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How much of the genetic differences between humans and chimpanzees are due to genetic drift?
Both natural selection and genetic drift play a part in changing our DNA over time. Are there trustworthy estimates how much of the differences over the whole genome between us and chimpanzees are due to genetic drift and how much is due to natural selection?

Interestingly, the rate of accumulation of new neutral mutations is independent on the population size and is equal to $\mu$ (per lineage), where $\mu$ is (also) the mutation rate at a given locus.

@Remi.b : Let's focus on the whole genome.

Note that most selection pressures will actually prevent divergence between two sister lineages as they act in the same direction. Only cases where selection differs between lineages will cause divergence. This type of selection is simply called divergent selection.

Following the neutral theory of molecular evolution, I would predict that most divergence is due to accumulation on neutral mutations. (+1)

@Remi.b I always learned that genetic drift is higher in smaller populations. This is discredited now?

@Rodrigo The loss of polymorphism through time (which is how one would quantify the concept of genetic drift) is higher in smaller population. Have a look to why-is-the-strength-of-genetic-drift-inversely-proportional-to-the-population-size.

@Rodrigo However, the rate at which neutral mutation fix is the same. The reason is that the probability of a neutral mutation to fix is $\frac{1}{2N}$. There are $2N\mu$ new mutations entering the population each generation and therefore the rate of fixation of neutral mutations is $\frac{1}{2N} \cdot 2N\mu = \mu$. This classic result is essential for phylogenetic reconstruction typically as we can infer time of divergence from the rate of neutral divergence without knowing anything about $N$.

The easiest way to track whether a particular protein-coding gene has diverged between two species because of drift or actively maintained selection is to look at the ratio of synonymous to nonsynonymous mutations within that gene. A synonymous mutation is one that doesn't change the identity of the amino acid within that protein; a nonsynonymous mutation is one that does. Synonymous mutations are neutral by definition; their presence gives us an idea of how much time has diverged and how frequently mutations in that protein coding region change over time.
A dN/dS (Nonsynonymous mutation to Synonymous mutation) ratio of 1 suggests that the primary driver of change between species is purely neutral change. That usually means that it doesn't matter what is going on with that protein and is a little unusual--I would primarily expect to see something like that in a gene that is on its way to becoming a pseudogene.
A ratio of less than one means that synonymous mutations are much more likely to persist in that region than nonsynonymous ones. This is usually a sign that purifying selection is happening--for whatever reason, it's important to the function of both species that those proteins stay relatively similar.
A ratio of more than 1 means that there is diverging or directional selection happening, and that that protein type is changing between the two species because selection is actively modifying one or both proteins.
Here is a paper specifically analyzing whole human and chimpanzee genomes using this metric.

You could improve this answer if you summarize what the linked paper concludes (in general, answers on StackExchange should stand on their own; links and references provide support, but we hope for answers here to outlast links that could change or go dead in the future).

"Synonymous mutations are neutral by definition" that's wrong. It doesn't change the shape of the protein but it does change protein synthetisation speed/amounts.

@Christian It's wrong in so far as it is a simplification/assumption, and a useful one at that.

@canadianer : I see no reason why there shouldn't be evolutionary pressure to increase or decrease the synthesis of a certain protein and that's what a synonymous mutations does.

Wildman et al. (2003) investigated 97 genes in humans and chimpanzees and show evidence that 30 of them (~31%) have evolved under positive selection. This is not per say an estimate of what fraction of substitutions are adaptive but it gives an idea.
Such estimates can be quite hard to get. I don't know any such estimates between human and primates but I know one on Drosophila.
Eyre-Walker and Keightley (2009) that about 40% of all substitutions between Drosophila melanogaster and D. simulans are adaptive.
Population sizes being larger in the Drosophila lineage than in the Hominidae lineage, I would predict that the fraction of substitutions that are adaptative would be significantly lower between humans and chimpanzees (prediction which agrees with Wildman et al. (2003)).
So, to the question How much of the genetic differences between humans and chimpanzees are due to genetic drift?, I would answer: More than 60%! But remain cautious realizing this is a vague estimate.


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Fold Coverage of sequence read?
What does it mean when N-Fold coverage of read of sequence? Details will be much appreciated if a link provider with brief explanation.

What you're asking is a little unclear to me...I don't know if this is what you're looking for, but typically, the fold coverage of a read represents the number of times that particular read was sequenced in a given run.

Fold coverage is often derived with respect to a genomic locus, not a read. In sequencing experiments, fold coverage of a genomic loci (coordinate along a reference assembly) will be the number of aligned reads that overlap the position.

It could also be the average coverage of a genome based on number of reads, read length and expected genome size.

Thank you for the additional detail. Absolutely, on a genome level the fold coverage is computed as: number of reads * read length / genome size, and genome size here be either the true genome size or the size of the fraction of genome that is captured for sequencing.

