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Why hasn't mother nature made us aware of our lizard brain?
In many personal improvement books I've read, people make a distinction between 2 parts of our brain:

the logical brain, dealing with logic, judgement, thinking; what makes Humans different than Animals
the lizard brain inherited from our ancestors, dealing with emotions and instincts, which takes shortcuts to react to the immediate problems, such as a saber tiger croping up to eat us.

The facts are, the lizard brain sometimes take actions/decisions without making the logical brain aware of that, which is at the origin of many brain biases.
I am wondering if there's a sound reason why Mother Nature didn't evolve us so that we would be made aware of our lizard brain decisions after the fact (i.e. a kind of summary for our logical brain). I mean, is there's something physical or an evolutionary reason that would prevent that?

The reason is that the “lizard brain” doesn’t exist, it’s pseudo-science sauce, as are almost all self-improvement books. In reality, the brain is much more complex than that.

I just looked this up. I am blown away by all the websites on lizard people. How can anyone believe David Icke.

@GabrielFair the Lizard Brain is not the same as David Icke's reptilian theory. The Lizard Brain thing seems to be just a simplistic way of describing a separate 'primitive' part of the brain (which doesn't exist), whereas David Icke thinks lizards secretly rule the world. While they are both stupid, I think Icke's ideas are insane, while the Lizard Brain thing is a basic misunderstanding.

@KonradRudolph you should make that an actual answer, so we can vote it up for visibility

-1 mother nature does not evolve us. That is a religious rather than a scientific view

I guess the problem lie in the wording: sorry but English in not my mother tongue and I am not in biology. Still, I'm surprised that this question has been closed as "non constructive". How can I improve this question? Maybe by removing the allusions to the lizard brain?

Two upvotes for this question?

Just to echo what others have said here, the term lizard brain is a remnant of "recapitulation theory" which rigorously proposed that the embryo develops through more primitive animals.  This is an intriguing idea when looking at embryos - early stage embryos of flies, birds, fish and primates really do resemble each other.  So the idea was that our lower brain, near the spinal chord was the brain of a lizard, whereas the prefrontal cortex, which is highly developed in humans compared to lizards, birds etc was 'added later' and represents a 'human brain'.  This idea is flawed because it basically assumed that the lizard part of us never evolved and was based on a linear idea of phylogeny, as opposed to Darwin's idea of evolutionary trees where lizards and insect continue to evolve.  In evolution there are no 'lower animals'.
In practice, the parts of the brain we have in common with lizards do handle more physiologically autonomous functions (heart rate, etc).  While cortex and prefrontal cortex do show greater activity in emotional and rational decision making.  This is now more of a rule of thumb, not a rigorous statement or a theory of development, merely the result that structures that were developed later tend to have newer functions.  A good discussion of this can be found in Gould's "Ontogeny and Philogeny".
Your question also asks why we can't rationally understand our lower brain functions...
Awareness itself is not an intrinsic property of the brain.  Some aspects of the rational mind and articulate self consciousness are so far fairly unique amongst brains.
I should mention at this point that I do not mean that conscious thought is unique to humans - its clear that primates are aware that they exist and have empathy for feelings of others. Its likely that other animals have similar amazing abilities we think of as human.
Just the same, the level of development in humans is distinctly unique.  Insofar as it is a unique development, not a typical brain function, we should understand that it is far from all encompassing.  Given all this, its not surprising that the physiological functions of the brain such as regulation of breathing, many hormonal levels, stress are not conscious.  I usually only know I've run too far and too hard because I can feel my chest heave - its actually only something I'm aware of because my brain is receiving signals from my chest that its heaving and my heart is beating rapidly.
The limits of our consciousness are the subject of much study now.  From cognitive psychology and behavioral economics we've been surprised over and over in the past 20 years how there are limits to the amount of information we can process at a time and, how limited we are in being rational to the point that we can make foolish decisions, and lastly how much of those decisions are made subconciously, only to be rationalized later by our thoughts.
I will give three examples.
1) Experiments in cognitive psych show that as subjects turn over cards in a deck, our pulse and respiration indicate they know that the deck is stacked before they consciously know.
2) Psychologist/Philosopher Joshua Greene is famous for observing that moral decisions are made in parallel in more than one region of the brain before the decision is rationally made.  This is a great radiolab podcast on this story.
3) Behavioral economists have shown that we don't even know a good deal when we see it.  We are often convinced by cues in the environment about the profitability of our decisions which comes from pre-set processes embodied in our minds.  Studies showing what happens when we pay CEOs too much money, manipulate decision making by offering too many choices and how poor people are more generous than wealthy ones.
This discussion goes back to Descartes, who felt we could be fooling ourselves to the point that we might even be deluding ourselves to believe in mathematics.
If there are ever times when people do things that don't make sense, we have often found that the faults go back to the limitations of our brains.   If you have never had that experience ... "Ill have what @Sylvain's having"!
Looking at references for cognitive dissonance, optical illusions will tell you a dozen more fascinating stories.  Highly recommend it :)

Whilst there is some interesting info in here, I think you should point out the fallacy in the original question (i.e. the lizard brain is not a thing).

added it - good point.


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Identify this waterfowl species?
I've been unable to find anything on the Google resembling this bird. I took the photo in Virginia Beach, VA around 2010, October, I think...
It appears to be between winter and summer plumage but I'm not sure. I tried looking on whatbird.com but couldn't find anything that really seemed to match up well.
Edit
I've added some more photos since people seem to question whether or not the white is snow, for some reason. Also note that most seem to have a red bill with a black tip, while the one with more white on its breast has a largely black bill with just a red band. Do bills change colors when plumage does, is that a thing, or perhaps it's just an anomaly or a gender trait?

I don't think there's seasonal plumage change going on here.  The white patches seem to be driven snow.  The bird on the left is plastered like the tree on the right.

There is snow, but it's not all snow. Also notice that the bills are two different colors.

It looks like a male and a female with the female being smaller and read beaked.

They don't really look like different sizes to me(at least, not drastic enough that I'd think it was a gender distinction...) the one on the left just has its head up and the one on the right has its head down.

Yes, looks like Cairina Moschata - Muscovy Duck. Native to Americas, domestic/semi-wild in Europe.

I am not an ornithologist, but using identify.whatbird.com and a simple google search, this appears to be a Muscovy Duck. Try a google image search for yourself! Some of the birds pictured have more ostentatiously red or larger caruncles, but some look very similar to the birds you photographed. For example: http://www.birdinginformation.com/birds/ducks/muskovy-duck/
From muscovyduckcentral.com and identify.whatbird.com:
The domestic breeds can come in a variety of colors, but are primarily black and white with red and white bills. The males are larger than the females -- around 15 lbs for a male and only 8 lbs for a female. Females are duller colored than the males. Muscovy ducks are indigenous to Mexico, Central and South America, but are now raised in many different locations. They are considered a good duck stock because they are large, breed quickly, provide good pest control, and are quieter than many other duck breeds.

I used whatbird.com for VA and that didn't come up ... (as mentioned in my comments) Well, your google-fu is obviously superior to mine. Thanks :D

Aaaah, that'd be why it dodn't show up in VA. I would've thought it would take migration into account tho. Huh.

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How do cancers eventually lead to death / other debilitating symptoms?
With regards to people I know or have read about who live with cancer, most of their symptoms are results of chemotherapy, surgical interventions, etc., which have the goal of eradicating the cancer. Assuming the cancer went untreated,* what kinds of symptoms would the cancer itself lead to, and by what mechanism would it cause death (in most cases)?
Please excuse my ignorance. I know that every cancer is different, and even different cases of a single type of cancer can present differently; so there may be many different answers to this question, but I'm not sure if they eventually lead to the same thing.
*I'm asking purely out of curiosity – I'm not "opposed" to chemotherapy or anything like that.

Where did you read about what symptoms? And I can assure you, cancers alone have a lot of nasty syndroms and outcomes.

Thank you for the comment--I would believe that for sure, I'm just wondering how specifically the cancer will kill / lead to the nasty symptoms. I'm mostly thinking about a personal case, where someone suffering from AML went through many rounds of chemo and developed a bad infection as a result of immunosuppressants. We didn't hear about symptoms of the cancer simply because the doctors detected it early and (thankfully) didn't let it get to that point.The book I'm reading is "The Emperor of All Maladies" by Siddhartha Mukherjee, which admittedly focuses on the history of cancer treatments.

This is a very general answer to a very general question.
So, in general, cancer occurs when cells stop behaving as they are supposed to.
Your body is made by something like 200 different kinds of cells (epithelial cells, neuronal cells, blood cells and so on) working together to maintain the body's functions. If many of those cells stop doing what they are supposed to do then your body will start malfunctioning. Different kinds of malfunctioning will occur depending on what kind and on how many cancer cells will spread throughout your body. This can eventually cause system failures.
If your lung cells are malfunctioning, for example, you may expect respiration problems.
Often cancerous cells spread all around your body (metastasis) and several tissues and organs will be compromised simultaneously leading to a complex pattern of symptoms.
Fatigue, pain, inflammations, and bleeding are common symptoms in many advanced stages of cancer since tissues and organs start to get seriously damaged.

Thanks for the answer--this explains what I was wondering about. Is it possible for a cancer to interfere relatively small amounts of interference with the function of healthy tissues? For example, with lung cancer, if the other lung would continue to function, or what remains of the healthy tissue of the cancerous lung. In these cases, would it be metastasis that leads to inhibition of vital healthy tissues around the body? Thank you again

Yes, small cancers can pass by unnoticed for a long time, they do not affect the overall function of the tissue or organ. It depends on how spread the cancer is. Indeed, in many cases, people start feeling sick after the cancer is already spread and so the doctors diagnose it when is unfortunately too late to remove it with a simple surgical operation. The problem is that sooner or later cancer will spread, so to eliminate the source of cancerous cells asap is important.

