Ion
http://en.wikipedia.org/wiki/Ion_channel

Ok, in other words.. the ions are too small and not uniformly purposed/moving to have such any such disruptive effect from hindering the AP process. Thanks for the insight, if I could trouble you for a source you surely would receive the BEST answer and this would be a resolved question.

This is elementary physics/chemistry. I don't need to show that atoms/molecules have no purpose, they undergo Brownian motion except when spatially hindered by a channel molecule. OK, I'll give suitable Wikipedia links.

Please forgive my elementary knowledge :) A good habit to source answers nonetheless, thanks!

Also remember that it is not Na+/K+ ions which go through the ion channels, but the solvated ions which are encased in a highly ordered water solvation sphere around them. The different sized sovlation spheres is what causes the difference in sizes for the ion channels. In a cell, negative ions would screen the positive charges from each other unless they were very close.

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Is Leptin Stimulated by Insulin Alone?
What is the mechanism of insulin stimulation in the human body?
Is leptin release stimulated by circulating insulin directly? Which other factors are involved in the level of insulin release? My goal is to identify nutrients that aid/trigger leptin production and release without causing undue inflammation or body-fat storage.

Welcome to SE.Biology. I think that you need to expand your question - it seems a little ambiguous as it stands. Do you mean stimulation of insulin release? Or perhaps insulin action in stimulating something else?

Is leptin release stimulated by circulating insulin directly? Which other factors are involved in the level of insulin release?
My goal is to identify nutrients that aid/trigger leptin production and release without causing undue inflammation or body-fat storage.

@Alan Would that be specific enough? I can go into more detail but thought keeping the question fairly general would make the answers be of use to more people.

You can edit your question, I have done that for you.

In the new version do you mean "Which other factors are involved in the level of insulin release?" or did you mean to say "Which other factors are involved in the level of leptin release?"?

I'm looking for how circulating insulin effects leptin levels in humans

This is a strange question, it is difficult to understand what you are really getting at. You should make it a bit clearer because at the moment it is an unintelligible series of poorly connected questions.

Okay: I want to know which foods best induce high leptin levels in humans.
If insulin is the primary simulator of leptin production and release then high GI carbohydrates will be more useful, and possibly some amino acids. If not, there might be other foods that can do a better job without spiking insulin.

I have to say that this seems like a really odd approach to figuring out your diet.  The question of whether insulin increases satiety has been more specifically studied in the literature, as has the satiety generated by equicaloric portions of various kinds of foods, as have the actual effects of various specific diets in human feeding studies.  If you do a bit of digging, I'm sure you can find studies relating high/low GI diets to medically important outcomes (weight loss, blood lipids, fasting insulin levels, etc.), as opposed to their effect on one proposed satiety/fat regulation hormone (leptin).  Your approach also ignores leptin and insulin sensitivity, which might be as important as the levels themselves.  As someone concerned with which foods to actually eat, empirical studies of actual diets seem like the best place to look.
Anyway, here are a few relevant citations to help answer your question:
This study found a increase in serum leptin levels in type I diabetic children who started insulin therapy:
Flück CE, Kuhlmann BV, Mullis PE. "Insulin increases serum leptin concentrations in children and adolescents with newly diagnosed type I diabetes mellitus with and without ketoacidosis." Diabetologia. 1999 Sep;42(9):1067-70.
http://www.ncbi.nlm.nih.gov/pubmed/10447517
A slightly smaller study asked the same question, and found no increase in leptin levels:
McCormick KL, Mick GJ, Butterfield L, Ross H, Parton E, Totka J. "Leptin in children with newly diagnosed type 1 diabetes: effect of insulin therapy." Int J Exp Diabetes Res. 2001;2(2):121-7. http://www.ncbi.nlm.nih.gov/pubmed/12369715
An in vitro study of rat fat cells does indicate a direct increase in leptin secretion/production when given insulin:
Barr VA, Malide D, Zarnowski MJ, Taylor SI, Cushman SW. "Insulin stimulates both leptin secretion and production by rat white adipose tissue." Endocrinology. 1997 Oct;138(10):4463-72. http://www.ncbi.nlm.nih.gov/pubmed/9322964 http://endo.endojournals.org/content/138/10/4463.full
...and in human fat cells:
Wabitsch M, Jensen PB, Blum WF, Christoffersen CT, Englaro P, Heinze E, Rascher W, Teller W, Tornqvist H, Hauner H. "Insulin and cortisol promote leptin production in cultured human fat cells." Diabetes. 1996 Oct;45(10):1435-8. http://www.ncbi.nlm.nih.gov/pubmed/8826983
Leptin levels are positively correlated with insulin levels and BMI (presumably as a proxy for fat mass?):
Lambrinoudaki I, Christodoulakos G, Panoulis C, Botsis D, Rizos D, Augoulea A, Creatsas G. "Determinants of serum leptin levels in healthy postmenopausal women." J Endocrinol Invest. 2003 Dec;26(12):1225-30. http://www.ncbi.nlm.nih.gov/pubmed/15055477
Thierry Thomas, Bartolome Burguera, L.Joseph Melton III, Elizabeth J. Atkinson, W.M. O'Fallon, B.Lawrence Riggs, Sundeep Khosla, "Relationship of serum leptin levels with body composition and sex steroid and insulin levels in men and women" Metabolism Volume 49, Issue 10, October 2000, Pages 1278–1284 http://www.sciencedirect.com/science/article/pii/S002604950041783X
This study found a positive relationship between changes in insulin levels and leptin levels, though it sounds like only in women. (I don't have the full text to check, and the abstract was ambiguous):
Widjaja A, Levy JC, Morris RJ, Frayn KN, Humphreys SM, Horn R, von zur Mühlen A, Turner RC, Brabant G. "Determinants of within-subject variation of fasting serum leptin concentrations in healthy subjects." Exp Clin Endocrinol Diabetes. 2000;108(3):208-13.
http://www.ncbi.nlm.nih.gov/pubmed/10926318
So based on an incomplete and cursory literature search, it seems likely that injecting insulin increases leptin production, as do some other activities that tend to increase insulin.  The evidence for causation in humans is not totally clear cut, though suggestive.

I agree - an odd approach to diet. Leptin does a lot and has several modes by which its expression is regulated. While the connections to insulin are well documented, I've brought to light here several other interesting characteristics of leptin.
LEP exerts its effects in the brain via the gene MC4R - see this.
HMGA1 strongly potentiates the capacity of the CEBPB (CCAAT/enhancer-binding protein beta) transcriptional factor to transactivate the LEP promoter (Esposito Fusco 2009 J Biol Chem 284:25998)
Subjects who watched a humorous video had changes in blood pressure and showed decreased levels of LEP as the level of GHRL increased, much like the acute effect of moderate physical exercise that is often associated with increased appetite.
After adjustment for gender and age SERPINF1 SNP rs12603825 revealed significant association with MRI-derived total adipose tissue mass and fasting leptin concentrations, as well as nominal associations with bioelectrical impedance-derived percentage of body fat and clamp-derived insulin sensitivity in humans, thus contributing to overall body adiposity, obesity-related insulin resistance and circulating leptin levels (Böhm Ordelheide 2012 PLoS One 7:e34035).
Leptin influences the development of eyes and ears in zebrafish and was shown by knockout to affect eye and ear development in mice (Londraville 2012 General Comparative Endocrinology J). There are many connections between blood lipids, lipid homeostasis and eye health; many genes important to both blood lipids and eye health are shared.
Lastly, the LEP gene shows altered H3K9/K14 acetylation in response to hyperglycemia (Pirola Balcerczyk 2011 Genome Res).

Leptin may not be as important as we think. A review in 2001 concludes:

Conversely, it is unlikely that leptin has evolved to prevent obesity
  when plenty of palatable foods are available because the elevated
  plasma leptin levels resulting from the increased adipose tissue mass
  do not prevent the development of obesity. In conclusion, in humans,
  the leptin signaling system appears to be mainly involved in
  maintenance of adequate energy stores for survival during periods of
  energy deficit. Its role in the etiology of human obesity is only
  demonstrated in the very rare situations of absence of the leptin
  signal (mutations of the leptin gene or of the leptin receptor gene),
  which produces an internal perception of starvation and results in a
  chronic stimulation of excessive food intake.

However, in a newer review it looks as if leptin is involved in more processes than mere survival:

Cloned in 1994, the ob gene encodes the protein hormone leptin, which
  is produced and secreted by white adipose tissue. Since its discovery,
  leptin has been found to have profound effects on behavior, metabolic
  rate, endocrine axes, and glucose fluxes. Leptin deficiency in mice
  and humans causes morbid obesity, diabetes, and various neuroendocrine
  anomalies, and replacement leads to decreased food intake, normalized
  glucose homeostasis, and increased energy expenditure. Here, we
  provide an update on the most current understanding of
  leptin-sensitive neural pathways in terms of both anatomical
  organization and physiological roles.