N-fold coverage usually refer to the average number of reads spanning across a particular region of interest. For example, if you are interested in a gene and would like to know how confident your data is, you may look for the coverage.
There is no absolute definition on how N-fold coverage is calculated. The most common method is to get the arithmetic average per base.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

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Identifying an Unknown Blood Type

The following case study has a student working with blood samples to
  identify their blood types (A, B, AB, and O). Consider the situation
  and answer the questions.
A student is given eight red blood cell suspensions, which contain
  only red blood cells, and the matching serum from each sample. (Serum
  is blood plasma in which fibrinogen has been removed.)
She is asked to identify each of the four different blood types
  present. To test these samples, the only materials she has at her
  disposal are a sample of type A red cell suspension and the serum from
  type A blood.
Describe the step-by-step procedure that she must use to identify the
  four different blood types present. In each step, interpret what it
  means if the cells in the sample clump together, or if they do not
  clump together.

I am mostly confused on what exactly "she has at her disposal are a sample of type A red cell suspension and the serum from type A blood." means..? What is a A red cell suspension?
I already know that:
TYPE A: has anti-B antibodies
TYPE B: has anti-A antibodies
TYPE AB: has neither anti-A nor anti B antibodies
TYPE O: has both anti-A and anti-B antibodies.

The passage:

To test these samples, the only materials she has at her disposal are
  a sample of type A red cell suspension and the serum from type A
  blood.

means, I take it, that she has available two containers: One has red blood cells from a known blood-type A individual suspended in a neutral fluid such as saline solution.  The other container has blood plasma (without red blood cells or fibrinogen) also from a known blood-type A individual.
These should be enough to determine the blood types of four individuals  from the unknown test tubes (four pairs of test tubes, each pair being one with cell suspensions and one with plasma, coming from four individuals having different blood types).

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Why alcohol can't help with OCD?
I was thinking about influence of ethanol on our brain.
We know, that ethanol can affect GABA receptors and increase flow of chlorine in our brain cells. So it makes signal weaker and slow our CNS activity down.
People with OCD usually take minor/major tranquilizers (and many other ofc.) that have similar effect.
I understand, that alcohol (ethanol) can't stay in our CNS as long as tranquilizers do and it also causes many bad influences, but if we put these bad effects away, could alchohol potentionaly help people with OCD for a short time?
I guess no, but i don't know much in neuropharmacology, so explain me please.
Thanks.

Interesting idea. How do you know it doesn't work?

The close-vote on the question being self-help is off. It is a legitimate question, especially in the light of the tendency for psychiatric patients to self-medicate. +1

https://www.quora.com/Why-alcohol-cant-help-with-OCD Got some answer on quora, if smb is interested.


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What is the evolutionary advantage of red-green color blindness?
Red-green colorblindness seems to make it harder for a hunter-gatherer to see whether a fruit is ripe and thus worth picking.
Is there a reason why selection hasn't completely removed red-green color blindness? Are there circumstances where this trait provides an evolutionary benefit?

Just a general note: evolution isn't a guided process. For a trait to disappear, there must be a strong pressure against that trait - usually either cost (e.g. cave fish eyes) or a more direct danger (e.g. black rabbit on snow). Dichromancy simply may not be disadvantageous enough (just like tetrachromancy, exhibited by some humans, isn't advantageous enough to spread). These kinds of variations are very important for the survival of the species - when the environment changes, that's the pool of adaptations evolution "picks" from :)

Note that the presence of a trait does not mean it's adaptive. Selection is not the only mechanism of evolution and others mechanisms can spread and maintain maladaptive alleles in a population.

Just to to Luaan 's point - and I doubt this is applicable for color-blindness - but sometimes a neutral or slightly disadvantageous trait (like color-blindness) may be bound together with a trait that is clearly advantageous.  So when evolution selects for the advantageous trait, it "accidentally" also gets the neutral/slightly disadvantageous one as part of the "package".

@BaardKopperud yes, a well-known example is Sickle-cell disease protecting against Malaria.

@StéphaneGourichon baard is describing linkage and genetic hitchhiking - sickle cell is an example of heterozygote advantage

It might have been "removed" at specific points in every generation that's ever lived. That won't guarantee that the same or very similar mutation won't happen again and again. There might someday be a clear advantage that isn't obvious today.

Short answer
Color-blind subjects are better at detecting color-camouflaged objects. This may give color blinds an advantage in terms of spotting hidden dangers (predators) or finding camouflaged foods.
Background
There are two types of red-green blindness: protanopia (red-blind) and deuteranopia (green-blind), i.e., these people miss one type of cone, namely the (red L cone or the green M cone).
These conditions should be set apart from the condition where there are mutations in the L cones shifting their sensitivity to the green cone spectrum (deuteranomaly) or vice versa (protanomaly).
Since you are talking color-"blindness", as opposed to reduced sensitivity to red or green, I reckon you are asking about true dichromats, i.e., protanopes and deuteranopes. It's an excellent question as to why 2% of the men have either one condition, given that:
Protanopes are more likely to confuse:-

Black with many shades of red
Dark brown with dark green, dark orange and dark red
Some blues with some reds, purples and dark pinks
Mid-greens with some oranges

Deuteranopes are more likely to confuse:-

Mid-reds with mid-greens
Blue-greens with grey and mid-pinks
Bright greens with yellows
Pale pinks with light grey
Mid-reds with mid-brown
Light blues with lilac