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What tests can be performed to test the purity and quality of the raw peptide HCG (Human Chorionic Gonadotropin)
What tests could be run to test the purity and type of HCG?
We are looking to purchase HCG from China but the purity and quality varies between labs, we are able to receive samples of the raw peptide and can use a contracted lab to perform tests but due to my academic background I have no clue which tests to request to determine the purity and type of the raw powder. The following is what we should be receiving from the labs in China.
Product Description
CAS Number: 9002-61-3
pI = 2.951
Extinction Coefficient: EmM = 3.88 (278nm)2
Synonym: Choriogonin, hCG
The molecular weight is approximately 37.9 kDa (with
approximately 31% carbohydrate by weight). The
theoretical molecular weight is 37.9 kDa based on the
native form, which contains 2 subunits. The α subunit
has a molecular weight of 14.9 kDa of which
approximately 10.2 kDa is for the polypeptide and
approximately 4.7 kDa for the carbohydrate. The
β subunit has a molecular weight of 23 kDa of which
approximately 16.0 kDa is for the polypeptide and
approximately 7.0 kDa is for the carbohydrate.3,
To answer Mad Scientists Question, the peptide is "supposed" to be CGA (1081) for use on humans. This is why it is so important for us to find a test that can define the qualities of the raw peptide.

What exactly do you want to do with it afterwards? The level of purity and the kind of contamination that would be acceptable is very different if you do some in vitro experiments or if you do in vivo experiments in animals, not to speak of giving it to humans.

A quick way could be a size analysis via a gel permeation chromatography, if you have access to this equipment.

A monograph from a pharmacopeia gives a good starting point for active pharmaceutical ingredient characterization. AFAIK there is no monograph for hCG nor your actual peptide of interest, but there is one for FSH (here for the european pharmacopeia monograph), which shares a subunit with CGA, meaning that modifications of it could suffice (though validating these modification will be a good amount of work, and will depend on the ultimate use for the peptide).
First, it is necessary to stress that even if the compound passes all assays, it would still be unsuitable for human use. It may be acceptable for animal experimentation. This is because the pharmacopoeia assumes a context where you have a non-adversarial relationship with your supplier, such that statement like "up to XX% remaining impurities" is an acceptable standard as the synthesis route & typical impurities are known. However, buying peptides from a random Chinese seller with no transparency on process is likely an adversarial situation.
Some keys to read the monograph:

Compound followed by the letter R ("water R", "glycine R"): these compounds have their own monograph. You could assay them accordingly, but for this use case understanding the R as "analytical grade" is possibly good enough.
"Follitropin CRS": chemical reference substance, a reference standard powder of follitropin obtained through reliable means (typically through EDQM for pharmaceutical purpose). Here also, substituting for an analytical grade standard from a reputable chemical seller could work.
Method followed with three numbers ("Bacterial endotoxins (2.6.14)"): reference a method monograph found in the given chapter/section. Apply methodology as described in the referenced text.

To adapt the assays to your peptide of interest, you need to understand which parts are specific to follitropin (and should be modified), and which applied to gonadotrophin-like peptides in general. For instance, for isoelectric focusing, the running conditions (pH, catholyte/anolyte) will be adequate, but the follitropin reference will be replaced with a CGA reference. On the contrary, the selective cleavage of peptide bonds assays is specific to the peptide, and will need extensive rework.

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Why don't plants get sunburned?
I just saw a video about the biology between sunburn, UVA and UVB and the different things we know about sunburn in humans. ( http://www.youtube.com/watch?v=ZSJITdsTze0 )
I wonder what keeps plants from getting sunburned?
By sunburned I meant that ultraviolet light injures the plant so that it requires some sort of healing process for the plant to be as healthy/strong/resistant to disease as a plant that isn't harmed.

First define what "sunburn" means with respect to plants.

It is seen that cyclic electron flow helps plants growing in high intensity of light.

they kind of do get sunburned. if they dehydrate their leaves become brown and shriveled.  it doesn't resemble animal sunburns.  when they are green they do have a lot of pigment that is the original sunscreen... it absorbs much of the light.

The following study shows evidence that UVB does damage plant DNA.

Rousseaux et al. Ozone depletion and UVB radiation: Impact on plant DNA damage in southern South America. Proc Natl Acad Sci U S A. 1999 December 21; 96(26): 15310–15315.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC24816/

Plants have more leaf surface area which is exposed to Sun and plants do need sunlight for Photosynthesis to produce food and oxygen. But how plants avoid getting sunburned ? (Sunburn for plants might mean like leaf getting dry or premature falling off etc). To explain this first we need to know the leaf structure and its mechanism to absorb light and heat.
Leaf structure:

(Image courtesy Complete Biology)
The major functionality of Waxy Cuticle on upper surface is(Leaf Terminology):

Insulation - Acts as an insulator preventing more heat absorption by the leaf surface. The lower surface of the leaf has 'Stomata' with 'Guard cell' which keeps the leaf temperature moderate by preventing maximum water evaporation. The plants have well adapted to various environment conditions by having various compositions in its waxy cuticle. This has prevented plants from losing water and getting leaf dry.
Light reflection - Surface of plant leaves also has hairy structures which will reflect the light and thus reducing the leaf surface from maximum light fall.
As we know the diffusion and osmosis process in plants to balance the water content in the cell across its body, we can say that depending on environment and temperature plants have mechanism to deliver water to leaves.

To summarize plants have developeb mechanism to prevent heating up of leaf surface which will dry it out. Hence they have evolved and adapted themselves to various environment to avoid getting sunburned. Similar question was answered here Why do plants do not burn
On the other side if there is any change in the environmental condition due to global warming or Ozone hole effect then dangerous rays from the Sun could damage the leaves.


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How efficient is the sodium-potassium pump ?
I am reading about transportation of ions in a cell. It is necessary to transport sodium back out and potassium back in, against their electrochemical gradient. This task is carried out by sodium-potassium pump, which transports three sodium ions out across the cell membrane for every two potassium ions carried inward. The source of energy for this transport process was hydrolysis of ATP.
My question is the order of the efficiency of a sodium-potassium pump.

The efficiency of a pump is equal to the work done by that pump divided by the energy that an ATP gave to pump and transform to ADP.

I couldn’t find a value for this but I have calculated an efficiency of 84 %.
Caution: this seems too high to me, so I show below my calculation, fully dissected, in case anyone can spot an error.
First of all the parameters. Ion concentrations are:
internal Na+  = 12 mM;
external Na+ = 140 mM;
internal K+   = 140 mM;
external K+   = 5 mM;
and membrane potential = -60 mV (negative inside the cell)
I use these values for constants:
gas constant R = 2 cal mol-1 K-1
Faraday constant F= 23,062 cal mol-1 V-1
and I’ll assume that the temperature, T, is 37℃ = 310 K
The Na+/K+ pump uses 1 molecule of ATP to move 3 Na+ out of the cell and 2 K+ into the cell.
The efficiency of the pump is therefore energy required to move these ions/energy released by ATP hydrolysis.
How much energy is needed to move the ions? In each case there is a contribution from the fact that the ions are moved along a concentration gradient (the chemical component) and from the movement along a gradient of electrical potential (because of the membrane potential). In considering these components we have to think about whether energy needs to be used when the ions move, or whether it is released.
For the chemical component we can use
ΔG = RTln(ratio of concentration, inside and outside), where ln = natural logarithm
The sign of this ΔG will depend upon how the ratio is expressed (in/out or out/in) but the absolute value will be the same. So I calculate an absolute value and then deduce the sign of the free energy change.
For Na+ ΔG = modulus(2 x 310 x ln(12/140)) = 1,523 cal mol-1
Since Na+ is being moved up a concentration gradient, work must be done so the free energy change is positive.
Applying the same formula and logic for the movement of K+:
ΔG = 2,065 cal mol-1.
(This value is greater than that for Na+ because the concentration gradient is steeper.)
Next I calculate the electrical components using:
ΔG = zFμ, where z is the charge on the ion = 1 in both cases, and μ is the membrane potential (in volts).
So for both Na+ and K+ the absolute ΔG value is 1,383 cal mol-1.
However, in this case Na+ is moving out, against the membrane potential while K+  is moving in with the membrane potential. Thus the value of ΔG is positive for Na+ but negative for K+.
Now I combine the chemical and electrical components to get the net free energy change per mole of ions moved:
Na+ ΔG = 1,523 + 1,383 = 2,906 cal mol-1
K+ ΔG = 2,065 -1,383 = 682 cal mol-1
Now I consider how to combine these two values. Each cycle of the pump uses 1 ATP to move 3 Na+ and 2 K+. Therefore each mole of ATP moves 3 moles of Na+ and 2 moles of K+.
Energy from 1 mole ATP that is used to move ions = (3 x 2,906) + (2 x 682)
= 10,082 cal
= 10.1 kcal
How much energy is released from hydrolysis of 1 mol of ATP? Estimates vary but a commonly accepted value seems to be 12 kcal mol-1
Thus efficiency of the pump = 100*(10.1/12) = 84%.
I think the free energy of ATP hydrolysis depends on ATP concentration, pH, and the amount of Mg present. For a well-fed brain, this is around 14 kcal/mol (see Journal Of Physical Chemistry B, 114 (49), (2010). 16137-16146). This gives an efficiency of around 70%, still too high but better...


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How does the immune system "learn" from a vaccine?
According to Wikipedia:

A vaccine typically contains an agent that resembles a disease-causing
  microorganism, and is often made from weakened or killed forms of the
  microbe, its toxins or one of its surface proteins. The agent
  stimulates the body's immune system to recognize the agent as foreign,
  destroy it, and "remember" it, so that the immune system can more
  easily recognize and destroy any of these microorganisms that it later
  encounters.

Question:  How does the immune system ""remember"" a foreign agent introduced via a vaccine?  And how does it learn how to deal with subsequent encounters?