Jéquier, Eric. "Leptin signaling, adiposity, and energy balance." Annals of the New York Academy of Sciences 967.1 (2002): 379-388.
http://www.ncbi.nlm.nih.gov/pubmed/12079865
Gautron, Laurent, et al. "Sixteen years and counting: an update on leptin in energy balance." The Journal of clinical investigation 121.6 (2011): 2087. http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21633176/

Would it be correct to say that this abstract indicates that leptin could be involved in preventing the decline of metabolism when a person has restricted calorie intake for a period of time?

It looks like it. However see the other review I added.


text:
Does the octopus have an anus? What does it look like?
Octopuses are cephalopods, which have separate anal and oral openings. Indeed, descriptions of the cephalopod GI tract clearly depict an anal opening.
However, I am very confused about how this applies to the octopus. I don't think I've ever seen the anus depicted - where is it? What does it look like? Does anything much come out?
My first instinct would be to simply do a google image search for this. Unfortunately, those results are flooded with unrelated hits (apparently the octopus is a popular motif for tattoos... in a certain part of the body).

The anus of Octopus is channeled into its siphon.

Image taken from Carina M. Gsottbauer
Note:

Siphon is a tube that leads from the mantle to the outside. Octopuses use their siphon to force water out in jets for propulsion and to flush waste products from the anus.

From Encyclopedia of the Aquatic World, Volume 6
By Marshall Cavendish Corporation

And here I was thinking that the siphon just ejects clean, harmless water... I'll keep this in mind next time I encounter an octopus!

I would imagine that you'd probably have to worry more about that poison gland than the highly-diluted waste that is ejected from the siphon.

@RobertHarvey Isn't the poison of Octopus injected through a bite? http://www.thecephalopodpage.org/octobite.php

@SanjuktaGhosh please add citations to your answer on where the image and quote originated. If you use images and/or text that are not your own words, you need to cite the sources.


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Is it possible for a substance to be absorbed by the hair or the scalp?
I've heard that the aplication of Monovin A in the hair would allow it to grow faster. Monovin A seems to be only A vitamin, according to the first website.
Could the application of A vitamin in the hair make it grow?
I'm thinking it's not very probable that applying it to the hair and the scalp would affect the hair growth. References will also be useful.

They have a lot of hair growth questions over at skeptics but not this one.

I've thought about asking this on Skeptics, But I believed here would be a more adequate place.

As to the subject line, yes, lipid substances or any non-polar small molecule will enter the skin cells and the body below. The reason is because cell membranes simply consist of fatty substance that behaves like a solvent for other lipids.
As to the specific question about this product, Monovin A. This is a veterinary product and the producer, Laboratórios Bravet, intends it to be injected into animals in case of a vitamin A deficiency. The main ingredients is a retinol ester in the amount of 2,000,000 IU (which usually means retinol equivalents in this respect).[1]
Indeed, retinol is a lipid and long-chain esters like retinol esters are non-polar, too, and can readily be de-esterified by esterases, making vitamin A (=retinol, retinal, retinyl palmitate, retinoic acid) immediately available to the surrounding cells and, via transport in the blood stream, to the liver, which is the body's store for it. Daily doses of 25,000 IU are known to be toxic when administered over a long time. Doses of 50,000 IU can be dangerous over weeks. In general, it appears that single high doses are better tolerated than long over-exposure.[2][3] So, do the math and dilute the stuff such that you get at most one hundredth of an ampoule, else...
Now the effects. Indeed, hair loss is one of the symptoms of heavy vitamin A-deficiency, and logically, that symptom can be cured with vitamin A. That does not mean that more results in more. While retinoids are important therapeutic agents for the management of many skin diseases, notably acne vulgaris, psoriasis, ichthyosis, and palmoplantar keratoderma, there exists something like retinoid-induced effluvium which is a side effect of such medication with tretinoin (ATRA).

Retinoid-induced hair loss (telogen effluvium) is among the most
  frequent and psychologically most distressing adverse effects of
  retinoid therapy, which results in premature termination of a
  clinically desired and often highly effective systemic therapy with
  retinoids.[4]

Since ATRA is readily produced from retinal, its concentration would be expected to be up, even if the original stuff was retinyl ester. In summary, I would expect no effect, or even hair loss, for you don't simply put such potent stuff on your head and elsewhere, and have no reaction from the body.
[1] http://www.bravet.com.br/pr-ceg-monovina.asp
[2] Vitamin A: Toxicity from Supplements In: Medical Sciences Bulletin 1995; Pharmaceutical Information Associates, Ltd.
[3] Hartmann S, Brørs O, Bock J, et al.: Exposure to retinyl esters, retinol, and retinoic acids in non-pregnant women following increasing single and repeated oral doses of vitamin A. In: Ann. Nutr. Metab.. 49, Nr. 3, 2005, p. 155–64. doi:10.1159/000086879. PMID 16006784
[4] K. Foitzik, T. Spexard u. a.: Towards dissecting the pathogenesis of retinoid-induced hair loss: all-trans retinoic acid induces premature hair follicle regression (catagen) by upregulation of transforming growth factor-beta2 in the dermal papilla. In: The Journal of investigative dermatology. Vol. 124, Nr 6, June 2005, p. 1119–1126. DOI:10.1111/j.0022-202X.2005.23686.x. PMID 15955085.

Great answer! I'm amazed that you posted some references. +1


text:
Free-flowing cells and those that are stuck together?
I've been thinking about the development of an embryo from the zygote stage.
How is it that when cytokinesis takes place at that stage, the cells all stick together in a little ball, but later in life, some are not bound to others (red blood cells, sperm cells, etc.)?
In other words, how is it that some cells are stuck together and some are separated? How does this property develop?

Cell-cell adhesion is a well-regulated mechanism, cells don't just stick together randomly, this interaction is mediated by specific molecules on the cell surfaces. The responsible proteins for that are the Cell Adhesion Molecules (CAMs) like integrins, cadherins and selectins. Which of these CAMs are present on the surface of a cell determines if those cells will bind to each other or not.
Cells can change their ability to adhere to each other or the extracellular matrix by expressing or not expressing different kinds of these molecules.
You can find a lot more information about this topic in the cell-cell adhesion chapter of "Molecular Biology of the Cell", available on the NCBI homepage.


text:
Could silicon oil block Na+ ion channels in the membrane of an axon and prevent Na+ influx?
Could silicon oil block Na+ ion channels in the membrane of an axon and prevent Na+ influx?
I have been wondering if Na+ influx could have been a diluting factor in anterograde fills.  If so, could coating the axon with silicon oil prevent this?

Why not directly using a Na+ channel blocker then?

No, silicon oil couldn't block an ion channel. Oil is a nonpolar substance, just like the membrane lipids, so if you can get your oil to that cell, it will mix with the lipids within the membrane. The ion channel, which sits in the membrane, too, is rather closed to the membrane interior and opens to the inside and outside of the cell which, contrarily, is a polar solution of soluble molecules in water. So, to block one of the openings you better have a polar molecule that is water-soluble.
http://en.wikipedia.org/wiki/Ion_channel
http://en.wikipedia.org/wiki/Polarity_%28chemistry%29

Ah, I think I see thank you. I wanted to figure out a less toxic way of blocking the Na+ pumps than say... TTX.

Things behave unexpectedly when you're at molecular size. Unfortunately, there are precious few videos with animations that could give a feel for it. Now, there is the next question.


text:
Why is most tissue cellular?
Most tissue is comprised of cells.  Why? It would seem inefficient to have so many individual nucleus, membranes, etc.?
Specifically: Not all tissue is cellular.  Much tissue is extracellular matrix.  Since the body can use noncellular tissue, what is the role of cells in cellular tissue?
Another way to ask my question: Do the cellular organelles directly contribute to the tissue and organ's function? Or are they just there to maintain the cell itself?
My hypothesis is:

In some cases, the cellular organelles directly provide the tissue's function.  Eg endocrine system - synthesized at the cellular level.
In other cases, individual cells function discretely in the tissue.  Eg, nervous or muscular tissue.
In other cases, the cell doesn't directly support the tissue's function.  But it's needed to grow and preserve the tissue.  Eg connective tissue.
And finally, in cases where preserving and growing the tissue is a small enough task, a small number of cells simply extracellular tissue.  Eg bone tissue.

The above is my hypothesis.  Is it correct? Fix, revise, or replace it with something better!

I am not sure I get your premise. Would you think that one gigantic cell would be more efficient then?