There are reports on the benefits of being red-green color blind under certain specific conditions. For example, Morgan et al. (1992) report that the identification of a target area with a different texture or orientation pattern was performed better by dichromats when the surfaces were painted with irrelevant colors. In other words, when color is simply a distractor and confuses the subject to focus on the task (i.e., texture or orientation discrimination), the lack of red-green color vision can actually be beneficial. This in turn could be interpreted as dichromatic vision being beneficial over trichromatic vision to detect color-camouflaged objects.
Reports on improved foraging of dichromats under low-lighting are debated, but cannot be excluded. The better camouflage-breaking performance of dichromats is, however, an established phenomenon (Cain et al., 2010).
During the Second World War it was suggested that color-deficient observers could often penetrate camouflage that deceived the normal observer. The idea has been a recurrent one, both with respect to military camouflage and with respect to the camouflage of the natural world (reviewed in Morgan et al. (1992)
Outlines, rather than colors, are responsible for pattern recognition. In the military, colorblind snipers and spotters are highly valued for these reasons (source: De Paul University). If you sit back far from your screen, look at the normal full-color picture on the left and compare it to the dichromatic picture on the right; the picture on the right appears at higher contrast in trichromats, but dichromats may not see any difference between the two:

Left: full-color image, right: dichromatic image. source: De Paul University
However, I think the dichromat trait is simply not selected against strongly and this would explain its existence more easily than finding reasons it would be selected for (Morgan et al., 1992).
References
- Cain et al., Biol Lett (2010); 6, 3–38
- Morgan et al., Proc R Soc B (1992); 248: 291-5

I'm red-green colorblind (not sure which flavor) and I can't tell the difference between the full-color image and the dichromatic image :(  that mannequin is wearing some really ineffective camouflage though.

I'm giving +1 for the last sentence. I doubt any selective advantage for colour blindness outweighs the selective benefit for colour vision so it's more likely to be a failure to be selected out of the population than anything that's actively selected in.

I can see the difference between the two images, but it's not clear to me why the man is supposed to be easier to spot in the image on the right.

I have full color vision, and still find the mannequin's camouflage to be wholly ineffective. If the fatigues were green and black, it might have been better than this green and white scheme.

I haven't found red-green color blindness to be as much of a hinderance as many people assume it to be.  A lot of my friends ask me how I tell apart traffic lights. The truth is that I can actually make out the difference, since I'm very perceptive to the difference in brightness between the lights.  Additionally, it's really easy to tell the state of the lights based on context (e.g., which cars are moving, etc.). The same applies to many other situations where normally-sighted people rely heavily on color. So it makes sense to me that color-blindess is not heavily selected against.

Also, tetrachromacy allows women with a heterozygous genotype (carriers) to see more color than an average person. This might be an evolutionary advantage to heterozygous carriers, similar to the sickle-cell gene protecting against malaria.

@jayhendren actually, traffic lights are intentionally designed with a shade of green that also has a lot of blue in it, specifically so that colorblind people can tell them apart from the red lights. Been that way for decades.

There seems to be some evolutionary advantages to red-green colorblindness. The paper in reference 1 (a summary can be found in reference 2) shows that people with red-green color blindness can differentiate between much more shades of khaki than unaffected people. This might help detecting camouflaged food in a green environment.
Reference 2 quotes an expert about this:

For example, it may have helped them spot potential food items in complicated environments such as grass or foliage, he suggests.

This fits with the observation that in a number of new world monkeys dichromatic and trichromatic animals are present in the populations. They found that the dichromatic monkeys have advantages in low light conditions.
References:

Multidimensional scaling reveals a color dimension unique to ‘color-
deficient’ observers
Colour blindness may have hidden advantages
A foraging advantage for dichromatic marmosets (Callithrix
geoffroyi) at low light intensity

Anecdotal evidence: both my brother and I have mild red-green colourblindness and our colourvision in the dark, is much greater than both our sisters. We also, in general, have much better nighttime vision than everybody we know who isn't red-green colourblind, to the point where , when most people can't see anything, we can still navigate comfortably (but obviously not nearly as well as if there's any real light). I can't say if this is due to colourblindness or not.

FYI: Your ref #1 is on deuteranomaly, which is anomalous trichromatic vision.


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Artificial reduction of NADP into NADPH by means of an electrical current
I've recently been attempting to artificially drive the formation of NADPH via the NADP reduction mechanism utilized by Ferredoxin-NADP Reductase in the Light-Dependent Reactions of Photosynthesis in plants. My goal is to reproduce the synthesis reaction in vitro only by means of an electric current.
Is there any way to replace the electron pair supplied by PSI in vivo, with one from a current going through a wire? Would conducting electricity through a solution of Ferredoxin, FNR, NADP, and a weak acid yield any desirable results?

It SHOULD work, theoretically. If it doesn't, try using strong acid (not so strong that it'd degenerate other chemicals) ;)

@another'Homosapien' Thank you for your answer! So you are fairly certain that simply conducting electricity through a solution of the chemicals would lead to the spontaneous synthesis of NADPH by the FNR enzyme? I have to conduct this experiment for a research project, and I would like to have confidence that my ideas would "work". Also, what is the most efficient way of detecting NADPH in an aqueous solution?

@another'Homosapien' So I don't have to "bind" ferredoxin to the metal electrodes, right?