Thanks for the excellent answers!  (There seems to be a lot I still need to learn)

Vaccines work by introducing an attenuated strain of the pathogen (or alternatively the antigens that are normally present on the pathogens surface) into the body, whereupon the body mounts an immune response.  As this will (hopefully) be the first time that the body has encountered the antigens on the pseudo-pathogen's surface, the response is called the primary response.
This consists of two main divisions: the cell mediated pathway and the humoral pathway.  In vaccination it is the humoral pathway that is important.  This is where a division of white blood cells (B-Cells) produce antibodies that are complementary to the antigens on the pathogen surface, causing a negative effect to the pathogen (death, inability to reproduce, de-activation of toxins, etc.).  However as each B-Cell produces a different antibody, there needs to be a mechanism to select the correct one:

Antigen Presentation (technically part of the cell-mediated-response) - a phagocyte engulfs the pathogen and displays the pathogenic antigens on its own surface.
Clonal Selection - B-Cells that are attracted to the invasion site attempt to bind their antibodies onto the pathogen's antigens.  It takes time for this to occur successfully as you are essentially waiting for the correct mutation to happen.
Clonal Expansion - Once a complementary antibody producing B-Cell has been found it is then activated with the help of a T-Helper cell.  This causes it to divide rapidly whereupon these cloned specific B cells can secrete their antibodies which will cause detriment to the pathogen.

It's at this point that I can start to answer your specific question.  The large clone of B cells will then sub-divide into two types.  Plasma Cells remain in the blood and produce antibodies to fight the infection.  The other type, much smaller in proportion, are called Memory Cells.  These cells have a very long lifetime and move to lymph nodes across the body (including the spleen), where they remain dormant until the same pathogen is found again.
When this is the case, the memory cells are activated by T-helpers so that they can divide into massive numbers of plasma cells to fight the infection the second time.  This secondary response is a much faster as the clonal selection stage does not have to wait for the right mutation - they are already waiting in the lymph nodes.  The response is also much stronger as each memory cell can produce large numbers of plasma cells - i.e. you can start with multiple activated B-cells (as many as you have memory cells) rather than just the one that has mutated into a complementary shape in the primary immune response.
The aim of the vaccine is for the secondary response to be so quick that potentially life threatening symptoms do not occur; the body has time to find and store the correct antigen in a safe environment as the pathogen has been deactivated.

I think there is some misinformation here. As far as I am aware, the point of memory B cells is that they are able to activate without T helper contact, solely based on pathogen contact. Surely if they required T helper contact, the memory response would barely be faster than the initial one.

MBQ and Rory M have already given decent answers on the "hows" of how the vaccine memory is formed. Now, for some twists:
There are three (general) types of vaccine, all of which are meant to make your body "think" its being infected and provoke an immune response, while at the same time not causing active infection. They are:

Live attenuated. These vaccines are made up of living pathogens that have, through a variety of methods, been rendered essentially harmless. Never the less, they are infecting you. It's a bit like getting into a shootout with people carrying Nerf guns. Good news is, the bullets are foam, but they're still shooting you. The advantages to these vaccines are that, generally speaking, they were easier to make, and because you are infected, you can shed the pathogen back into the environment, spreading the vaccine around a bit. The disadvantage? Sometimes the pathogens de-attenuate, and cause disease.
Killed. Dead pathogen - your body responds to the presence of foreign antigens, develops an immune memory, and that's that. You gain safety, but lose the secondary spread of vaccinating attenuated pathogens.
Virus-Like Particles. This is the sexy new class of vaccines, that is both dead and...not real. Synthetically produced, these vaccines (like the HPV vaccine) are both harmless and provoke an immune response, and can be customized - they can have antigens to different strains, etc. that you can't do just with attenuating or killing pathogens in the wild. They're awesome, and brilliant, and expensive as hell to develop and produce.

Once your body "learns" from the vaccine, how well it retains that memory also may vary. Some vaccines provoke a strong immune response, and the pathogen they target is genetically stable enough that you're pretty much set for life. Others, like the chicken pox vaccine, wane over time as your body isn't challenged by new exposures to the pathogen, and needs to be "reupped" now and again by giving you another dose of the vaccine, known as a booster. For some vaccines where your vaccine-triggered immunity may wane over time, we might not bother with a booster because you're now old enough that you're out of danger. The HPV vaccine comes to mind again - we're not sure you're immune for life, but if we can make sure you're immune until say, 65 or 70, it doesn't really matter, because it will take years for cervical cancer from an HPV infection to develop anyway.
Still others target diseases that mutate rapidly enough that your body's memory doesn't last long. The yearly flu vaccine is an example of this. A year after you get your vaccine, you body may "remember" the previous year's strain well enough to fight it off, but that's not the strain of influenza going around that year. This is also a problem for the hypothetical development of an HIV vaccine.

I've never heard of "spreading" a vaccine by shedding live attenuated pathogens into the environment (although the explanation makes sense). Can anyone give more information about how often this occurs and how effective it is?

@adamj537 Best example is live polio vaccines

If you want a shorter version, but with some key terminology in there, here you go:
When the body is exposed to an antigen (a substance that stimulates an immune response), antigen-presenting cells (e.g. macrophages) engulf them and present them on the surface of their cell membrane. Then, T cells bind to it and in short, they eventually get activated. Then activated T cells activate B cells, which then divide by mitosis to form a clone with plasma cells and memory cells. Remember, these plasma cells are specific to that antigen. The memory cells are the one that causes a quicker secondary immune response as it recognises the antigen when the body is exposed to it again and causes a greater number and faster production of antibodies.


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How To Avoid Macro-Evolution Confusion?
I regularly encounter students who believe humans came from amoebas and when asked why they often say Macro-Evolution has been scientifically proven.
Macro-evolution is defined as evolution at or above the species level, which leads to the problem: Scientific evidence does exist for speciation at the Biological Species Concept (BSC) level, but not for all species concepts and only if a helpful definition is employed. Lions and tigers are considered different species and have been know to reproduce--sometimes with fertile offspring. Therefore, what benefits are there to such a broad category as macro-evolution?
The distinction between lions and tigers is so much smaller than feathered vs. scaled creatures! Surely the current definition of macro-evolution is overly broad and confusing to newcomers. Only the fuzzy edge of the macro-evolution definition has been proven. Proving that 1 inch of a yardstick exists does not prove that the rest does. There is a distinct lack of rigor to the statement that "macro-evolution has been scientifically proven."
Surely the definition of macro-evolution could be chopped in half with the goal of distinguishing between relatively trivial changes (Lion vs. Tiger, but beyond micro-evolution) and relatively non-trivial distinctions (either at and above the genus or the family level). The "trivial" changes could be termed "Middle Evolution" and work something like this:
1.) Middle evolution: evolution at or above the species level, but below the family level.
2.) Macro evolution: evolution at or above the family level.
Substitute the word genus for family in the above definitions if that seems better. I admit that line would be somewhat arbitrary, but would not the term "Middle Evolution" be informative?

Two observations: 1. Species speciate. Genera don't generate. 2. Any taxonomic distinction above the level of species is meaningless.

Macro-evolution is a nonsense terms as far as biologists are concerned.  All it really means is evolution over a long time-period.  All the macro/micro/middle is dishonest manufactuvorsey foisted off by liars and deluded individuals.

Would not a better term be Mesoevolution?

This is really more of a discussion than a question and not a good fit for this site.

The only place that the terms "macro-evolution" or "micro-evolution" are generally used, are in creationist rhetoric. They are not terms used by biologists. This is because there is no need to create distinct categories. In reality there is only "microevolution". Macro-evolution is not a different thing, merely an accumulation of many micro-evolutions.

what benefits are there to such a broad category as macro-evolution?

None. Which is why such a term has been abandoned.

“They are not terms used by biologists” – that’s not true. They do have a biological meaning … which is of course distinct (but sufficiently similar to cause confusion) from what creationists mean, and has been around long before they started using the term. I try not to use the terms myself due to the confusion that has been engineered by creationists but some biologists do use them.

@KonradRudolph I know they have meaning, but that doesn't mean they're used still. Our advancing understanding of evolution has made them irrelevant.

No, they still have meaning and are still used by evolutionary biologists. They have been made irrelevant only insofar as there are other terms that can be used instead, but not because “macroevolution” is an inadequate term (it isn’t, it’s a well-defined, actively studied concept), rather in order to avoid confusion because it’s being misused.

There were 1920 scientific works in Google Scholar with the keyword or title "macroevolution" in 2018. https://scholar.google.com/scholar?q=macroevolution&hl=en&as_sdt=0%2C14&as_ylo=2018&as_yhi=2018


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Why does the exercise level impact the nail growth rate?
I read on https://en.wikipedia.org/w/index.php?title=Nail_(anatomy)&oldid=863800434#Growth:

Actual growth rate is dependent upon age, sex, season, exercise level, diet, and hereditary factors.

Why does the exercise level impact the nail growth rate?

Had you looked up the reference that wikipedia cites?

@BPinto i tried but it's behind paywall.

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


text:
Does constant pressure cause muscle atrophy, and if so, why?
I read on https://en.wikipedia.org/w/index.php?title=Gluteal_muscles&oldid=876760828#Clinical_significance:

Sitting for long periods can lead to the gluteal muscles atrophying through constant pressure and disuse.

However, the statement isn't supported by any reference. Does constant pressure cause muscle atrophy, and if so, why?

I tried to find some references stating that constant pressure causes muscle atrophy, but I haven't found any so far. The following information sources don't list constant pressure as a cause of on muscle atrophy:

https://en.wikipedia.org/w/index.php?title=Muscle_atrophy&oldid=884590568
https://vet.uga.edu/ivcvm/courses/VPAT5200/02_injury/atrophy/atrophy01b.htm  (mirror)

I think it's likely you found a scientifically unfounded and (if we want to be very pendantic) inaccurate sentence on Wikipedia. It's unsourced, and colloquially stated. Disuse causes atrophy, and pressure is simply something that doesn't help. Pressure probably does not lead to atrophy; hearts don't atrophy simply due to being exposed to ever-present pressure from circulating blood. The pressure might even slow down atrophy in such cases. One could make a case for sitting restricting blood flow to the muscle, which could be a mild contributor in the long run.