Why "one gigantic cell"? Why cell at all? Why have zillions of small parts (nucleous, membranes) which don't directly contribute to tissue function? As a note, very few artificial machines work that way (though perhaps integrated circuits could be argued to).

membranes are extremely important for things like compartimentalization and signalling. For instance, neurons could not work without membranes, as they are required to generate electrochemical gradients. One very important signalling pathways is that of DAG/IP3, one of the components of the membrane. Membranes allow for storage of calcium ions in high concentrations. And I could go on listing other millions of functions.

Also, the comparison of a cell to a machine is not really a good one. A cell is more like a factory, where you have the CEO's office (the nucleus), an assembly line (the ER) with workers (ribosomes), a packaging department (Golgi), power plants (mitochondria) and so on (blatantly copied from this PDF)

Also, I wouldn't trust anything artificial longer than 100 years, from experience. Eventually something gives, and then where is the repairman if it cannot repair itself like a cell that simply divides to survive?

Since cells are the origin of every life, any tissue must at least be based on cells. Some tissue matter is outside the cells (plant cell walls), some apparently non-cellular tissue is really a bloated organelle. Both happens. As to your theses,

yes, an example are oil reservoirs in plants
no, these are just big cells. A striking example is spinal cord nerves that can be very long; irreparable if injured, because you can't repair single cells
connective tissue is cartilage, bone, adipose tissue, blood, hematopoietic tissue and lymphatic tissue. These together fit in both the organelle and extracellular substance slots, so you would have to differentiate
bone belongs to connective tissue

So, yes, you can differentiate between functions belonging to whole cells, cell organelles, or extracellular material. And there is no reason to narrow this question to humans.

Thanks - can you clarify: Does the cellular nature directly contribute to tissue function? Do organelles directly contribute to tissue function? Why are cells the origin of every life? Has this question been explored ever?

Yes and yes, by their physical and chemical properties and those of their content, respectively. Because evolution started with cells and it proved the best solution over the years. And there is even enough evidence to see why it all starts with cells: because lipids will form spheres by themselves in water, with or without content. It's just the physical optimum.

Please give an example of the "bloated organelle" you refer to.

Biological tissue by definition is tied to cellularity. To start this post, it might be useful to include important definitions:
A definition from wikipedia:

Tissue is a cellular organizational level intermediate between cells
  and a complete organism. A tissue is an ensemble of similar cells and
  from the same origin, that together carry out a specific function

The ECM or extracellular matrix, as the name suggest is a matrix.

WP: In biology, matrix (plural: matrices) is the material (or tissue)
  between animal or plant cells, in which more specialized structures
  are embedded, and a specific part of the mitochondrion that is the
  site of oxidation of organic molecules. The internal structure of
  connective tissues is an extracellular matrix.

Lastly,in chemistry, matrix generally refers to any chemical species which is not of direct immediate regard to the context of the observer (e.g. a chemist), but may or may not have significant effect on the chemistry or chemical environment in question.

Do the cellular organelles directly contribute to the tissue and organ's function?
No, they do not directly contribute to the tissue and organ's function but organelles contribute indirectly:

There is a hierarchy of structure: Everything is composed of smaller
  things and is a part of something larger. The character of structures with different
  scale changes according to the interplay of various physical forces. Quantum
  phenomena control the small scales, while gravity dominates on large
  scales, and both come into play at the beginning of the universe.

(Source: The Little Book of the Big Bang: A Cosmic Primer, pg 6 By Craig J. Hogan).
Mathematically the matter of hierarchies in science is tractable through renormalization. That isn't directly relatable to (structural) biology, but theoretical scientists have applied it.
Or are they just there to maintain the cell itself?
Out of necessity, the cell's organelles take part in the function of the cell, yes. The reason is that the organelles are enclosed by the cell and as such all prerequisites for sourcing energy are "enclosed by one additional level" as well. That being said, the organelles must maintain themselves, structurally (referred to as turnover) and information-wise. Information may not always be as accessible as through a designated external information carrier molecule, but may be a molecules properties or even another's  molecules properties, serving for instance as a "nucleation template".
Thus, the word just in your question is not applicable.
Lastly, I would like to give you a few pointers related to cellularity and the question of "why" in a context of evolution.
Cellularity may be a universal restriction that follows from the laws of thermodynamics. These laws are by consensus equally valid anywhere in the physically tractable universe. To do any work you need to have a gradient of a physical property, which is relatable to an interconvertable form of energy. To do work in an open environment in a sustainable manner over a long-term period, it is good to have insulation.
On this planet, inhabited by carbon-based lifeforms with evolution being confined to immediate (geo)chemistry**, that meant the use of lipids. Conveniently, lipids form micelles through intermolecular self-organization, in order to allow the system to reach a mimimum free energy state.
Chemical systems with say ions too spontanously assemble given favorable energetic conditions,- all you have to do is let table-salt water evaporate, yielding you little salt-cubes which even shed a bit of insight into the underlying makeup of the crystal's unit cell. But the energies of bonds that make up the insulation layer must be in a reasonable vicinity of the local thermal energy (k*T), where k is the Boltzmann constant, and T the temperature in Kelvin.
Thus, chemical species where the weak London forces outweigh any other intermolecular forces, is ideal for self-assembly of an insulation layer in a biological context. It is not the only solution that evolved. But the insulation layer crucially determines your abilities and interactions as an unicellular or multicellular organism in the tempo-spatial regime. (How large can you get? How fast can you hunt? How fast can you bud something off or engulf? How flexible are you towards shifts in your environment? Those things...)

(Dileptus - a predatory protozoan - hunting, hiding, and playing around)
Self-organization can be observed across many hierarchies, serving the minimization (or optimization) of one or several properties.
A lipid membrane is ideal on a planet whose surface is covered by an extremely polar molecule. Insulation-wise lipids are impermeable to ions to allow the formation of an membrane potential. As electrical insulators lipids are excellent thermal insulators, locally confining electrons, and finally at providing mechanical insulation. Additionally lipids can serve as fuel, nutrients, signalling molecules, and many other tasks - which really just follows from or less local molecular evolution.
Evolution:
Speaking of evolution. Just like biology doesn't make sense without the context of evolution, evolution doesn't make sense without the context of energy.  For science, evolution starts at the earliest physically tractable point and transitions across many hierarchies. Matter itself is just another form of energy, and as poorly defined as space: as "anything that has mass and takes up space".
Concluding:
No-one can conclusively tell you what any given organelle is for (yet).
But science has furnished a comprehensive picture, by looking at the molecules that make up the organelle and tracing it back to genes to let scientists marvel at an organelles function from a bioinformatical perspective. What greatly helps the exploration of organelle function are many high-resolving imaging techniques, with a plethora of labeling techniques. This array of labeling methods was amassed over the course of a century. Recently imaging equipment has seen a rapid increase of better resolutions in the time domain, which is very important as each level of hierarchy has its own sort of "time-signature" - which is of course strongly influence by the masses (or inertial forces) involved.
The entire picture of organelle function is however subject to a major revision-cycle with the ongoing efforts to map out entire cells at an atomic level, with large scale preparations already underway.
This post isn't thoroughly sourced, and much of it is only a layman's perspective. Consider this only as a starting point.
Disclaimer: universe-review.ca has been around for almost a decade, despite an unclear author backing this project- for obvious copyright reasons of the textbook contents. it is scientifically sound.
***Immediate [geo]chemistry* would exclude anything from say Alpha Centauri, but not for instance Kiuper belt objects that may have had a significant role in the composition of earth's geochemistry. This subject is so far outside my field, I cannot give you any better information.

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DAM enzyme distances move along the genome
I am fusing a protein with a Dam enzyme (http://en.wikipedia.org/wiki/Dam_(methylase)).  The idea is that when the protein binds to the DNA, the Dam enzyme will start methylating nearby GATC sites, thus helping identify the protein binding region (using DpnI later on, and microarray technology).  However, I have no idea, in theory, how many (bps) will the enzyme traverse across the genome from its starting location.  I.e., how far (in terms of bp) from its starting location will the enzyme methylate the GATC sites.
There are methods for finding protein binding regions along the genome that use such technology, such example here: http://www.nature.com/nbt/journal/v18/n4/abs/nbt0400_424.html

I am not sure about this but I believe there is not minimum or maximum distance. Each Dam protein will cut and then disassociate from the DNA. I don't think it moves along while remaining connected. If this is correct (again, I am not sure, not my field) then there will be no min/max distance between restriction sites. It will just float around until it finds another DNA molecule and cut the first site it finds. This could be adjacent to the previous one or kilobases away.

get it, thanks terdon.  I think you may be right, in my case completely not my field I am a EE...

Is there a restriction enzyme called Dam? It isn't included in the rather extensive list on Wikipedia. The only Dam that I know of is the Dam methylase of E coli which modifies the A at GATC sites immediately after replication.