I said it SHOULD work, not it WILL work. There could be some problem at any step. I am not expert in using biochemicals in vitro, so I can just say that yes, theoretically it is possible. Ferredoxin carries electrons from PS-I to NADP, and since PS-I is the only source of electrons there, so ferredoxin is attached to the membrane. But as electrons would move from one place to another in solution, ferredoxin need not be attached at electrode.

@TomD Would a 100mM solution of acetate produce a pH below 5? Also, would serial dilution do for the experiment, since 100 micromoles for the NADP is a bit too sparse for our lab equipment? I don't know if your setup would yield a significant result, either. Finally, I would like to know how you came up with your numbers regarding the concentration of the chemicals. Could you clarify a bit more? Thank you!


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An experiment to test if a bacterial resistance gene is on the plasmid or chromosome?
So I have an E.coli strain phenotypicall resistant to the antibiotics ampicillin and rifampicin. How do I test if the AmpR gene is carried on a plasmid and not on the chromosome?
In summary, I thought perhaps you could isolate the plasmid, put it in an ampicillin sensitive bacteria, then see whether or not the bacteria die.
I also thought you could use PCR on the plasmid with primers complementary to sequences adjacent to the AmpR gene. I'd use a positive control with the gene of interest and a negative no template control.
Do these sound about right & are there any other methods or controls I should consider?

I remember another method. Isolate the plasmid and use restriction enzymes specific to ampR (Pvu I & Pst I). If the plasmid is cut, then the resistance gene should be on it.

You could try to isolate a plasmid, transfer it into non-resistant bacteria and see, which resistances they develop through the transformation.

Based on the situation you have described, isolating the plasmid from the ampicilin-resistant strain of E. coli and allowing it to be taken up by a separate, non-resistance strain of E. coli would be the most efficient, and cost effective method of determining whether or not the AmpR gene is located on the plasmid or the bacterial chromosome itself.
In order to do this, you would need to first grow a culture of the ampicilin resistant strain, from which you could induce lysis of cells in order to obtain a solution containing free plasmids.
Several different plasmid isolation or mini-prep procedures exist that are typically quite effective, if done correctly.
Additionally, many specific "plasmid-isolation" and "plasmid-purification" kits exist that would offer the materials and instructions needed to undergo this process: Isolating your Addgene Plasmid DNA from Bacteria
After properly isolating the plasmid from your ampicilin-resistant strain, you would then need to insert that plasmid into a non-resistant E. coli strain. Bacterial transformation via electroporation is a commonly used technique that causes increased permeability of bacterial cell membranes, enabling the plasmid to enter or be taken up by the cells.
Once these cells have been allowed to "recover" they can then be grown in liquid or solid culture containing ampicilin. Growth would indicate the AmpR gene is present in the bacterial strain, and that the plasmid is responsible for carrying this resistance. Likewise, no growth would suggest that the gene must have be present on the bacterial chromosome instead.


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Is there a difference in cytoplasmic pH between prokaryotes and eukaryotes?
The cytosolic pH in human cells is around 7.4, but fluctuates as the cell is replicating. Prokaryotes and eukaryotes are vastly different in many ways. One thing they share is cytoplasm. Is there any general difference in the pH between these two cytosolic spaces? Any pointers to a previous investigation into this would be hugely appreciated. Ideally I'm after a quantified numerical comparison from a peer reviewed reference, but given the obscurity of the question that might be a tall order!
Googling was to no avail. It's swamped with pH survival data.

In the article "pH of the Cytoplasm and Periplasm of Escherichia coli: Rapid Measurement by Green Fluorescent Protein Fluorimetry", by Jessica C. Wilks and Joan L. Slonczewski, the pH of E.coli cytoplasm was mentioned as 7.2 - 7.8. I just took E.coli's pH range as a common example of prokaryotes.
Reference link: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1951819/


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Does the Michaelis-Menten equation take in account the non-enzyme formation of products?
I only recently learned about the Michaelis-Menten equation, since I am not studying biology or anything related. Let's write the equation as
$$\frac{d[P]}{dt} = V_{max} \cdot \frac{[S]}{K + [S]}$$
If I'm not mistaken, this equation describes the rate at which products are formed ($\frac{d[P]}{dt}$) as a function of substrate concentration $[S]$ in steady-state. In a translation of Michaelis' paper I read that $V_{max}$ can be written as $k [E]$, where $k$ is a constant and $[E]$ is the total enzyme concentration.
Mathematically one would say that when the total enzyme concentration is zero ($[E] = 0$), the rate at which the product is formed should equal zero. If I recall correctly, in several reactions products are formed without enzymes (Enzymes only enhance the reaction rate?). Is the Michaelis-Menten equation specifically used for situations where $[E]>0$? If so, how does it account for very low enzyme concentrations where product formation from non-enzyme reactions cannot be neglected?