@S Pr: But bedsores are caused by constant pressure on areas of the body, including people in wheelchairs: https://www.hopkinsmedicine.org/health/conditions-and-diseases/bedsores  Though I doubt that normal sitting would be sufficient.


text:
What causes tenocytes to migrate from intact regions of tendon into the wound site, and how do they move?
The 2018 study {1} mentions that:

The healing process
  of injured tendons includes tenocyte migration which occurs
  from intact regions of tendon into the wound site.

What causes tenocytes to migrate from intact regions of tendon into the wound site, and how do they move?

References:

{1} Dursun, Gözde, Mersedeh Tohidnezhad, Bernd Markert, and Marcus Stoffel. "Effects of uniaxial stretching on tenocyte migration behaviour." Current Directions in Biomedical Engineering 4, no. 1 (2018): 313-317. https://doi.org/10.1515/cdbme-2018-0076


text:
Which hardware specification should one be looking for to optimize the visualization of a tendinopathy through ultrasound?
The 2019 study {1} reports that hip abductor tendon pathology is better visualized by 3.0 Tesla MRIs than by 1.5 Tesla MRIs.
The 2014 study {2} also mentions the usefulness of high teslas for tendon analysis:

MRI of tendons and ligaments benefits from high spatial resolution. Stronger magnetic fields lead to higher signal-to-noise ratios and improvements in image resolution; for this reason, 3-T MRI may be more sensitive than 1.5 T for detection of partial thickness tears [26]. Alternatively, higher resolution may be achieved by using a local surface coil [27]. Imaging with shorter echo times improves sensitivity to tendon changes, although this may come at the expense of specificity [28,29]. T2 weighted images are helpful for identifying fluid signal in tendon or ligament tears (Figure 5) as well as for demonstrating changes in the surrounding tissues [30]. If the orientation of a tendon changes over its course, magic angle effects may be problematic; it may therefore be helpful to acquire images with a sufficiently long echo time to avoid these artefacts.

Which hardware specification should one be looking for to optimize the visualization of a tendinopathy through ultrasound?

References:

{1} Oehler, Nicola, Julia Kristin Ruby, André Strahl, Rainer Maas, Wolfgang Ruether, and Andreas Niemeier. "Hip abductor tendon pathology visualized by 1.5 versus 3. 0 Tesla MRIs." Archives of Orthopaedic and Trauma Surgery (2019): 1-9. https://www.ncbi.nlm.nih.gov/pubmed/31243547; https://doi.org/10.1007/s00402-019-03228-1
{2} Hodgson, R. J., P. J. O'Connor, and A. J. Grainger. "Tendon and ligament imaging." The British journal of radiology (2014).
Harvard ; https://scholar.google.com/scholar?cluster=16366672343955449638&hl=en&as_sdt=0,22 ;
http://www.birpublications.org/doi/full/10.1259/bjr/34786470

Why do you give background on MRI while asking a question about ultrasound?

@BryanKrause to give an example of an important hardware specification for another imaging device also commonly used to non-invasively visualize tendons.


text:
Keyword based literature search
I understand this is not a biological question but this is often a problem whenever I look for literature.
How to look for a reference for some fact based on keywords. For instance you know about a fact such as - Cell signaling responses are faster but short lived compared to transcriptional responses. How to find the literature which actually says this. I often end up getting irrelevant results.
In other words, how to represent a fact using appropriate keywords. Is there an algorithm which can generate synonymous statements [like MeSH terms in pubmed] and search for those.
Or is there any way of setting up a hierarchical search.
PS: If someone finds a reference for "Cell signaling responses are faster but short lived compared to transcriptional responses" then please let me know

You may want to have a look at Gene Ontology and at GOPubmed

GO is about functional annotation of genes. That's not what I am looking for. GOPubmed is cool. I need to see if it has the function of search levels

I would either cite an advanced molecular biology or developmental biology textbook or if you must cite a paper, find the relevant chapter in the textbook and look at its references.

I think the statement above is slightly misleading. There are many many types of cell signalling, anything from RTK (at the cell surface or when its endocytosed), to steroid receptors, which operate on different time scales and produce different results depending on the type of signalling. Also it depends on what you are measuring/defining as a signal/response in lets say "cell signalling" because you could define cell signalling response as protein phosphorylation at any point in a signalling cascade or it could be the transcriptional activation itself (consider the MAPK pathway in Drosophila, at which point do you consider a response is produced? when Raf is activated? or when transcription factors such as pointed bind to their ETS binding site and start to transcribe as measured by luciferase? as you can tell the time difference between the two is quite large, well as far as I know after RTK activation in Drosophila it takes ERK 20 minutes just to translocate to the nucleus). A cell signalling response could also constitute changes in the rate of cell migration, cell shape etc, which can either be slow or fast depending on the signal in question. so I think the above question needs major rethinking and redefining.
Now getting back to your questions about key search terms, in my experience, over time you just end up developing a knack for what you consider to be key words after you carefully define the question and think bout its different aspects. A rule of thumb that I use is typing at name of proteins (e.g. JNK or RAS etc) or processes (transcription, phosphorylation etc) and use a word like rate, time-scale, half-life, turn-over or something like that if its measuring changes in time you are interested in. Just play around with words.
Also as a general advice you don't have to reference every snippet of every fact like "water is liquid at RT in standard atmospheric pressure" etc. References are meant to be there to acknowledge the work of others like "how DNA was discovered" so that people can't just lift paragraphs or pages out os someones research without acknowledging them and passing it as their own work.
Hope this helps.

Thanks Bez. What I meant by fast and slow is the response time. Protein phosphorylations are much faster than transcriptional activation. Which I know for sure. Just wanted a review sort of thing which summarizes the response times of different processes in a cell.


text:
How are collagen fibers in skin aligned with respect to skin surface?
I read in one paper that collagen fibers in dermis are randomly oriented in direction with respect to the skin surface. I can't locate that paper now. However, I came across this paper that indicates that collagen is always aligned parallel to the skin surface (page 3). Which one is correct?

Does epidermis have collagen?

Oops, sorry i meant dermis. Edited.

Collagen underneath the epidermis is not completely randomly oriented, in fact mostly they are directed along the muscle fibres beneath them.
This was first observed by Karl Langer and hence was given the name as langer's lines( of skin tension). This peculiar arrangement of collagen is responsible for maintaining integrity of skin at times of stretching force developed on them by the muscles. Had they perpendicular, then skin would tear easily.
This also has clinical relevance because during surgery if an incision is made along these lines the scar would be minimum.

Source: https://en.m.wikipedia.org/wiki/Langer%27s_lines

Great answer! Does this vary with age?

I don't think so


text:
What is the mechanism of labeling a DNA molecule with deuterated water?
I have seen a paper in which deuterated water was used to follow dividing cells. The assumption was that deuterated water will be incorporated into newly synthesized DNA molecules. Is there any direct incorporation of water in the replication process? Is there any proton exchange?
The paper describing the method can be found here:
http://www.pnas.org/content/105/16/6115.full.pdf

Please add a reference for the method. I imagine that deuterium could be incorporated at several points in the pathway for de novo synthesis of dNTPs, either into the bases or the deooxyribose.

proton exchange always happens (i dont have anexact reference right now but i have read about it in spectroscopy texts) .. and hydrogen incorporation is also there as @AlanBoyd said..

@WYSIWYG Exchanging protons wouldn't be useful to follow cell division as they exchange all the time. The deuterium would be incorporated into both new and old DNA, and would also be gone if you remove the D2O again.

Thank you all for the comments and answers. Just added the reference. The de novo synthesis pathway of dNTPs sounds like a reasonable place to start looking. Thanks, Alan.

I would assume that the labeling occurs in the reduction of NTPs to form dNTPS.
This process (catalyzed by ribonucleotide reductase) involves protonating the hydroxyl group on the 2' carbon, allowing it to leave as water, and then adding a hydride to the newly formed carbocation. The two hydrogen atoms (the proton and the hydride) come from two thiols on the enzyme, which in the process are oxidized to form a disulfide bond.
The crux is that, in the presence of heavy water, the two thiols would rapidly exchange their hydrogen for deuterium. That means that the hydride that gets added to the carbocation would be a deuterium, and the resulting dNTP would be deuterium labeled.
This is the only step that I can imagine the labeling working for, as a carbon-hydrogen bond is formed (which doesn't exchange rapidly with the solvent) using the hydrogen from a sulfer-hydrogen bond (which does exchange rapidly with the solvent).


text:
Does Sympaticus and lymphatic circulation cause feeling of thirsty after short shower?
I have been reading blogs, Guyton and Pocock about what triggers the feeling of thirsty.
I am not convinced that is the fact of

warm water
time is short so not much water lost

Assume that the water's temperature is the same as body's temperature.
Of course, there is little temperature change caused by air and water, but I think it is not that much.
I think more important is the steady, continous irritation of skin as a mechanism.
I wrote my suggestion for the answer below.
Do sympaticus and stimulation of lymphatic circulation cause feeling of thirsty?