I'll second Alan's comment, please clarify which enzyme you mean exactly. Dam is a methylase, it doesn't cleave anything.

guys you are all completely right, there is not such a restriction enzyme but rather a methylase enzyme!

Dam methyltransferase methylates large DNA molecules in a processive manner, with an effective range of up to 7 kb on either side of an initial methylation reaction.
My answer is taken from this paper:

Urig, S. et al. (2002) The Escherichia coli Dam DNA Methyltransferase Modifies DNA in a Highly Processive Reaction J Mol Biol 319 1085-1096

The authors report on a kinetic analysis of E. coli dam methylase. For anyone using this system as described by the OP, this paper is essential reading. Their conclusion is that the methylation process is highly processive, which is to say that a single dam-DNA interaction leads to multiple methylations before the enzyme dissociates from the DNA.
I'll restrict myself to describing just two of their experiments:
Figure 5
In this experiment they analysed the time course of methylation of an end-labelled 879-mer with 4 GATC sites, using DpnI digestion to detect methylation. In this experiment all DNA was found to be either fully methylated or unmethylated - no evidence for the presence of partially methylated DNA molecules was detected.
Figure 6
In this experiment they analysed the methylation of λ DNA (48.5 kb) and were able to detect partially methylated molecules. A kinetic analysis of the data results in the following conclusions (MTase; methyltransferase):

From these simulations, we [determine] a processivity of nav=3000. This means that after binding to the λ-DNA and starting the one-dimensional diffusion process, one MTase on average meets 3000 dam sites before it dissociates from the DNA. Since the enzyme performs a random walk, it will hit many sites more often than only once and the effective range of processivity corresponds to the square root of nav. Therefore, the dam MTase is able to methylate approximately 55 GATC sites on λ-DNA in a processive reaction in vitro. In this simulation, 4.6 associations of an MTase molecule to the same molecule of λ-DNA are required to obtain fully methylated DNA.

In a random DNA sequence GATC should occur on average every 44 = 256 residues. This suggests an approximate range of (55/2)*256 = 7 kb on each side of an initial methylation reaction.

couldn't ask for a better answer!  thanks so much.


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Why do we think chronic inflammation can cause cancer?
Why do we think chronic inflammation can cause cancer? I know the pathway is not fully understood, but what makes scientists believe that inflammation causes cancer?

There are good epidemiological data for this.

Links between cancer and inflammation were first made in the
nineteenth century, on the basis of observations that tumours often
arose at sites of chronic inflammation and that inflammatory cells
were present in biopsied samples from tumours.
There are many triggers of chronic inflammation that increase the risk
of developing cancer. Such triggers include microbial infections (for
example, infection with Helicobacter pylori is associated with gastric
cancer and gastric mucosal lymphoma), autoimmune diseases (for
example, inflammatory bowel disease is associated with colon cancer)
and inflammatory conditions of unknown origin (for example,
prostatitis is associated with prostate cancer). Accordingly,
treatment with non-steroidal anti-inflammatory agents decreases the
incidence of, and the mortality that results from, several tumour
types.

Cited from Mantovani, Alberto, et al. "Cancer-related inflammation." Nature 454.7203 (2008): 436-444.
http://www.sld.cu/sitios/reumatologia/temas.php?idv=21500

We don't think inflammation causes cancer - we know inflammation causes cancer. The mechanisms are still being identified, but chronic inflammation causes cellular turnover and proliferation that appears to lead to the development of cellular damage and subsequent mutations.
Chronic inflammatory states are clearly associated with the development of cancer in a number of diseases. One of the most common that comes to mind is hepatitis, which literally means "inflammation of the liver". Chronic hepatitis B and hepatitis C infections are two of the most common causes of liver cancer (hepatocellular carcinoma) world wide. This is why we vaccinate people for hepatitis B - it has greatly decreased the incidence of liver cancer.
There are a number of review articles that discusses potential mechanisms available on Pubmed that are freely available and worth taking a look at for more information.

I don't disagree with your answer (we do know inflammation causes cancer) but HCC in viral hepatitis is more of a counter example. HBV is an oncogenic virus and causes cancer directly. HCV might be an oncogenic virus, but the jury is still out. HCC is very rare in autoimmune hepatitis, which suggests that, in HCV (and HBV) it's the viral infection rather than the inflammation that leads to cancer.

Inflammation and the inflammatory response can lead to tissue damage, and these stresses at the cellular and DNA level can lead to changes in the cell's programming. One example I can think of is neutrophils and macrophages--inflammatory cells--releasing reactive oxygen species (ROS)--reactive oxygen radicals--at the site of inflammation, which can damage normal tissue and their DNA. With enough changes and damages--in particular, mutations and translocations to genes that regulate cell growth--the cells can undergo anaplasia and ultimately dysplasia and neoplasia (cancer).
Check our wikipedia for these term, "reactive oxygen species" and the section on caner (https://en.wikipedia.org/wiki/Reactive_oxygen_species) as well as the textbook "Robbins and Cotran Pathologic Basis of Disease" if you can get your hands on it.

Welcome to Biology and thanks for your interesting answer. Would you happen to have some references to back your answer up?

Chronic inflammation also appears to mediate epigenetic changes that serve as a fertile ground for the evolution and origins of fully transformed, neoplastic cells. In fact, there are inflammatory conditions such as chronic periodontitis where this is pretty well established. Paper here
There is also evidence for genetic and transcriptional disruption induced by inflammation in model organisms. Paper Here


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Exactly which amino acids are phosphorylated in higher plants during state transitions?
I know it is usually stated as the threonine residue near the N-terminus of either light harvesting complex (lhc) b1 or lhcb2, but if this is somehow lost, say in a mutant, is the system flexible enough to compensate by phosphorylation at another site such as a serine residue or will state transitions just cease?

The protein in question from Arabidopsis has this UniProt entry. In the comments you read: The N-terminus of the protein extends into the stroma where it is involved with adhesion of granal membranes and post-translational modifications; both are believed to mediate the distribution of excitation energy between photosystems I and II. As known PTMs we have (see Sequence Annotations) Threonine-38 and Arginine-36; below you can see known mutations. My guess, though, is that they are a few years behind and so it's better to look at recent work.
Let us then take the PMID 11113141 referred to in the above entry and see the citing papers, e.g., via CiteXplore where I see at least a few relevant references on the topic of LHC phosphorylation. If there were a review, it would be listed there. Apparently, there is also a plant phosphorylation site database PhosPhAt which might help, see PMID 22723801.
In summary, not much is known, lacking even a single review on the subject.

is the system flexible enough to compensate by phosphorylation at another site such as a serine residue

If we are just talking about substituting a residue, I think that functionality would be dependent on the associated kinases. Perhaps the plant phosphorylation database rwst mentioned could be of help?
According to my biology book (S377 Book 3), threonine-serine kinases can usually phosphorylate both residues due to their similarity. There are also tyrosoine kinases, and hystidine kinases; the latter occurring in plants only. The book states that these are the only residues that are known to be phosphorylated. It is uncommon for a threonine-serine kinase to be able to phosphorylate tyrosine, but some rare kinases can do both.


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Are these objects we found ambergris? How to distinguish ambergris from other deposits/minerals
These two objects below were found on the East Coast of the North Island of New Zealand on seperate occasions but within 5km of each other.
They both had a strong and unique, neither pleasant nor displeasing scent to them which has since faded.
The larger of the two is slowly shedding/crumbling small white clumps, presumably as it continues to dry up, a little lump of a resin like material has also become dislodged. The smaller of the larger two lumps has stayed fully intact.
Are they ambergris?
How can an amateur determine if they are or not? What else could they be?