In any study of enzyme kinetics it is essential to subtract all 'blank' rates and to ensure that the measured rate is due only to enzyme catalysis.
That is, in kinetic 'parlance', the velocity vs [enzyme concentration] should be linear and go through the origin.  Doubling the enzyme concentration should double the (enzymic) rate, and halving the enzyme concentration should halve the (enzymic) rate.
Failure to subtract blank rates may give rise to a variety of spurious kinetic effects such as downwardly-curving double-reciprocal plots (Lineweaver-Burk plots).
Downwardly-curving Lineweaver-Burk plots are diagnostic of negative co-operativity, but such a conclusion may be artefactual if blank rates are not subtracted.
A very good reference to this sort of this is Enzymes, (1979) by Dixon, M, Webb, E.C.,  Thorne, C.  & Tipton, K.F. (3rd Edn), Longmans,  in particular pp 461 - 462.

Just for confirmation; the product formation rate would thus be $V_{0} + \frac{V_{max} \cdot [S]}{K+[S]}$ if blank rates were not subtracted? Is there a different notation/name for the rate of product formation when $V_{0}$ is not subtracted?


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Molecules, Targets and Isoforms
I have a question. Given a molecule A and two isoforms of a gene X, Y, and the knowledge that A targets X. Can I infere from this anything about whether A targets Y?
As a motivation think about Furosemide (= A) and SLC12A1, SLC12A2. From Drugbank I know that Furosemide targets SLC12A1, and from KEGG I know that Furosemide targets both genes. I wonder whether I can infer the KEGG knowledge already from the Drugbank knowledge...
Best,
Alex :)

The short answer is no.  What matters is whether the sequence and folding (if you are talking about binding of A to proteins instead of DNA) of each isoform of your gene still results in the binding of A.
I other words, A may bind to X. Y, an isoform of X may not have the same sequence that A likes to bind to. Or, in the case of proteins and A, Y may fold slightly differently, preventing accessibility of A to Y.


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Why does the intensity of an action potential once generated at the trigger zone remain undistured throught the axon?
What causes this consistency?
I read the previously asked questions on this site none of them carry an answer to this question.

If my / Thawn's post doesn't answer your question, then you should place a bounty on your question, and if it does answer, then please select it as correct answer. Don't just leave the question unanswered.

If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered.

Actually, it would be better to say that action potential does not travel but is regenerated anew in a sequence along the axon.

I would like to elaborate how this happens and why this is the reason why the action potential stays constant:
In rest state, there is an ion gradient across the membrane of each cell. This causes a small voltage between the outside and the inside of the membrane, the so called transmembrane potential.
Once the cell membrane becomes permeable for ions (normally this occurs when an ion channel is opened), the potential causes ions to flow across the membrane, the membrane becomes depolarized.
In the axon, the membrane contains so called voltage-gated ion channels. As soon as the membrane is depolarized at the trigger zone, the depolarization of the adjacent membrane causes voltage gated ion channels to open in that adjacent memrane as well, causing ions to flow also across the adjacent piece of membrane. This process continues in a wave along the whole membrane, this is what we call the action potential. Because the ion gradient across the membrane and the density of ion channels is constant along the whole axon, the amplitude of the action potential stays constant along the whole length of the axon.

Your opening offers a very nice point of view +1

@Thawn Could we say that the ions (Na+) moving across the length of the axon cause conformational change in the voltage gated ion-channels and thereby opening adjacent ion channels, inducing a second action potential in new (adjacent) region of axon?

@SanjuktaGhosh Yes, that's how action potential reaches the adjacent areas. Na+ entered inside from one place diffuses to nearby region which causes voltage to rise (above -70mV), and as soon as that reaches threshold limit, action potential is generated in that region while the previous region is busy in repolarizing.

@another'Homosapien' I have just a small addition to your comment: while the influx of Na+ ions causes the depolarization of the membrane and initialized the action potential, the conduction of the potential along the length of the axon happens by the movement of any ion (K+, Na+ and even Cl-) since this is simply the conduction of a charge through a salty solution. Also, this movement is NOT simple diffusion but a directed motion driven by the difference in electric potential.

I am afraid I can't completely agree with you. Since action potential is largely governed by Na+, its movement through length of axon thus plays a major role in transmitting action potential (though other ions may have some effect too as you said). Also, it is indeed simple diffusion of Na+. It also reaches depolarized areas, but though it is already in recovery phase, so it cannot play its role there. But since polarized areas have (almost) no Na+ inside, so its diffusion qyickly generates action potential.

I would like to request someone to join this discussion. @Christiaan if you please, add your views.

@another 'Homo sapien' I was also wondering if the other ions could influence conformational changes.

@SanjuktaGhosh Simple answer- they cannot. I have put a diagram in my answer (first image) which clearly shows that ion channels are only for Na+ and K+. Other ions are either freely permeable (eg: Cl-) or impermeable (eg: amino acid/protein anions) through neural membrane, so they cannot cause conformational changes.

@another'Homosapien' You need to separate two ways that Ions move during signal transduction: 1) across the membrane. As you state correctly, there are specific channels for Na+ and K+ which only allow these ions to pass. 2) along the axon. This conduction is important for the action potential to reach neighboring voltage-gated ion channels and move along the length of the axon.This conduction is not limited by any membrane and therefore all availabel ions (mainly Na+,K+ and Cl-) take part in this conduction. Also the latter conduction is not driven solely by diffusion but also by the voltage.