I think the mechanism is the stimulation of the skin systemically i.e. the most important endocrine organ which we have.
The irritation of skin in the shower is

mechanical turbulent stream of water in acceleration

1) hitting (start) your skin from different directions (many flows) in many different flows
it's you who causes the systemic stimulation effect!
water steam in acceleration all the time; moving its direction; in ellipsoidal tracts
water stream flowing slowly on your skin towards periphery mostly
causing smooth but continuos irritation of your skin

activation of smooth muscles in synchronous order which boost lymphatic circulation

mechanical turbulent stream of air (temperature change of skin)

this one is not in accelerative move, since there is no forces which keep the subsequent air and skin together
very little impact, unless extreme situation (etc in Alaska)

I would think that the increased lymphatic circulation irritates the walls of lymphatic circulation which causes an increase in the need of water there.
So water would diffuse from vascular space inside blood vessels (extravascular space) into the lymphatic system.
The decrease in blood pressure through baroreflexive arch and hypothalamus (some nuclei too) would then be sensed as the feeling of thirsty.
Water in shower on the skin accelerates, since it changes its direction all the time from the beginning of the stream until the end.
I think it is the steady change of irritation's location in ellipsoidal tracts that stimulates hypothalamus.
I think it is not the strength of the stream but the changing direction that is cause of the irritation.
Of course, there is little changes in the strength of the total stream.
I think this is not so significant than the change of the direction of the water flow causing the irritation.
In short, I say that accelerative water streams massage lymphatic system in ellipsoidal tracts.


text:
Which processes are included in the process called cells eating themselves?
I am reading about atrophy and I am thinking to which processes the phrase cells eating themselves refer to.

Cells need something to survive these difficult times. To decrease
  protein synthesis to survive. If insufficient, cells start
  to eat themselves. Then, ubiquitine-proteosome pathway and autophagy
  pathway.

I am not sure if it is only apoptosis.
It can refer here to longer cascade.
I think it can at least refer to autophagy where one cell degrades its components.
Which processes does the phrase cells eating themselves include?

The processes are mentioned in the quote you provided: "ubiquitine-proteosome pathway and autophagy pathway". As far as I know, apoptosis per se is not utilized for recycling.

Please, make that an answer, since it answers the question.

So:
the processes are mentioned in the quote you provided: "ubiquitine-proteasome pathway (note: it's proteAsome) and autophagy pathway". As far as I know, apoptosis per se is not utilized for recycling.


text:
What's the explanation for those shivers/shudders that happen at random times?
They happen at any time, presenting as a sudden urge to shiver/shudder all at once. It originates in the neck and shoulders, feels like instant gooosebumps then out of total reflex shoulders roll back and neck cringes. Happens every couple of months and comes out of nowhere, then gone without a trace.
I have read about myoclonic jerks but this doesn't sound the same.
Where do these impulses come from and what's the physiological explanation?

You should remove all personal references (and the line about ghosts). Everyone experiences these random shivers so you can edit your question to make it general. Also, we would highly appreciate if you can add some of your own research on this question.

Nice question, I'm curious too. Lets see what answer do you get. ;)

It is just like a muscle spasm but generated from your nervous system. If the problem persist you are lacking in a certain vitamin that your body needs to function correctly.


text:
What can be the reason for yellow and dark marks on leaves?
The plant in our office started to have this strange marks, what can be the reason for that kind of marks? how can we cure the lovely plant?

Yellow leaf spots have various shapes, depending on the cause. Downy mildew starts with angular pale yellow spots. In cucumbers (Cucumis sativus) and other cucurbits, powdery mildew causes pale yellow spots followed by powdery white patches.
The location of the yellow spots may help you determine the cause of the symptom. Some diseases, such as powdery mildew, cause spots on older leaves first and then spread to younger leaves. Yellow spots from powdery mildew can occur on upper and lower leaf surfaces. Downy mildew spots occur on the upper sides of leaves between leaf veins that give the spots their angular shape.
Now lets jump into the causes :-

1 -Moisture Stress

Over-watering or under-watering are the most common culprits when a plant's leaves turn yellow.
If plants don't receive enough water, they drop leaves to prevent transpiration (essentially, a plant's way of sweating) and conserve water. Before they drop, though, the leaves will typically turn yellow.
Too much water can be just as damaging to leaves. When the soil doesn't drain well, an overdose of water leaves the soil waterlogged and root systems can literally drown. Without oxygen, roots start to die.

2-Normal Aging

As many plants age, the lower leaves will turn yellow and drop off.
However, to solve this case, don't worry. If the plant becomes too leggy, consider trimming back the main stem to promote new growth and bushiness.

3-Cold Draft

Now let's first understand what a cold draft is. A cold draft is a current of cold air being drawn indoors.
A plant sitting near it is giving off more heat than it receives from the room. Remember, heat travels from places of higher temperature to places of lower temperature.Cold drafts on tropical plants will often cause the leaves to turn yellow and drop.
To solve this problem, particularly If your plant is near an air-conditioner vent in summer or a drafty window in winter, move it to a less turbulent place.It's also a good idea to mist tropicals that you're overwintering to increase the humidity.

4- Lack of Light

A plant that is yellowing from a lack of light will typically yellow on the side that is away from the light source.
To solve this, move the plant to a sunnier location and see how it does. If window light is tough to come by in your home—especially in winter—you might need to rig up an artificial plant light or two.

5- Nutrient Deficiency

This can be caused by too much calcium in the water if you're using hard water, or by a nitrogen deficiency.If this is the problem, the plant's top leaves may be the first to go yellow.
However to solve this issue, since it is species specific, its important to diagnose the problem firstly and them take some remedies.

6-Viral Infection

If your plant has a viral infection, it might show up as blotchy, spreading yellow patches on leaves throughout the plant. This may be accompanied by deformed leaves and stems, as well as discolored flowers.
To solve this , discard any plants that you suspect are infected since viral infections can not be treated.

7- Fungal infection

If caused by a fungus, there is nearly always fungus growth of some type in the spot, particularly in damp weather. This fungus growth may be tiny pimple-like structures, often black in color, or a moldy growth of spores.
To solve this, you can use sulphur(in dust form) and milk.
Sources - https://www.thespruce.com/reasons-for-yellow-leaves-on-houseplants-4150680
https://www.hunker.com/12140067/how-to-diagnose-cause-of-yellow-spots-on-leaves
www.uky.edu/Ag/PAT/cat1/leafdis.htm

Its Chlorosis, degradation of Chlorophyll.
gradually it will lead to necrosis.
it might be due to lack of nutrients, especially manganese, zinc or iron.
it might also be due to poor drainage or root damage.
provide more space for the roots to grow. Treat soil by providing nutrients.
your problem should solve.


text:
Identify this caterpillar

Could anyone try to help identify this caterpillar, there are loads of them all over my garden and I've got three of them in a makeshift caterpillar house. I've had them for about a week and they've grown to about 3 or 4 centimetres in length and I am yet to see any of them form pupae. I am from London by the way.
EDIT: they don't seem to be too fussy about what they eat, I have found them on honeysuckle, rose bushes and even some nibbling on the bind weed I've pulled recently.

@rg255 thanks, once I am home I will take some closer pictures, I believe there were a lot on my honeysuckle but I will give a full list later.

@rg255 I have added new, closer images and a brief description of the plants I've found them on. Two of the ones I have been looking after have seemed to now be staying close to the dirt level I've put in the tank (possibly going to cocoon under ground or in the floor???).

Actually, the animal is not a caterpillar but larva.
The species is Abia lonicerae Sawfly, discovered by Linnaeus 1758.
(Another picture)

Is the sawfly considered a pest? Should I worried about the massive population of them in my garden?

Thanks for the response, that explains why I couldn't find them anywhere on the Internet by searching for caterpillars!

Are you sure that it's that particular species (if so, what characters are you using?), or could it be a related species (Abia sp.)? +1

@fileunderwater I am, actually... the images are related to specific species from the answer.

How do you distinguish it from other species in Abia?

@user16370 With regards to pest status, the larvae will eat the plants in your garden, potentially causing damage.  The adults are relatively harmless.

Larvae of this species do feed on honeysuckle (Lonicera) foliage


text:
What is basis of multifunctionality of "master glands" in the endocrine system?
I have just started reading about the endocrine system and I am having some difficulty understanding the basis of distribution of glands and associated hormones.
I am using multifuntionality to describe the amount of relatively independent input and output that are shared through a same organ or proximal space. Many of these organs have a heterogenous mixture of endocrine cells sharing the same glandular space.
There appear to be some glands that are considered "master glands" such that they take a variety of relatively independent input, apply some control logic via a diverse set of endocrine cells and tissue and secrete a diverse hormonal output. The pituitary and hypothalamus are the best examples, however the adrenal cortex and the pancreas also fit this definition to a certain extent. Many times the diversity of hormones and cells within an organ have no obvious connection (eg thyroid). Some glands appear more specialized with a relatively straightforward endocrine axis of input and output (eg testes).
Some of this multifunctionality seems unnecessary, in that insulin secretion could occur anywhere and be effective in the manner of an insulin pump, or contain risks due to excessive centralization as in a pituitary tumor or renal artery stenosis, so there must be some advantages I do not understand.
My textbook (Headley, Levine, 6th) seems to minimally cover multiplexing, signal cross-talk and competition between diverse endocrine cells sharing an organ. Its focus on discrete pathways and axes suggests these are evolutionarily unfavorable.
Are there synergistic advantages in shared endocrine infrastructure such as vascularity or metabolic pathways?
Is there some overlying logic that can be used to explain this distribution of glands and hormones regarding multifuntionality-specialization, or is it necessary to view the distribution of vertebrate endocrine system as the outcome of evolutionary contingencies?
Thanks

In this text, Pituitary is referred to as master gland. But in one of the sessions that I participated, referred Thyroid gland and Pancreas as master glands. So I am curious to know the answer here myself. Are you referring to the shape of the particular gland by "Spoke-Like"?

No I mean centralized as in diverse endocrine cells and tissue with diverse inputs and outputs that may be unrelated sharing a same organ or proximal space. The testes appear to me to be strictly male reproductive organs with a relatively straightforward endocrine axis of androgen production of primarily testosterone based on LH input, although a role of FSH in sperm production.

@WYSIWYG "they also affect the development of the physical and metabolic characteristics that are distinct for a sex" : Totally. Specially in terms of females, these glands (ovaries) seems to be even more crucial. Isn't it?