This is unlikely to be ambergris. As I understand it, ambergris tends to darken with age and be a waxy substance with a low (~60 C/140 F) melting temperature. and should melt a little in your hands to give a waxy feel. The smell should be animal- or fecal-like.
Your last image shows a crystalline substance with obvious fracture planes, which means that it is some sort of solid.
I think this is almost certainly the resin from a species of coniferous tree. As you are on the East Coast of the North Island, it could well be pieces of *Agathis australis (Kauri) gum/resin, especially so if you are in Northland or the Coromandel. Kauri are only found about as far south as the bottom of the Coromandel/Kaimai range in the East and down to around Kawhia in the West.
If it is Kauri gum, it will be hard and have a pinetree-like scent, especially when scratched. You should also be able to polish it with turpentine. Kauri gum is semi-fossilized and a form of amber.
Auckland Museum has some pieces of Kauri gum that resemble what you have, and you can find this image on Wikimedia Commons:

Auckland Museum, CC BY 4.0 https://creativecommons.org/licenses/by/4.0, via Wikimedia Commons
Or this one from Te Ara (The Encyclopedia of New Zealand):

Interesting, I shall gently warm some up and see what happens

I don't have very good temperature control, but it does melt under a heated knife. However I read that kauri gum also readily melts ¯\(ツ)/¯

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Method of determining base values of traits in isolated populations
Prelude: I came across a discussion about the correct formula for calculating the average IQ of offspring, which goes something like the following
$$ 100 + \frac35 \left( \left(\frac{\text{father's IQ + mother's IQ}}{2} \right) - 100 \right) $$
but it does not matter for this question, and I do not know or particularly care if this is the correct formula.
As you all know, there is regression to the mean, i.e., if both parents have a freakishly high IQ of, say, 160, but come both from a "base population" with average IQ 100, the formula calculates the average IQ of the offspring to be lower than the arithmetic mean, because the parents are both outliers of their own "base population". Now, the above formula supposedly takes regression to the mean into account (and the mean it takes into account is IQ 100). As some people then pointed out, there is assortative mating, and very smart people descend often from very smart people, so the formula does not work for couples of "good pedigree".
I take it that this regression to the mean happens because these outliers with high IQ still carry some of the genes of the base population with IQ 100 and those are likely to be inherited by their children, thus lowering the IQ of offspring in comparison to their high-IQ parents.
My questions are:

How many generations of ancestors of average IQ, say, 110, do you have to have, in order for the regression of the mean to go towards IQ 110?

More generally and more interestingly, how do you determine what is the average value of a trait of a reasonably isolated subpopulation, that stems from and still lives inside a larger population? I am specifically interested in subpopulations as small as families, families with mean values of traits that deviate significantly from that of the overall population.
Obviously, the first family-generation with a mean IQ of 110 does not make it likely that the mean of the offspring will be 110 as well if the direct ancestors, i.e., the zeroth generations and those before average around 100. At what stage or how many generations in can we reasonably assume that the IQ 110  is the value that the mean regresses to, under the assumption that there is constant assortative mating regarding intelligence and no freakish outliers occur in the family tree?

I guess it boils down to the following. How big do the two family trees of a couple have to be in order to reliably infer the average value of a trait — like intelligence, highly heritable, polygenous — in future offspring?
(No eugenics, no one gets selected other than by their mates, no evil scientists lurking.)

Consider a couple where the male has an IQ of 125 and the female has an IQ of 100.  What average IQ does the formula give?

Update
I put in an answer to this question, with some reservations noted below, as there is a somewhat straightforward genetics answer to at least part of it. I'll leave the answer up for a little while as a sort of placeholder, up to the point that the question hopefully gets taken down.
Original answer
I'll first note the strong "yikes!" aspect of this question, which is closely related to e.g. eugenics.
Question 1
However, I believe that you will be most interested in the "breeder's equation", which is I believe the source of some of your values:
$\Delta Z = h^2S$
$\Delta Z$ = change in mean trait value in a population per unit time (generation usually)
$h^2$ = narrow-sense heritability
$S$ = strength of selection.
I suggest going to that resource for more information.
I will quickly note that this model is strongly dependent on a number of assumptions:

You have accurately estimated the narrow-sense heritability.
You have a large, panmictic population (you have raised this with assortative mating).
a lot of other stuff

(1) in particular is a big deal for IQ or really nearly any human, where there are reported heritability estimates in the 50% range from twin studies, but we honestly don't have a good estimate of this stuff, and there is really strong confounding from environmental variation (contra evo psych). I would not expect ("normal") IQ variation to respond very strongly to selection if environments were held constant. (There are obviously very clear examples of systematic environmental effects on IQ).
When I say "normal" variation, I mean among people who do not have cognitive disabilities related to specific variants of large effect (such as abnormal karyotypes). If you include those, you will get a large initial response to selection due to selecting on that unambiguous variation.
Question 2
Why not just measure the trait of interest?


text:
Why is coconut a fleshy fruit?
Firstly, I understand that it is classified as a drupe and its mesocarp is fibrous hence its hardness. However, how did botanists conclude such? Putting both mango and coconut side by side, we can at least see that the mango has fleshy mesocarp and soft exocarp. I would argue that the coconut's structure bears more similarity to the durian yet the latter is a capsule (or dry).
With that in mind, I cannot comprehend how the pericarp is distinguishable in 3 layers in coconut but not in durian yet they seem to be same? If coconut is like a deviant under drupes due to its fibrous mesocarp, (1) how'd they even distinguish that it was a mesocarp and (2) what is the clincher that made them conclude that coconut is indeed a fleshy and drupe despite seemingly deviant from common examples such as mango?
Apologies for not being articulate enough to explain.

The drupe definition from other answers is correct: it is a fruit with a fleshy outer part (exocarp and mesocarp), and a single hard endocarp. A drupe does not split open on its own (it is indehiscent).
A coconut fruit matches this description. The exocarp and mesocarp are fibrous (which botanically counts as fleshy), and the endocarp is hardened.

The hard shell of the shucked coconut is the endocarp, and is derived from the ovary wall. The white flesh is part of the seed, called endosperm, and the outermost layer of the seed is the seed coat. The seed coat is a very thin layer between the hard, dark brown endoderm and the endosperm.
A coconut also only contains one locule, or chamber of the ovary.
A durian, on the other hand, is a very different fruit architecture. A durian fruit contains multiple locules, and these will eventually split apart once the fruit is ripe enough (it is dehiscent). This makes it a type of fruit called a capsule. Capsules are normally described as "dry fruits" by botanists, but that descriptor is a little stretched here since the exo- meso- and endocarp that make up the walls and structure of the ovary chambers are, if not soft and pulpy, not exactly hard or papery.
The soft fleshy part of the durian that people eat is a part of the seed called an aril. Not all seeds have an aril—it's an extra fleshy bit on the outside of the seed that usually enhances seed distribution. (The red juicy bit of a pomegranate seed is also an aril.)
Finally, often the layers of a fruit can be hard to distinguish because they are compressed or of a similar structure. Botanists can identify fruit layers by tracking the development of the fruit and what the young tissues become.

A [drupe][1] is defined as a fleshy fruit, that does not open at maturity, with a single seed enclosed in a hard shell. Against all evidence, a coconut is a fleshy fruit - that corky brown husk around the seed is botanically the same as the flesh of a mango or a grape. Coconut fruits never contain more than one seed, and that seed is contained within a hard, woody shell. So, coconuts meet all of the technical criteria to be drupes.
EDIT:The fleshy part of a pomegranate seed is a sarcotesta, a fleshy outer seed coat, not an aril, which is a growth separate from the seed coat attached to the seed's hilum.
[1]: https://en.wikipedia.org/wiki/Drupe


text:
Nicotine levels in non fruit/edible parts of plants (that are not tobacco)
I am an ex smoker who now vapes (uses e-cigs). Various authorities are equating vaping with smoking by calling it a 'tobacco product' - which is in a sense true given that the majority of nicotine sold is extracted from the leaves of tobacco. I am interested in the practicality (or otherwise) of extracting nicotine from other botanical sources.
Of course, it is not just tobacco that contains nicotine, it is common in other plants of the nightshade family, as suggested by The Nicotine Content of Common Vegetables & Nicotine: Occurrence and biosynthesis. The second source notes:

Nicotine is a natural product of tobacco, occurring in the leaves in a range of 0.5 to 7.5% depending on variety.[84] Nicotine also naturally occurs in smaller amounts in plants from the family Solanaceae (such as potatoes, tomatoes, and eggplant).[85]

Reference 85 points back to the first link, which shows this table.

But looking at the numbers, it seems unlikely. At even .5%, the 'low nicotine' tobacco leaf comes in at 5 mg/g, which is 5,000,000 ng/g - around 50,000 times more concentrated than eggplant. In fact, here is a graph of the log10 value (2 is ten times larger than 1) of each.

On the other hand, the ability of a plant to produce nicotine is retained and handed down to ancestors because nicotine is a pesticide that ..discourages insects from eating the plant, and larger herbivores will also get sick if they eat too much of it. Logically, levels of nicotine would be higher in the leaves and stems of a plant than in the fruits/food that we & animals are more interested in eating. That again makes sense, since most fruits are 'designed' to be put through the stomach of a larger animal as part of the process of regeneration.
That logic seems to be borne out by the levels of nicotine in tomatoes, that start around 40 ng/g in green tomatoes, but end up at just over 4 ng/g in ripe tomatoes (not sure what's going on with that 'pureed tomato' level of over 50 ng!). The drop suggests to me that's the plant's way of preventing consumption while the fruits are still developing, but making them safe(r) to eat once ripe.
But what about the nicotine content in the leaves of those plants? Logically they might have a higher nicotine content. Does anyone know of studies of the levels of nicotine in the other parts of plants of the nightshade family?

Apparently someone thinks this question is less than optimal. Would appreciate any suggestions on improving it..