@Thawn thanks for the suggestion, I added that part too in the answer :)

Descriptive Answer- A nerve impulse is the movement of an action potential as a wave through a nerve fibre. A wave of negative charge on the surface of an axon marks the position, at any moment, of the action potential. Action potentials are self-generated along the axon. The events that set up an action potential at one spot on the nerve fibre also transmit it along the entire length of the nerve fibre. The changes in membrane permeability at one site upset the normal membrane permeability at the adjacent area. The action potential then moves to the neighbouring region of the nerve fibre till it covers the whole length of the fibre. Action potential is propagated along a nerve fibre without any change in the amplitude. It is, thus, a nondecremental (not decreasing) phenomenon. Actually, it would be better to say that action potential does not travel but is regenerated anew in a sequence along the axon.
Explanation- To know why nerve impulse transmission is consistent, lets first know how it is transmitted, for which we should know how it is generated.
Generation-
At rest (no impulse), outside of neuron i.e. ECF (extra-cellular fluid) has more positive charge and inside of neuron has relatively less positive charge or more negative charge. This is maintained by keeping Na+ outside and allowing K+ to move freely between inside outside. It is done by action of voltage-gated ion channels like closing of Na+ channels and keeping K+ channels open, and through Na+/K+ ATPase which transports 3 Na+ outside for bringing 2 K+ inside, and K+ can again freely move outside down the concentration gradient. This results in a resting membrane potential of -70mV i.e. depolarization.
When neuron receives a stimulus, its Na+ channels open and K+ channels close which causes an influx of Na+ which results in more positive charge inside and negative charge outside. This is the action potential of neuron of about +30mV (value varies, I have taken from here, for variations in AP see this). It lasts for less than 1/1000 of a second as Na+/K+ pump  starts working again immediately and K+ channels open and Na+ channels close again to recover the resting potential of neuron i.e. repolarization.

Source
Transmission-
Breaking of resting potential i.e. action potential at one place stimulates action potential at the adjacent place. Actually, action potential is not transmitted through the neuron, it is regenerated at adjacent areas in a sequential manner from one point to another in the axon. Opening & closing of ion channels at one point causes opening & closing of ion channels at the next point by which action potential is transmitted through the axon.

Source
This also explains why nerve impulse does not travel in reverse direction i.e. due to repolarization state of neuron at the previous site during which it cannot transmit any impulse.

Source
Now, for why nerve impulse is consistent through the neuron i.e. why it does not decrease during its course through axon. This is because of equal charge throughout the length of axon. Resting potential is -70mV throughout the axon, and action potential is +30mV at any point in the axon, due to which no charge is dissipated and the nerve impulse remains consistent. For detail about it, refer to the all or none law of nerve impulse which states:

The all-or-none law is the principle that the strength by which a nerve or muscle fiber responds to a stimulus is independent of the strength of the stimulus. If that stimulus exceeds the threshold potential, the nerve or muscle fiber will give a complete response; otherwise, there is no response.

i.e. if a stimulus has the threshold potential (-40mV to -55mV), it will always generate nerve impulse of same action potential (+30mV) otherwise no action potential will be generated and transmitted i.e. it will be consistent everywhere.
Source- Pradeep's : A textbook of Biology for Class XI, chapter 22- Neural control and coordination.
Similar answer has been posted by @Thawn too. I have added some more explanation and citation to this answer.
EDIT 1- You may find an answer to How does a change in the potential across a neuron's membrane get turned into a signal that is sent down the axon? helpful which says:

the sodium gates open the more positive the voltage is, which in turn opens more sodium gates. If a patch of neural membrane is depolarized, the charge diffuses into the nearby patches of neural membrane. This will open the sodium channels of the nearby membrane patch. Now once enough sodium channels open, the neuron will fire a action potential, at this point potassium channels open and potassium rushes out of the cell repolarizing it(making it more negative). Furthermore the sodium gates close at positive voltages which further repolarizes the neuron and prevents back propagation.

EDIT 2- Thus propagation of ions in axon can be, as pointed out by @Thawn, categorised as:
1. Perpendicular to length- this type of movement is responsible for generation of action potential. It is perpendicular to length of axon i.e. through neuron's membrane. This type of movement of ions is governed by voltage-gated ion channels, which ensure charge difference between inside and outside of axon.
2. Along the length- this type of movement is responsible for transmission of nerve impulse through the axon. It is parallel to length of axon. Since there is no membrane in length of axon, this type of movement is thus governed only by diffusion. As Na+ enters cytoplasm of axon, it diffuses to adjacent areas. But since previous (depolarized) area already has high concentration of Na+, so its net movement is towards the next (polarized) area, which becomes the cause for depolarization of that area. This is similar for K+, Cl- and other ions (like protein-derived anions).


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Are seedless fruits considered life?
From school, I remember that for something to be considered life, it must be able to reproduce.  With the creation of seedless fruits (such as watermelon), would this be considered life as they don't have seeds so they can't reproduce?

Why wouldn't they be? They are part of a plant which are indisputably living in almost anyway that matters. Fertility is not a pre-requisite for life - just a common way to pass on genes to the next generation. I'm voting to close this question because it's not clear what your question is without a robust definition of life.