@WYSIWYG I misspoke and meant strictly reproductive and endocrine. I then attempted to describe how that organ has a straightforward endocrine axis. Testosterone has a diverse set of outcomes in cells, however I refer to the number and diversity of testes outputs, which is primarily testosterone. Testosterone injections in castrated chickens maintains a relatively stable phenotype with regard to endocrine status.

@hkjairam Then you should not use the term "centralized" and rather emphasize on multifunctionality (and cellular diversity?). Another point: endocrine glands don't have ducts.

@WYSIWYG. True, fixed the ducts. My connotation of "centralized" conveys the structural proximity of specialized cells with unrelated tasks, better in a more network-centric fashion,  but that is my subjective opinion. I do not understand what you mean by "cellular university".

@hkjairam I had to write "diversity" and I wrote "university". I have no clue how I did that. (PhD effect I guess!!). Regarding centralization: even in a network perspective, the out-degree would denote how many tissues does a gland affect (conversely for in-degree). That will still not convey the actual question which is "In how many different ways does a gland affect the body". I hope I am understanding correctly.

@WYSIWYG I think there are flaws in the word "centrality" as a central node may also have a single input and output but is commonly traversed, but I thought the popular understanding of "central", with the idea of a hub and spokes would accurately convey the gist of my question. I thought "multifunctional" would lead to answer regarding versatility of tissue and not the endocrine pathway architecture.  I am open to changing, but I do not how widely the word choice is leading to misunderstanding.

@hkjairam If you do not mean multifunctional then I am still failing to understand what exactly you are referring to. You tagged this question as anatomy and you are talking about architecture of signalling pathway. Am I missing something here? Are you trying to ask how proximity correlates with shared signalling pathways or in other words, whether a heterogeneous gland has higher number of local signalling paths between component tissues?

You should also add a link to your text book or if it is not openly available then illustrate the topic that it minimally covers. This would give others an idea about what you are really expecting.

If I'm understanding this question correctly you're asking why we have a mix of "master glands" like the hypothalamus that regulates a bunch of different tasks uncoupled by control logic (oxytocin doesn't influence ADH or TSH) and also specialty glands like the ovary, which do "only one thing" (yes there are many inputs and many outputs to lots of different tissues, but they're all coupled). Rolling all the glands together for efficiency would make sense, but distributing them might also make sense. Why a blend? Is that right?

It would seem to me that in the examples that you have listed that proximity to necessary input is the overriding logic behind gland geography. Take the hypothalamus as the first example. This gland receives input from diverse regions of the brain from the amygdala and hippocampus to the retina and brainstem. The brain can tweak levels of various releasing hormones entering the  hypothalamic-hypophyseal portal veins in order to produce a response that is appropriate to the situation perceived by the brain. It makes sense to have all of these co-located because they are all receiving input from the brain. Similarly, it makes sense to have all of cells that are uptaking the releasing hormones close-by to protect these vital peptides from degradation in the systemic circulation. Their collectively unique circumstance makes sharing a specialized vasculature a logical choice.
The pancreas is a good example of the importance of cross-talk within some endocrine tissue. Within the islet, alpha, beta, and delta cells are feeding back on each other to get the balance of insulin and glucagon just right. To whit, glucagon secretion provides a paracrine signal for insulin secretion. This makes sense because the body knows that once glucagon is released the blood sugar will soon rise. Ergo, it makes sense to trigger some insulin secretion as well in preparation. Their co-location makes that possible.
In short, I would say the overriding logic to the placement of each of these glands is their proximity to the necessary inputs and outputs that each of these glands interacts with.

Nice answer but one correction....The pancreas, although in proximity of the duodenum, does not sample fluid from the duodenum that is absorbed. Nutrients absorbed from the duodenum are mostly transported to the hepatic portal circulation and then back into the peripheral venous circulation via the hepatic veins. These nutrients then flow to the arterial circulation and then back to the pancreas. The liver may be a better example of being in a good 'geographic' location for your answer as it 'sees' all portal nutrient flow and can buffer nutrient levels in the peripheral blood.

Thanks for the catch. I vaguely remember learning in a physio class that elevated local levels of glucose in the ecf can stimulate glucose release, but I can't find a source for it other than my notes. Since it can't be sourced I've removed that point. I would add the liver case because it's a good example of the importance of geography, but I can't find a good link to why it's necessary for endocrine function per se.


text:
Hill's function for translational regulation
Transcriptional regulation is generally modeled as a Hill's function (similar to Michaelis-Menten Kinetics):
$$\frac{dm_X}{dt}=\alpha _{m_X}.\frac{R}{K+R} -\beta _{m_X}.m_X$$
Where $m_X$ is the mRNA for some gene-$X$, $R$ is a Regulator $\alpha$ and $\beta$ are formation and degradation rate constants respectively. This equation denotes a saturation kinetics; increasing activator wont cause indefinite increase in transcription. Sounds logical because all promoter sites will be occupied at some point.
In case of a repression the equation looks like:
$$\frac{dm_X}{dt}=\alpha _{m_X}.\frac{K}{K+R} -\beta _{m_X}.m_X$$
I want to model repression of translation using a similar equation. However, the issue is that even though a single mRNA can be saturated by a regulator, increasing mRNA will require more regulators. So effectively the regulator available for a single mRNA molecule will be total regulator ÷ total mRNA.
My question is that whether in such a case the following equation is logical:
$$\frac{dX}{dt}=\alpha _{X}.m_X.\frac{K}{K+R/m_X} -\beta _{X}.X$$
Where $X$ is the protein.
Which means we are taking into consideration the effective concentration of a regulator per mRNA. In other words the Hill's constant $K'$ should scale with mRNA concentration. ($K'=K\times m_X$)
Assumptions:

Well mixed system
System at thermodynamic limit
Amino-acid pool infinite
Ribosomes infinite

I am confused are we talking about regulating translation or transcription? By translation for example there can be competitive inhibition caused by RNA intereference afaik, so it does not depend only the amount of mRNA... And ofc there is a max speed which depends on ribosome count.

Oh no no.. No complications involved. This is just some regulator (mechanism unknown). Ribosomes are plenty (they are not considered variables). I mentioned transcription so that those who have seen that equation for transcription regulation can draw parallels with the equation that I mentioned.

Ohh okay. So ribosome count can be considered infinite in this case, and only mRNA count and the regulator affects the speed of the translation. Am I right? If yes, then please edit your question with these details!

Does X mean the amount of proteins in your equation?

See the edit. "Speed of translation" is not affected; just the rate of protein formation.

Yepp you are right they are different things. :-)

For me it makes sense if we are not talking about ribosome count, and we assume that the regulator instantly finds free mRNAs (and if R regulates the translation in your equation). Now I think these constraints taking us far from reality, but who knows...

It can be assumed that ribosomes are not limiting. If they were then protein synthesis would be globally affected which doesn't generally happen during the usual gene regulation (happens under drastic conditions such as UPR and stress). Regulator may not instantly find mRNA. We can adjust the rate constants accordingly. My doubt was mainly regarding normalizing regulator concentration with total mRNA for the hill's equation

I checked some articles, and almost all of them use f(r), r = (mx, X) to describe regulation and they are talking about regulatory networks. So you'll probably need Fourier transformation and such nice mathematical tools to understand them.

Articles about regulatory models of transcription and translation - http://arxiv.org/ftp/arxiv/papers/1204/1204.5941.pdf - http://arbor.ee.ntu.edu.tw/~brdai/papercollection/Bioinfo/chenmg99.pdf - http://bioinformatics.oxfordjournals.org/content/22/14/e489.full.pdf+html - http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.100.9757&rep=rep1&type=pdf - http://psb.stanford.edu/psb-online/proceedings/psb03/dehoon.pdf - http://www.uv.es/gfl/documentos/TIG.pdf - http://www.ihes.fr/~zinovyev/papers/MorozovaRNA2012.pdf - as far as I understand none of them used your approach by translation...

It looks right to me. I don't have references at hand right now, but iirc even Hill functions in the context of deterministic models assume the ratio of TF concentration to the number of TF binding sites to be large; otherwise, you would have to consider binding ratios even at the level of transcription modeling, similarly as to what you are doing now for translation. E.g. consider a hypothetical situation where 10 TF molecules would compete for binding to 5 different promoter regions, each having 10 binding site repeats. (cont.)

Similarly, in your specific case, introducing the ratio of regulator per each mRNA may not even be necessary if this ratio is large, effectively leading to saturation levels anyway. If this assumption cannot be made, then your reasoning makes sense. One thing you could consider doing is establishing system reactions, then deriving Hill-free ODE equations according to the law of mass action; you could then compare this model to the one you propose. Furthermore, performing a stochastic simulation might make sense (I can recommend tools if desired). Let me know if you need help with any of this.

@w128 Thanks for the answer. I have also been discussing this issue with my PI and he also said that adding scaling in the equation is not necessary if the dynamics are not very different from unscaled one. I would do stochastic simulations later. Thinking of using fortran for implementing Gillespie's algorithm. Can you post this as an answer because this seems logical. You can add some logical/mathematical explanation. I don't need references (I don't think anyone has modeled translational regulation as saturation kinetics). PS: If you do it in 24h you will get the bounty :)

@w128 "Similarly, in your specific case, introducing the ratio of regulator per each mRNA may not even be necessary if this ratio is large, effectively leading to saturation levels anyway".. I agree but unlike promoter sites the mRNA concentration is not static and so the number of mRNA-sites will keep changing with change in mRNA levels. That's why I thought scaling should be important. Otherwise the model would mean that the regulator is just repressing the ribosome allocated to this mRNA.