It might be an opinion about nicotine in general. This question has quite a bit more data than an average question, but I'm not aware of large nicotine levels in other parts of plants. I assume tobacco will still have the highest nicotine levels, because that's what people have been selecting for for centuries. I also assume that the FDA doesn't like e-cigarettes because they still have nicotine, regardless of source. Nicotine is addictive at low doses and toxic at high doses. They really don't like candy flavored nicotine products that might attract children.

"..I'm not aware of large nicotine levels in other parts of plants. I assume tobacco will still have the highest nicotine levels, because that's what people have been selecting for for centuries." I suspect therein lies the answer. "I also assume that the FDA doesn't like e-cigarettes because they still have nicotine," As do nicotine patches, lozenges, gum and puffers (inhalators).. "Nicotine is addictive at low doses and toxic at high doses." Not much. There is no single instance of getting a lab rat addicted to it. It is largely the other things in tobacco smoke (like WTAs) that ..

.. are so addictive. Most people that can transition from smoking to e-cigs typically drop the nicotine levels gradually. Not a great sign of an 'addictive substance'. "toxic at high doses" Yes, The dose makes the poison, and a 2014 study estimated an LD50 dose of 500 mg for an adult human. It is not to be treated lightly, and should be kept in bottles with child-proof cap, out of reach of children. "They really don't like candy flavored nicotine products that might attract children." Umm.. nicotine lozenges are designed in yummy ..

.. flavors, and check this graph of adult taste distributions for e-liquids. Further, a) kids often vape with no nicotine, and b) in states of the US where vaping is restricted, show a slower drop in smoking rate. Since the 1970s, tobacco controllers have recognized that "People smoke for the nicotine, but die from the tar". E-cigs have no tar, no carbon monoxide, and when used responsibly, provide an effective and 95% safer way for smokers to satisfy their desire for nicotine. Thanks for bringing those matters up. :)

BTW - I recognize that you were speculating about what other people might be thinking. I suspect the same reason was behind the down vote. The thing is, there are powerful forces aligned against the e-cig industry at the moment, including the CDC, FDA, ALA, AMA, CTFK.. and states deeply in debt to the MTSA.. They spread much fear, uncertainty and doubt for ..whatever reasons. That's why I'm investigating 'nicotine from other sources'. It has become a largely political point that nicotine is sourced from tobacco. Next stop would be, synthetic..

Note that the nicotine is not the problem and never was the problem. There are, apparently, some studies that link nicotine itself to certain cancers but the reason that smoking is bad for you is overwhelmingly because you smoke it. Take away combustion and most of the problem basically disappears. Therefore, the source (or even presence) of nicotine is essentially irrelevant. That said, please don't use this forum as a soap box to tout the improvements of e-cigs over smoking. I happen to agree with you 100%, but this is not the place for it.

Would look forward to finding out more when you get back to your computer, @kheironiscus.

why would hte lack of nicotine in other plants be relevant, many plants produce high concentrations of specific compounds that is relatively rare in most other plants.

.. I'm not aware of large nicotine levels in other parts of plants. I assume tobacco will still have the highest nicotine levels, because that's what people have been selecting for for centuries. .. - user137

That logic seems compellingly sound.
Based on that, why would a researcher even bother to measure the nicotine content of the other parts of non-tobacco plants?

They are not being eaten by consumers & thereby have little or no risk of poisoning them.
The levels of nicotine would be expected to be so far lower than the 'commercially viable' tobacco leaves as to be of no interest (purely for their nicotine content).

So in answer to my own question.

Does anyone know of studies of the levels of nicotine in the other parts of plants of the nightshade family?

No, because it is unlikely any such research has been performed.

Tomato leaves have something like 184 ng/g of nicotine, in the same ballpark as tomatoes (the fruit) and not close to tobacco.  I think this is not peer-reviewed, but it cites other papers that are: Nicotine Analysis in Several Non-Tobacco Plant Materials
And this is a PDF of a slide deck providing a simple presentation of the results from the same article: Nicotine Analysis in Several Non-Tobacco Plant Materials - PDF

"I think this is not peer-reviewed" No problem here. I've read enough papers from people in tobacco control that have passed peer review, which completely disagree with other peer reviewed papers, that the 'not peer reviewed' status does not bother me in the slightest. Thanks for your answer!

I take issue with the previous answerer's assertion that it is extremely unlikely that previous research on nicotine concentrations has ever been performed; in fact, it was very well established decades ago that alkaloids in Nicotiana (and other Solanaceaes) are predominantly synthesized in the roots and, in the case of grafting studies, translocated through the stalk into the scion, which findings rest on measurements of alkaloid levels throughout the plant.  The research is very much out there.
Reference
G. R. Waller and E. K. Nowacki,“Alkaloid Biology and Metabolism in
Plants,” Plenum Press, New York, NY, 1978. Pages 121-141 for the nicotiana grafting discussion.  No doubt there is more recent work out there, though.


text:
Suggestions for self-studying experimental techniques
I would appreciate any suggestion regarding self-studying experimental techniques used in biology for a theoretical scientist (candidate).
Maybe I should be more specific. I'm a biology major, but took as little experimental courses as possible, and I didn't paid much attention to those I took. (shame on me, right). Then I got a MS in applied math. When I revisit my molecular biology/genetics and biochemistry textbooks, I realized that they are mostly descriptive.
An experiment/technique oriented textbook would be very helpful for me, especially if it will also provide an overview of the methods.
My purpose is not the make up for the lost undergrad years, change my research orientation or master experimental skills. I'm aware that this is not achievable by reading some texts. My sole purpose is to not get lost on theory/experiment interface. When someone asks how something could be proven experimentally, I want to know what options are there in the field.

and I also wonder, why there is no self-study tag on biology.SE

Are you mostly interested in molecular biology oriented methods?

yes, especially genome sequencing and transcriptome quantifying methods

My undergrad mol. biol. book showed a lot of the original experimental data for establishing mol. biol. mechanisms, but it's pre-shotgun sequencing. It doesn't have a lot of the new, PCR-based stuff, because much of the basic biology was worked out before then. Should I hunt down that textbook title?

thank you, but I think I need something which covers also moder techniques.

I cannot more highly recommend Molecular Cloning 4 ed.. It is a really comprehensive text which covers numerous molecular biology experimental techniques including different types of PCR.
EDIT: Also, there are some great suggestions for other books and websites that also cover molecular biology techniques in the answers to this question: Short, concise, practical manual for doing experimental biology


text:
Is excessive hydration a risk factor for cancer in humans?
I was reading a book on radiation biology, and the book describes the process of "indirect action", where radiation can first ionize a water molecule forming a free radical, which then may interact with important cellular molecules, such as DNA.  This contrasts with "direct action" which involves direct ionization of a key cellular molecule.
The book states that as hydration increases, the probability of indirect action occurring increases.  Given that indirect action normally predominates over direct action in cells, could this mean that over-hydration could be a risk factor for developing cancer in humans? Has there been any research into this?
In addition, would larger humans, who obviously have a larger bodily water content, have an increased risk of developing cancer compared with smaller humans?

What do you mean by over-hydration? Humans consist to a high percentage of water - it is present in every cell and necessary for out biochemical reaction, so there is already plenty of water present.

@Chris, I don't mean any strict definition of "over-hydration".  If a human is dehydrated, the intracellar water volume will decrease, and if a human has renal impairment leading to anuria, it is likely intracellular water volume will increase.  So by overhydration I simply mean more intracellular water than otherwise, that may result from increased water intake, or decreased water excretion.

In the most technical sense, yes. In a practical sense, no. Average background radiation dose from food and water sources is ~.3 mSv according to the UN. Given that it takes 1 full Sv to increase cancer risk by ~5-6%, it seems unlikely that, under normal conditions, variability in consumption of water will change risk in a significant fashion.
Now, when dealing with highly contaminated water, there may be a more exaggerated effects, scaling with an increased concentration of radioactive particles per unit of water. Of course, in highly radioactive situations the risk of radiation poisoning may be a more immediate worry.


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Any benefit to low dose radiation?
Is there any survival benefit in humans that can be obtained from chronic exposure to low dose radiation, or is any dose of radiation a potential harm?  Has any research been done into this?

What kind of benefits do you expect?

@Chris, the book on radiation biology I was reading said that animals exposed low doses animals were observed to have a decrease in mortality compared to those exposed with no radiation.  The book is quite old so I'm not sure what recent studies suggest.  The books said the cause of this phenomenon was unknown and controversial, but stated some scientists hypothesized low dose radiation could prevent some diseases occurring.

http://journals.lww.com/health-physics/Abstract/1982/12000/Physiological_Benefits_from_Low_Levels_of_Ionizing.1.aspx

This is not an easy question - I can have a deeper look into this after the weekend, if not somebody else does it.