I'm voting to close this question as off-topic because it is a nice candidate for Philosophy.SE

What's life isnt a matter of Biology but Philosophy? Hmm.. for once thing, there are 4 tags labeled "life" in this SE, one of them with its own definition of life. And some of the definitions out there of "life" says "Life is a characteristic that distinguishes physical entities that do have biological processes" (hard to think that idea came from Philosophy and not Biology) and some of the definitions out there of Biology says "Biology is the natural science that involves the study of life and living organisms". How can you study life if you dont define what it is?

Definition of life
The definition of what is alive and what is not is not a matter of biology but a matter of philosophy. Most definitions are based on:

Physiology

Existence of a metabolism

Evolution

Ability to reproduce and have heritable traits

Ecology

Ability to respond to the environment

There are plenty of possible definitions of "life". Note also that behind the complexity of defining what is alive there is the issue of defining the unit (the individuality if you want) on which the concept of life applies.
Your definition of life
You suggest a quick and simple definition so let's consider it.

to be considered life, it must be able to reproduce

If you talk about the watermelon tree
If this is your definition, then Citrullus lanatus is definitely alive as it is able to reproduce (otherwise we would not be able to cultivate them).
If you talk about the watermelon fruit
Now you may ask is the fruit itself alive. Then, using your definition again, I suppose the answer is no because a given seedless watermelon will not be able to give birth to other seedless watermelons (even via the make-up of a watermelon tree).
Note that following the same logic one could argue that one's head is not alive either as one's head does not reproduce. Only your gonads do. Your dog might not be considered alive either. A castrato (singer) would not be alive either. A woman, after menopause, cannot reproduce either! Arguably, a cloud replicates or a fire replicates and could eventually be considered alive following your definition. So really, as you can see your simple definition hardly fit your intuition of what should be called alive.
My opinion on your definition
Personally, I am not a big fan of your definition but again it is nothing but a matter of preferences. I don't like that your definition is unclear because there are plenty of limit cases and because there are plenty of cases we would want to call alive that we can't anymore (like a woman after menopause for example!) Every definition of life would eave limit cases but with your definition, it really easy to find these limit cases.
Is this question about Biology?
No, it is not. It is a question of philosophy.
Other interesting post on Biology.Stack
You might want to have a look at why isn't a virus alive.

And if being able to reproduce is a criteria for being alive, then my dogs are not alive, since they've been neutered.  Since one of them is now shoving his head under my hand in order to get me to go out and play, I'd say they're quite definitely alive :-)

Thanks! I inspired from your example to add that to my answer.

Yes, they are considered life

Seedless fruits can develop in one of two ways: either the fruit develops without fertilization (parthenocarpy), or pollination triggers fruit development, but the ovules or embryos abort without producing mature seeds (stenospermocarpy). Seedless banana and watermelon fruits are produced on triploid plants, whose three sets of chromosomes make it very unlikely for meiosis to produce fertile gametes. This is because one of the three copies of each chromosome can't pair with another appropriate chromosome before separating into daughter cells, so these extra third copies end up randomly distributed between the two daughter cells from meiosis 1, resulting in the (usually) swiftly lethal aneuploidy condition. Such plants can arise by spontaneous mutation or by hybridization between diploid and tetraploid individuals of the same or different species. Some species, such as tomato,[4] pineapple, and cucumber, produce seedless fruit if not pollinated, but do produce seeded fruit if pollination occurs.

They fulfill all processes which are required for anything to be considered as life

Metabolism
Respiration
Sensitivity (responding to stimuli like gravity and sunlight)
Nutrition
Excretion (getting rid of CO2)
Growth
Reproduction
Homeostasis

Sources

http://www.scientificamerican.com/article/how-do-seedless-fruits-ar/
https://en.wikipedia.org/wiki/Parthenocarpy

Which definition of life are you using? Answering yes or no to this question suggests that there is such a thing as a scientific, objective definition of life, while there is none.

@Remi.b I am using the definition by the encyclopedia britannica, which states that there is a definition, at least to some extent, what makes things life

The vast majority of scientist disagree on a given definition and they all agree that any definition would leave limit cases. Wiki gives tens (or hundreds) of citations.

According to Wiki:
Life is a characteristic distinguishing physical entities having biological processes (such as signaling and self-sustaining processes) from those that do not, either because such functions have ceased (death), or because they lack such functions and are classified as inanimate.
If we consider, let say, infertile animal, it has signal system and that maintain homeostasis so we can definitely say that is life, but it's life.
I understand, that the question is about species, but if we can say, that
such plants can arise by spontaneous mutation or hybridization between diploid and tetraploid individuals of the same or different species, how can we deny mutations that occur in our life in a natural way and state that it is not life?
In my opinion, when someone says that something is not life, it's inanimate.
But that is out of the question, i guess.


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How to obtain a list of proteins sorted by the ~1400 unique protein folds?
The databases CATH and SCOP both have around 1400 unique protein folds recorded from analysis of the PDB.  However, I do not see any method to access this particular data.

A list of each of the 1400 folds (just an id number, and/or a descriptor)?
For each individual fold (of the 1400), a list of PDB IDs for proteins which are known to adopt each individual fold?

Is https://www.rcsb.org/search/browse/scop suitable?