Your logic looks correct to me. Essentially, what you are doing is uniformly distributing the regulator among the available mRNA.
Note that even when using Hill functions to model transcription, the ratio of transcription factor (TF) concentration to the number of TF binding sites must be large - otherwise, you would have to consider binding ratios even at the level of transcription modeling, similarly to what you are doing now for translation. E.g. consider a hypothetical situation where 10 TF molecules compete for binding to 5 different promoter regions, each having 10 binding site repeats - you need to somehow distribute the available 10 TF molecules among 50 target binding sites. Clearly, this is not something accounted for by the standard Hill equation, which would in such case wrongly assume that 10 TF molecules are regulating each construct.
In your specific case, introducing the ratio of the regulator per each mRNA may not even be necessary if this ratio is large, effectively leading to saturation levels anyway. Note that the maximum level that $m_x$ can reach (at steady state) is equal to $max(m_X) = \frac{\alpha_{mX}}{\beta_{mX}}$. If you can ensure this value to be much smaller than your translational regulator concentration, you will get similar results even if you use simply $\frac{K}{K+R}$ for translation modeling.
If the latter assumption cannot be made, then your reasoning makes sense. For each individual mRNA molecule:
$$\text{X produced per mRNA} = \alpha_{X} .\frac{K}{K+R'}$$
where $R'$ is the amount of mRNA bound to this molecule. If $R$ is the total available regulator concentration and uniform binding affinity is assumed, this means that $R'=\frac{R}{m_X}$. Summing this over a total of $m_X$ mRNA and considering degradation yields exactly your final ODE.
Note that another important assumption you are making is that regulator binding/unbinding to/from mRNA is fast compared to translation, and that no cooperative interactions are present.
If you want to verify things further, you could establish system reactions, then derive Hill-free ODE equations according to the law of mass action. You could then compare this model to the one you propose. Furthermore, performing a stochastic simulation might make sense. If you want to go down this road but don't want to implement Gillespie's algorithm on your own, you can use e.g. SGNSim or COPASI.

Thanks for the answer. This was helpful. I understand that there are many considerations to be made to make the right model. I had to simulate different kinds of regulatory motifs so I wanted to keep the equations simple while at the same time allowing saturation.

authors: Тигран Хачатрян


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How can alcohol cause blindness?
Strong alcoholic beverages (e.g. moonshine) are reported to have caused blindness amongst some people.
How exactly can alcohol make someone go blind?
Is that because different forms of "rubbing" and homemade alcohol: ethanol, methanol, isopropyl and moonshine cause damage to the optic nerve?

Disclaimer: I am interested in what exactly is the biological process of certain alcohols on the optic nerves and what in particular triggers the blindness.

It'd be better if you cite such a report.

Why do you first talk about homemade alcohol (moonshine) and then about rubbing alcohol? Both have no connection. Can you please clarify this?

Methanol is probably the culprit in those cases. As little as 30mL of pure methanol can kill a person. While it's pretty safe to handle as long as you don't drink it, my lab here in Japan won't let me use it outside a hood designated for toxic substances. The reason it's so toxic is because it gets metabolized to formic acid.

@user137 As long as you do not drink it or pour it in large quantities over your skin (it will be taken up to some amount) you are pretty safe. This is the typical overreaction of safe guard measures.

@Chris They won't even let me put 70% ethanol down the drain, it's an organic solvent and must be disposed as such.

@user137 Formaldehyde is the toxic product. Formic acid is not that toxic.

@WYSIWYG I got the information from Wikipedia, " The conversion to formate via ALDH proceeds completely, with no detectable formaldehyde remaining. Formate is toxic because it inhibits mitochondrial cytochrome c oxidase, causing hypoxia at the cellular level, and metabolic acidosis, among a variety of other metabolic disturbances." This suggests that the formaldehyde doesn't stick around long enough to be an issue, and that formate itself is also toxic. Wikipedia could be wrong though.

Methanol is rapidly absorbed not only after oral ingestion but by inhalation or after cutaneous exposure and becomes oxidised in the liver to formaldehyde and to formic acid, metabolites which are more toxic than methanol itself and which inhibit mitochondrial ATP production.
Histopathologically, circumscribed myelin damage behind the lamina cribrosa of the optic nerve has been reported. The electrophysiological changes following acute methanol ingestion suggest that methanol affects photoreceptors, Muller cells, and the retrolaminar portion of the optic nerve.

Source : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1771266/
Several years ago there were numerous cases of blindness and death due to Methanol in Estonia.
If you ask : What exactly happened?
Waste from wood (sawdust, shavings), and other cellulose-containing materials (paper, rags, etc.) can be processed by applying excessive heat and acids, resulting in degraded cellulose into sugar (glucose). Sugar obtained is fermented to get ethanol. However as a side-effect, some methanol is produced as well. This compound is not safe to drink. Basically, someone sold it (illegally) as an ethanol drink (I am not sure if they stole it and tried to monetize it this way.).
There was a (stupid) joke that somewhat popularized knowing about this problem:

(roughly translates to) "Guys, let's drink faster, it is getting dark."

Other impurities in the alcohol could have similar effect, but I can confirm at least the methanol part.

You can perhaps add that the toxicity is because of formaldehyde which is formed by oxidation of methanol in the body.


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Synaptic pruning and selective elimination during adolescence
How does Synaptic pruning occur during pre-adolescence, adolescence and post-adolescence, after there is blooming overproduction of synaptic connections until the years of late childhood, and how does during this stage of brain development, "selective elimination" of synaptic connections occur, which is depended on the activity of synapses which are involved in  primary functions?
Also, why, how and to what extent does the brain, after approximately age 6, receive the urge to cut back certain synapses?
Update 1: what exactly is triggered before and during adolescence, so that the brain receives the urge to perpetrate synaptic pruning? I know how synaptic pruning is carried out, I am however very intrigued in the specific processes that occur, from the signal that the brain receives to do it, to why exactly it occurs in such an early stage of life

What do you mean with "how does..occur"? Could you specify your problem? It's kind of vague.

@Christiaan I mean "how does... occur"? as in what biological process takes place during synaptic pruning, and what exactly happens to the synapse during the given age range.

Don't you think that makes the question kind of broad? There are many processes going on, from plastic synaptic changes to cellular mechanisms leading to the pruning itself triggered by certain events. I think you cannot expect anyone to lay the full process out for you. Could you specify your issue?

@Christiaan I am in no way expecting anyone to explain the whole process to me, apologies if the explanation of my question is too broad, trying to be more specific: my question would be what exactly is triggered before and during adolescence, so that the brain receives the urge to perpetrate synaptic pruning? I know how synaptic pruning is carried out, I am however very intrigued in the specific processes that occur, from the signal that the brain receives to do it, to why exactly it occurs in such an early stage of life - hope this is more specific


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Iron metabolism in the brain
I did an expression profiling from publicly available RNAseq data for mouse tissues. While for liver and testes I am getting expected proteins in the top highly expressed mRNAs, for brain I am getting ferritin (Ferritin heavy chain 1: Fth1) as the top expressed mRNA!
There are a few studies which report elevated ferritin and iron in neurodegenerative diseases while some others have implicated its role in ageing.
I haven't come across any study on iron metabolism in the normal brain. Does iron metabolism play an important role in the function of the brain?
PS :

The data that I am talking about, has the SRA accession number- SRR652247 (I tried all three runs submitted in SRA)
The mice used in the experiment were 11 weeks old
I used bowtie -> eXpress for quantification of RNAseq reads.

Look at the study summary - it describes expression profiling in testis. Do you think they might have mis-labeled the organ?

I don't think so.. because testes sample has high level of protamine expression which is not there in brain. Also, the highest expressed transcript (all RNAs) in brain is Bc1 - a ncRNA known to regulate translation at synapses.

As usual, association of NDD or age with Fe does not mean it's the causative agent, nor vice versa.

Many articles focus on the pro-oxidant function of iron (and globins in particular). It makes sense that levels may be higher in the CNS due to their role in respiration, which is increased secondary to the “absolute requirement” for glucose facilitated by constitutive GLUT3 expression. So perhaps ferritin is increased to maintain supply for neuroglobin synthesis?
Another thing to consider, Ferroportin1 (FPN1) (iron export protein) is expressed at relatively low levels in the brain when compared to i.a. bone marrow (HPA 2018). You could hypothesise that increased storage is required as a result of decreased transport. But I would look at expression of import proteins; TFR, DMT1, and ZIP 8/14, as that could very quickly throw this theory off.
References:
The Human Protein Atlas (HPA) 2018, SLC40A1, The Human Protein Atlas, 11 September 2018, www.proteinatlas.org


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How does the value of K determine number of local optima in NK model?
BACKGROUND
The NK model of fitness landscape considers N states which can interact with K other states. For example N is the total number of genes in a haploid genome and K is the number of other genes that each gene may interact with.
In this article Kaufman says:

The fully connected NK model yields a completely random fitness
  landscape. For K = N - 1, the fitness contribution of each site
  depends on all of the other sites in the sequence and therefore
  altering any site from one to the other value, 0-1, alters the fitness
  contribution of each site to a new random value. Thus the fitness of
  any 1-mutant neighboring sequence is completely random with respect to
  the initial sequence. The landscape is fully random. As was shown in
  Kauffman & Levin (1987), Weinberger (1988), and Macken & Pereison
  (1989), such random landscapes have very many local optima, on
  average, 2N/(N +1).