@Mew I found a non scientific article: http://www.hiroshimasyndrome.com/radiation-the-no-safe-level-myth.html which has many citations. So it is possible that low level radiation is beneficial. I think you should read more in the topic to reach a conclusion.

@Mew Another article: http://www.snm.org/docs/Radiation_Hormesis_JNMT_March_O3.pdf and wikipedia article: http://en.wikipedia.org/wiki/Radiation_hormesis

As @ inf3no indicates in his links: the general term for a beneficial effect to a low exposure of a stressor is called 'hormesis': http://en.wikipedia.org/wiki/Hormesis. A very interesting and exciting topic indeed.

Thanks everyone for your input so far, I'll keep investigating and looking at the links you have provided.

This is an interesting - and highly debated question. Generally there are two completely different directions of thinking when talking about dangerous substances (this applies to dangerous chemicals as well):

The linear no-threshold model (LNT).
The hormesis model, in our case the model of radiation
hormesis.

Summarizing the models the LNT model says that every dose has a negative response, so there is nothing like a stimulating dose and exposure should be avoided at any means. This reflects the policy in the handling of radioactive substances. If you look at the figure below, the curves a + b (supra-linear and linear) reflect the LNT model (the figure comes from here):

The radiation hormesis model says that there is a dose range in which the radiation above the background level is not only not harmful, but beneficial. High doses are (in line with the LNT model) also considered harmful. This can be seen in the curves c (linear-quadratic) and d (hormesis) in the figure above. The benefits are thought to take place through the activation of repair mechanisms (which are only activated by radiation) which protect against changes in the genome and thus also protect, once activated, against changes which are caused by other agents and reasons. See reference 1 for more details about radiation hormesis.
There are a number of studies which observe this effects in the laboratory and this is also one of the major critic points: To my knowledge it is currently unknown if these effects can also be seen outside a controlled laboratory environment.
Other critique points are low study publications (which makes studies prone to statistical errors), using wrong models (cell culture) or too high doses. See references 2 and 3.
Since our environment contains naturally radioactive substances as well as cosmic and UV radiation, we have developed pretty efficient mechanisms to deal with these problem. Additionally measurable effect of radiation on the activity repair mechanisms can be seen (and this is not debated at all), but the main question is if these effects can also have a beneficial effect. It is also not known, if all radiation ($\alpha, \beta$ and $\gamma$) have the same effect, or if some of these like $\alpha$-radiation is more dangerous.
So I think it may be possible that there is some positive effect, but until this is proven, I would rather be safe than sorry.
References:

Evidence for beneficial low level radiation effects and radiation
hormesis.
Uncertainties in studies of low statistical power
Health Risks from Exposure to Low Levels of Ionizing Radiation

I would be inclined to say yes based on the current wording of your question. There is more than one type of radiation out there, so I'm not exactly sure which you are interested in.
Ultraviolet is the one I will focus on though. Within the ultraviolet spectrum there are three types of ultraviolet radiation. The types are UVA, UVB, and UVC. UVC is primarily blocked by the atmosphere, so it never reaches us on the Earth's surface. UVB is perhaps best known for causing sun burns and skin cancer. UVA is the least powerful of the three. In chronic doses as you suggest it is probably far from good, but it can be beneficial at low doses.  UVA is linked with the production of Vitamin D which strengthens bones. It also stimulates tanning of the skin, which helps to protect the body from UV damage. Here is a link to The WHO describing some of UV's health benefits:
www.who.int/uv/faq/.../en/index1.html

Well, if we're considering UVB, Vitamin D is an obvious candidate to considering benefits of "radiations".  Even though, initially, Vitamin D synthesis was just a mechanism of protection for early marine organisms against UVB DNA damages. There are now so many metabolisms affected by Vitamin D.


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Biology view on trait variability
In reading the annotated Origin... I have come to the following note by Costa on p. 168:

Again, modern biologists would disagree with Darwin's idea that especially well-developed traits vary to a greater degree than expected simply because they have been varying and undergoing selection in the past (as evidence by their considerable development)...

I am not sure I understand what the problem with Darwin's view is. From reading his work I understood that he, Darwin, is simply saying that traits that have been more recently acted on by natural selection would vary more than those that have been acted in the past and over a longer period of time (given that conditions remain relatively the same - I assume).
What is the modern view of biologists on this?
P.S. The excerpt to which this side note refers, follows:

In these remarks we have referred to special parts or organs being still variable, because they have recently varied and thus come to differ; but we have also seen in the second Chapter that the same principle applies to the whole individual; for in a district where many species of any genus are found - that is, where there has been much former variation and differentiation, or where the manufactory of new specific forms has been actively at work - there, on an average, we now find most varieties or incipient species.

Could you please clarify? Do you mean well-developed (whatever that means really) or recent? The two are not synonymous. Could you maybe include Darwin's original sentence that we modern types are supposed to disagree with?

I cannot really clarify it as I don't really understand what the author means. I can, and will, include the original passage to which this side-note refers.

In fact, I can't find what Costa is saying in Darwin's words, as it seems Darwin is saying complete opposite.

The variance of a trait's allele frequency can follow different trends over time depending on several factors such as whether one or several of the alleles are consistently selected for or the population dynamics. For example Disruptive Selection will tend to increase the allele variance. On the other hand Directional selection, or Stabilizing selection will tend to decrease variance by driving the allele frequency to one side of the distribution (in the first case) or by "cutting down" its sides in the second case. It is true that stabilizing and directional selection processes are more common especially under relatively stable environments. Therefore for the majority of cases, during the first phase of selection for a trait variance will most commonly decrease . This, however, is not a rule.
There are additional, rare, but from an evolutionary point of view extremely important cases where allele frequency variance can see a sudden "ballooning". Consider for example the case of selection processes after mass extinction events. Then, because of the sudden availability of previously occupied niches, genetic drift due to small population sizes as well as changed conditions the previously stabilized traits will start...well...drifting. The same is true for almost any circumstances that will destabilize equilibrium and lead to speciation.

But that has little to do with the actual theory, which is trying to explain the "general principles" of things. The events such as catastrophe will in a sense "revert" things back to an earlier time, after which the quickening of variability will commence. BUT it will still tend to slow down, eventually, and vary to a lesser degree, again satisfying the theory. N.B.: I haven't read about the Disruptive Selection or Directional Selection yet, so I am only talking about your latest point here. Thank you and excuse me!

Now that I've read about Disruptive Selection, I don't see how it impacts the argument. For once the selection is stabilized, it will tend to vary less. E.g. in the example of white/black rabbits - once the black color is chosen, it will vary very little compared to when the rabbits were initially specialized from, say, previous-rabbit-species, which were, for example of green color. Nor is there anything in Drawin's theory to suggest that simultaneous "genes" cannot exists in species at the same time, if selection deems them useless.

Directional selection sounds just like a regular natural selection to me. Perhaps I am missing some fine detail? Excuse my ignorance - I am just starting this subject!


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Reattaching body parts
Is there any living organism that has the ability to remove and reattach body parts at will?
I'm not talking about regeneration (like in starfish). Say I'm chasing prey, and I decide that my tail will be a hindrance. So I leave it behind, and reattach it after the hunt.

I've never heard of reattachment... that would be a very exotic trait :)

I dont think this would be possible from the simple idea that all cells need energy, and if there's no nutrient flow, then how would the cells inside the detached body part stay "alive".  Doctors can currently reattach body parts right now if it's within a certain amount of time, but no animal yet can just reattach at will.


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What is the purpose of measuring both VS (volatile solid) and TS (total solid)?
In the biogas process you often measure Volatile solid and Total solids. Can any one explain these concepts more accurately and why it is interesting to look at these properties.
The biogas process I refer to is a process of fermenting waste food materials and slaugther house waste in to bio fuels, consisting largely of methane. The fermentation is conducted in anaerobic milieu in large plants.
Total solids and Volatile solid are measurements on the sludge the currently fermented waste,(the gooey stuff that is in the bio-reactor).

Can you elaborate on what the "biogas process" is?

Total solids (TS): The part of the sludge that remain after drying at 105$^{\circ}$C for 20 hours:
$$ TS(\%) = \frac{\textrm{weight dried at } 105^{\circ}C}{\textrm{wet weight} }\times 100 $$
Volatile solids (VS): The part of the sludge that is combusted at 550$^{\circ}$C after 2 hours:
$$ VS(\% \textrm{ of TS}) = \frac{\textrm{dried weight at }105^{\circ}C -
 \textrm{dried weight at }550^{\circ}C}{\textrm{dried weight at }105^{\circ}C}\times100$$

For the definition, see Pelle's answer.
For the reasons, both are easy and cheap to measure and can tell you a lot about your material if you have similiar mterial to compare. TS is often used to asses howa material can be handled (pumpable, stackable)
In agricultural biogas applications for example, a sometimes used assumption is 1g COD = 1,6 g VS
In AD, VS is broadly associated with digestible biomass, and depending on input one third to one half of VS will be converted to gas. In fact, gas yields are often given per mass of VS because of this.
Note that solutes that are actually volatile, like alcohol, will be evaporated when testing for TS. Laso note that the points give na bove only work if you compare similiar materials.

VS and TS are very important parameter when it comes to Biogas production, in the following ways.
VS = Represent organic matter of the feedstock (excluding the inorganic salts, ash). Having in mind that bacterial action is on Organic mater and not Inorganic. meanwhile,
TS = Denote all the organic as well as inorganic matter in the feedstock.
Finally, VS/TS for different feedstocks can be model to give the biogas production.


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Why can't you taste food when you have a cold?
It is a common observation that food is tasteless when we have a cold. Why is that so?
What is the cause of inability to taste when we have a cold? Are the nose and ability to taste connected?

There are many factors that contribute to the flavor of food - the five "traditional" tastes (sweet, sour, bitter, salty, umami), smell, texture, spiciness, "coolness" (like peppermint), temperature, etc. Smell and taste are detected in similar ways, by chemoreceptors expressed in taste pores by specialized cells of the lingual epithelium (tongue), and in the nose by the olfactory epithelium. Both are affected by upper respiratory tract infections like colds and the flu, leading to diminished senses of taste and smell, and a corresponding reduction in the overall flavor of food.

This doesn't answer the "why" question.

@Kevin: yes it does... receptors are also on the olfactory epithelium.

When we eat something,the aroma of the food particles enters our nostrils and travel through nasal passage.While passing,through hair cells present in our nose,the information (flavor & taste) is sent to the brain.But during Common Cold,our nasal passage get clogged with mucus which don't allow the aroma to pass.Due to this, the brain becomes unable to determine the taste and flavor of the food.

Can you please [edit] your answer to add some references that would support your answer?


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Bacterial cell lysis buffer used in proteomics procedures
What kinds of detergent-free bacterial lysis buffers exist? The proteins we're extracting will be later analyzed by LC-MS/MS, and we're looking for a lysis buffer that won't interfere with this downstream analysis.

I'm a HUGE fan of FASP (filter-aided sample preparation) which is an in-solution preparation/digestion. It is very fast, allows you to not worry about a protein precipitation step, and gets rid of all MS incompatible substances with the wash steps (so doesn't matter what lysis buffer you use). It requires very few, inexpensive materials (a pack of 100 centrifuge filter units is less than 250 USD from VWR) and has great recovery. This is the link to the Nature Methods paper that the linked protocol is based on (the linked protocol is an updated, faster version of the Nature Methods one).

There are a few techniques available for this.
Some recommend a urea-based technique, others recommend a chloroform. Do you have more information about your specific needs?
A Chloroform-Assisted Protein Isolation Method Followed by Capillary NanoLC-MS Identify Estrogen-Regulated Proteins from MCF7 Cells

why not use a french press?   put a few thousand PSI on the sample and the cells just pop open.  The lysis buffer contains no detergents:
Lysis buffer:
50 mM Tris-HCl pH 7.5
50-200 mM NaCl*
1 mM MgCl2
5 mM DTT
1 mM PMSF

the salt concentration is variable and you could probably do without the DTT too if thats a problem ...

As pstew mentioned, SDS based lysis followed by FASP is a very good way. However, FASP can lead to sample losses. I would use it only if you have large culture of bacterial cells.
If you want totally detergent free method then, lyse cells in 8 M guanidinium hydrochloride buffered to pH 7.5-8.2 using 50 mM Tris buffer or 50 mM freshly prepared ammonium bicarbonate. If your cell pellet is approximately 20 uL then add 60 uL 8 M GuHCL buffered solution so that final conc of GuHCL is ~ 6M, heat to 65 degrees C and shake for 30 minutes or so. Spin down to remove any insoluble debris. Measure protein concentraion, if you want to, using BCA assay. Then, reduce with 10 mM DTT for 30 minutes at 56 C, alkylate with 25 mM iodoacetamide at room temperature and in dark (for this step it is crucial that the pH of your sample is around 8.0 otherwise iodoacetamide will cause side reactions). Dilute at least 8 times and digest overnight with Trypsin.


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Punnett Square Help
In fruit flies, red eyes are dominant over white eyes. Show a cross between two white-eye fruit flies.
My question is...
How do I know if the white-eye fruit flies are homozygous or heterozygous?

This looks like a homework question, you should take a look at the policy on asking homework questions - it is important to demonstrate an attempt at an answer and make sure it is tagged as homework http://meta.biology.stackexchange.com/questions/266/homework-policy-for-faq

Just to add an extended perspective to all of the answers submitted so far.
The classic white-eye phenotype in Drosophila is associated with a gene, white (or w) that is carried on the X chromosome (females XX, males XY) i.e. it is a sex-linked phenotype. Male white-eyed flies are therefore technically not homozygous, they are hemizygous since they only have one X chromosome and thus one copy of the gene.
There are other white-eyed phenotypes due to segregation of two genes (brown and scarlet) - this is the standard two-factor cross example in many genetics courses. In this case (no sex linkage is involved) a white-eyed fly is homozygous for the recessive allele at both loci.

In fruit flies, red eyes are dominant over white eyes.

Red is dominant (A) which means we can deduce that white is recessive (a). Therefore AA individuals are red eye, and so to are Aa because the dominant red allele overrides the white recessive allele. Then the only way a fly can be white eyed is with aa.

Show a cross between two white-eye fruit flies.

Both white eyed flies are aa so all four possible outcomes are aa in a single locus punnet square.

In order for any recessive trait to be expressed, it must be homozygous for that recessive trait. If an individual was heterozygous, the recessive allele would be masked by the dominant allele, giving it the dominant phenotype.
Therefore, since white eyes are recessive, fruit flies with white eyes will always be homozygous (aa) for that recessive trait. A fruit fly that is heterozygous (Aa) for this trait would have red eyes.

Because red is dominant over white, in order for the flies to express the recessive white eye trait they must be homozygous for the recessive white allele - I.e (no pun intended) rr.

If the question allows you to assume that eye-colour is a typical gene with two alleles, then we can figure out the answer. If flies' eye-colour has two alleles - dominant and recessive - then the phenotype will be dominant (red - A) or recessive (white - a). Dominant traits need only one dominant allele, so the genotype can be Aa or AA. The only other combination is aa, and that codes for the recessive phenotype of white eyes. There can be no heterozygous white eyed fly.


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How do people who have lost both of their legs produce red blood cells?
As far as I know, just leg bones produce red blood cells. So, how people who lost their both legs produce red blood cells?

Can you point to a reference?  Any bone with sufficient marrow can produce erythrocytes.  It may be that the largest number are made in the femur and tib/fib, but they aren't exclusively the point of production.

Red blood cells are produced in the red marrow which...

"is found mainly in the flat bones, such as the pelvis, sternum,
  cranium, ribs, vertebrae and scapulae, and in the cancellous
  ("spongy") material at the epiphyseal ends of long bones such as the
  femur and humerus." - Wikipedia

So you are partly right; the femur is associated with red blood cell production, or Erythropoiesis to give it it's technical name, but there are other bones within the human body that also do this job. The process of erythropoiesis is stimulated when the kidneys detect low levels of oxygen in the blood stream and stimulate production of the hormone erythropoietin. Further, the role of the tibia and femur in erythropoiesis also decreases with age whereas...

"the vertebrae, sternum, pelvis and ribs, and cranial bones continue
  to produce red blood cells throughout life." - again from the wiki page

So I'd suggest it is unlikely that loss of the legs would have a major impact on the production of red blood cells in adults. I imagine that with the loss of legs comes some reduction in functionality of erythropoiesis but also a lower requirement of red blood cell production (less blood capacity = less blood cells needed = less blood cells need to be produced). I can't find any studies which explore the ability or needs of amputees and non-amputees with regards to red blood cell production.

While researching earlier I did find some reports on post-amputation anaemia. Clearly the compensation by other bones does not always work, but this was a minority of only about 7% iirc.

@Armatus Thanks, I guess people will be affected differently, I couldn't find any evidence of prolonged problems myself but did find cases of transfusions being required in the days/weeks after surgery but that is probably more related to the blood loss and maybe the other bones "learning" to compensate.

Red blood cells are produced in the red marrow, and white blood cells are produced in the yellow marrow. The marrow is found in the flat bones (i.e.long bones) which is the pelvis, sternum, ribs, and vertebrae. If the long bones are no longer attached the the pelvis and the ribs with have to work harder in order to produce the blood cells needed.

can you give a source for that information? Also, see comments on question that are listed above.