I did not read the references mentioned in the text but I read the related section in Kaufman's book: Origins of Order: Self-Organization and Selection in Evolution.
In the book he says that the fitness of a genotype can be ordered and given ranks; the probability that a genotype is fitter than its neighbours (local optima) is same as its probability of ranking higher than its N neighbours. So this probability:
$$P_m=\frac{1}{N+1}$$
and if each gene can have only two states lets say on or off then the expected number of optima with respect to one-mutants (i.e. the difference between a gene and its neighbour is just one mutation) would be:
$$M_1=\frac{2^N}{N+1}$$
What I don't understand is the role of K in this expression. This reason should be valid for any number of K (See the quote above). Even in the book this explanation is given in the case where K is maximum i.e. N-1. I can understand that K can affect the ruggedness of the landscape but can anyone explain how K affects the number of optima? (or are they just two separate statements written together, which is confusing me)

Let's take the opposite extreme, $K=0$, so that each site has an independent effect on fitness. Without loss of generality, we can say that at each locus $n$, the $1$ allele confers an advantage $s_n$ over the $0$ allele. Then there is just one local optimum, the global optimum, at $\vec{1}$, so $M_1=1$ (and $P_m=2^{-N}$).
The key difference is that in the $K=0$ case each fitness comparison of a focal genotype with a neighbor is independent of the rest: the fact that mutating the first gene decreases fitness, for instance, doesn't make it any more likely that mutating the second gene will decrease fitness. For any $K$, it is necessarily true that the focal genotype has a probability $1/(N+1)$ of being fitter than all of a set of $N$ other randomly chosen genotypes, but we're interested in comparing it to its neighbors, which are not a random selection, and are only equivalent to a random selection when $K=N-1$.

Thanks Daniel. Sorry I for the late response. Was out of town and didn't check. So except for the N=0 case, it is not straightforward to predict the number of optima from the value of K or is it monotonously increasing?

No need to apologize! I think that it's monotonously increasing, but I'm not sure if it's been proved in general. There are a couple of papers by Vlada Limic in Ann. Prob. (2003 with Rick Durrett, 2004 with Robin Pemantle) that look at related questions.


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Why do Phobia exist if they aren't advantageous?
A phobia is usually the irrational fear of something, and the individual experiencing it is often unable to justify whether there is such detestation of something which might not even be threatening.
I am aware that there are:

Agoraphobia
Social Phobia
Specific Phobias such as Arachnophobia (fear of spiders) or Ophidiophobia (fear of snakes)

My question is, why do some people have e.g. Arachnophobia but not something closely related such as Entomophobia (fear of insects)?
And why do phobias even exist at all? To me they don't seem to serve a purpose (protection), and do not seem to be of advantageous existence.
Furthermore, I am curious to why exactly a phobia exists – and in some cases manages to be  passed on from the parent to the offspring.
DISCLAIMER:
I am aware of there being several psychological processes involved in this such as events that occurred in early years, or if there is a relative with anxiety, the risk of you suffering of a phobia is significantly larger. I also heard there is a high incidence of people developing phobias after traumatic brain injuries.
However, I am interested in the biological aspect of a phobia, and that why if it isn't advantageous to us, why does it exist?

Why do you say that there aren't people with a phobia of insects in general? Can you support that claim? Also, not everything that exists has advantages. Lots of non-advantageous things exist. Phobias, for example are maladaptive. Fear, on the other hand, is often adaptive.

I think the fault in your reasoning is the assumption that phobias are not advantageous to us. As an example of a potentially useful phobia, consider the fear of heights. Now consider two different ancestors: one who was afraid of heights and one who was not. Generally speaking, the ancestor who was afraid of heights would likely avoid such environments and thereby reduce the likelihood of, say, falling off a cliff or high precipice. In evolutionary terms, we would say that natural selection confers an advantage to the phobia-possessing individual(s). This website in particular has some interesting reading:

Others believe that phobias exist because of evolutionary development to avoid danger in order to improve survival. There are several stimuli that are shared by the most phobic people (heights, insects, crowds, etc.) These phobias, with a couple of exceptions, relate more closely to pre-technological societies. Thus, some scientists, such as Martin Seligman, believe that people are inherently "prepared" to fear certain objects. ((5))) In other words, our phobias relate closely to the perils of our ancestors, as through natural selection, those who feared the dangerous stimulus survived while those who didn't, died off. Prepared fears appear to be very easily conditioned. Some scientists, such as LeDoux, believe that preparedness and the ease of conditioning are the result of certain preexisting neurological connections that exist evolutionarily. These connections are turned on with relative ease.

I get your point and appreciate the example, however I am still curious as to why someone could be a sufferer from Arachnophobia but not Entomophobia? Both could be seen to have similar features, would you not agree that it is odd, to see someone having a phobia of something, but not of something which is closely related to the other angst. I'd be very grateful, if you could provide me with some resources/informations on that.

I think there is a difference between rational and irrational fear. Irrational fear is not advantageous; rational fear is. A fear of heights is rational; a phobia is not. A phobia is something that actively disrupts someone's life.

@anongoodnurse: Why is a fear of heights (or of anything) advantageous?  As opposed to sensible caution, of course.  From what I've seen, it actually makes injury more likely, as the phobic person either freezes, or runs in panic.

Okay, so I see the distinction now, sorry that I was unable to answer that in my post. @jamesqf Per the definitions we are using, "rational fear" would certainly be advantageous if it leads to avoidance of the risky/dangerous/fear-inducing situation to begin with. So as I pointed out in my fear of heights example (which imo is a rational fear), the person would avoid precarious and elevated scenarios altogether. Granted, this may be a disadvantage if the person needs (for some reason) to be in such a location. For most of the part, though, it would prove advantageous.


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Can magnetoreception occur in humans?
Magnetoreception is a sense which allows an animal to detect the Earth’s magnetic field in order to perceive direction, altitude, or location. Magnetoreception is present in bacteria, arthropods, molluscs and members of all major taxonomic groups of vertebrates.

There are several hypotheses that magnetoreception could occur in humans due to cryptochromes, which are a class of blue light-sensitive flavoproteins, because they have been observed to detect magnetic fields in a number of species.

Furthermore, I read somewhere that magnetic bones exist in the human nose, specifically in the ethmoid sinuses. $^1$
Is there more research on those "Magnetic bones", and to what extent is magnetoreception possible in human-beings?
$^1$nature.com/nature/journal/v301/n5895/abs/301078a0.html

What is the dislike about?

Where did you read about "magnatic bones"? Do you have a citation?

@kmm Yes, I do actually – http://www.nature.com/nature/journal/v301/n5895/abs/301078a0.html

Do be aware that most biomagnetism (even those published in Nature) can turn out to be bogus. In this preprint, Markus Meister debunks 3 recent nature papers claiming biomagnetism. Nowhere in the referenced Nature paper do I see an attempt to link the magnetic field range of the ferrous ions and the range needed for the biological function that aids bone growth and repair. It's just an exciting hypothesis as far as I can see.

@James That sounds logical, the idea of magnetoreception in humans would just be too awesome! Thanks for the useful link btw

When we talk about 'can something happen', then I don't think the answer would need a reference.
Of course, humans can attain the ability of magnetoreception, but the main question is What good will it do to us? Instead it'd prove to be disadvantageous as:

We already have smartphones, compass for identifying magnetic field, so why will the body prefer to waste energy on something which can be done without wasting energy?
We all know that the earth has its own magnetic field. So whenever you wake up or go for a walk (just do any movement), you'll feel an irritating magnetic sensation. Why would that be useful?

Even if we don't talk about disadvantage, then also magnetoreception wouldn't prove to be much useful in whole human population. Randomly, some guys might get a few genetic mutations which would allow them to feel magnetic field, but that wouldn't be of any use to them.
BUT, to your interest, humans do have magnetoreceptors, in retinas. See this article:

But cryptochrome isn’t unique to birds – it’s an ancient protein with versions in all branches of life. In most cases, these proteins control daily rhythms. Humans, for example, have two cryptochromes – CRY1 and CRY2 – which help to control our body clocks. But Lauren Foley from the University of Massachusetts Medical School has found that CRY2 can double as a magnetic sensor.

or this Wikipedia article:

Humans are not thought to have a magnetic sense, but there is a chemical (a cryptochrome) in the eye which could serve this function.(2)

Source                                                           Source
So, acquiring magnetoreception might be easier than you'd expect, but it doesn't happen even in this condition. Why?, who knows? Maybe because our body rejected magnetoreception as useless. Maybe at some point of time, humans had the ability to feel/see magnetic field, but this feature now seems vestigial.
EDIT: Regarding "magnetic bones", every article that I could read only points to this Nature article you referred to in your question. So it doesn't seem like there has been much research on it, or maybe this article itself is enough to conclude the topic.
References:
1.http://blogs.discovermagazine.com/notrocketscience/2011/06/21/humans-have-a-magnetic-sensor-in-our-eyes-but-can-we-see-magnetic-fields/
2.https://en.wikipedia.org/wiki/Magnetoreception
3.http://www.ks.uiuc.edu/Research/cryptochrome/
4.http://www.microsystem-components.com/html/magnetoreception.html
5.http://www.nature.com/nature/journal/v301/n5895/abs/301078a0.html


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Do single nucleotides spontaneously bind to ss DNA?
Do single nucleotides spontaneously bind to ss DNA? AT. GC. I realize the rhibisome is usually needed for making a strand, but what about randomly hbonded base pairs? Does this occur?

note that a binding might be thermally unstable; e.g.: assume 1-2 nucleotides in various approximations for annealing temperature of oligo-nucleotides such as https://jeltsch.org/annealing_temperature and note that annealing temperature would be very low, and potentially at a temperature where water is frozen

“I realize the rhibisome is usually needed for making a strand”. If this is indicative of your knowledge I suggest you do some homework by reading a book on molecular biology before asking questions of this type. An introductory section on basic chemistry would also not come amiss.

Potentially, transiently. There’s an entropic penalty for a single nucleotide to bind a DNA strand which would not be offset by any enthalpic gain (if there is any). I’ve no idea where that equilibrium lies, but it’s probably far away from base pairing.

I am no expert on the topic, but single stranded DNA is commonly found during DNA replication, when DNA helicase splits apart the DNA strands so that the DNA can be replicated. When this occurs, the two DNA strands naturally have a high affinity for each other, bearing complementary base pair sequences, and another molecule must be present in order to prevent the two DNA strands from re-binding. These are single-stranded binding proteins, and they bind to ssDNA to prevent re-binding from occurring. As this prevents the DNA from binding to the antiparallel strand, I would imagine it has a role in preventing single DNA nucleotides from binding to the DNA strand as well.

Please reference your response!