If there is a simple way provided to do this it is very well hidden. The tedious and stupid way to do 1 (get a list of folds) would seem to involve rolling your own:

Go to http://scop.berkeley.edu/ver=2.07 (or whatever is the latest version).

Click on each of the 12 classes in turn. e.g. (a) all alpha proteins will take you to http://scop.berkeley.edu/sunid=46456 .

Save the source of each page as text.

Write and run your own parser to pull out the sunid () from the http://scop.berkeley.edu/sunid= and the description line if you wish. (This assumes you program.) I think this sunid is the fold id.

If you can than find some database or table that has PDB and sunid values in it, you can write another program to find the answer to 2.
Alternatively… (appended January 2021)

Download dir.cla.scope.2.07-stable.txt (or the latest version)
Save as a text file.
Open in Mircorsoft Excel. (Just dragging onto the app icon formatted it properly on my Mac. Your mileage may vary.)
You can just select the column with the ids, paste into another sheet, and then remove duplicates to get all the different fold ids. (Alternatively, you have about 276,000 entries to do with whatever you wish.)

As this popped up again after about five years, and I have actually used this recently, I have added a non-programming method to get at the info, just using an Excel spreadsheet.

It looks like you can download the full database in SQL format or parse-able text files from here:  SCOP Download - Berkeley
The link has a link to the Schema as well:

Thanks for the answer, but it doesn't answer the question.  Being able to download the database doesn't help.  The schema might have been useful - except that none of the tables have around ~1400 rows, or at all mention folds/topologies in the table name or description.

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


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Why do we only initially feel the bending of a hair?
In my neurobiology class, my professor prompted us to take the tip of our pencil and fold or push down a single strand of hair on our arm or leg in the opposite direction that it grows in. He then commented on how we are able to detect the initial stimulus, but how after a while we no longer feel the hair being bent.
My question is thus, why does this occur? Why would we suddenly no longer be able to feel the stimulus of the hair being forced back?

Short answer
Touch receptors become unresponsive after continuous stimulation, a process called neural adaptation.
Background
There are various touch receptors in the skin (Fig. 1). One of them is the hair follicle receptor. These receptors form sensory nerve fibers that wrap around each hair bulb. Bending the hair stimulates the nerve endings.
All the afferent fibers of the skin receptors in the skin show neural adaptation. A rough classification of the various skin receptors is grouping them in rapidly and slowly adapting fibers.
Rapidly adapting fibers respond mainly to pressure changes. Typical examples are the Pacinian and Meissner's corpuscles, but also the hair follicle receptor.
Fig. 1. shows a static stimulation of the various receptors. Upon initial stimulation, the hair follicle receptor (Fig. 1a) vigorously fires action potentials. Because the hair follicle receptor rapidly adapts, however, it soon stops responding when the hair is continuously, statically bent in that same direction. Once the stimulus is removed it fires another volley of action potentials because the hair moves again.
In other words, the hair follicle receptor responds to strokes, stretch and skin vibrations, as it is a novelty detector; it detects change, just like Pacinian and Meissner's corpuscles do (Fig. 1b,c). This opposed to Merkel cells and Ruffini endings (Fig.1d,e) - these receptors are designed to continuously fire action potentials upon a static pressure stimulus (Fig. 1), although even these receptors eventually give up and become unresponsive.

Fig. 1. The skin receptors and neural adaptation. source: Delmas et al., (2011)
Reference
- Delmas et al., Nature Rev Neurosci (2011); 12: 139-15


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What is synaptic clearance?
Please explain what the term synaptic clearance means. For example, what would dopamine synaptic clearance be? It is important to me in context of dopamine signaling variation due to difference in synaptic clearence level.
Some gene alleles are associated with greater synaptic clearance in dopamine pathways. It used to explain dopamine level variation and throught it some brain areas activity (for example Nucleus Accumbens) difference among people with different genotypes. For more information see for example. Also, reduced synaptic clearence related to greater dopamine signaling levels. So I was interested in this term from prespective of brain activity in areas with dopamine receptors

We generally appreciate if you provide some background and show some of your own research effort. Background means some details on where you encountered this term. Background provides the context of the term  and helps in understanding its meaning (especially for not so popular terms). Research effort refers to any information that you were able to gather by searching the web or books.

Great.. Can you please add this to your question by editing it? Usually people would not go through the comments and secondly comments do not show up in searches. Finally, a question should be complete in itself.

"Synaptic clearance" is referring to the clearing of a neurotransmitter from a synaptic cleft.  A synapse is a place where one neuron can stimulate another neuron. The tiny gap between the neurons is called the synaptic cleft. The presynaptic (stimulating) neuron releases a neurotransmitter (such as dopamine) into the cleft and some of the neurotransmitter is recognized by receptors in the membrane of the postsynaptic (stimulated) neuron.  In order for the synapse to stimulate the postsynaptic neuron a second time, the concentration of the neurotransmitter in the cleft must be reduced to its original levels.  This reduction is called clearance, and can occur in several ways (mainly dependent on the type of neurotransmitter).  The neurotransmitter may be transported back into the presynaptic neuron for reuse; this is called reuptake.  The neurotransmitter may also be degraded (broken down chemically) into an inactive form.  To a lesser extent, neurotransmitter can also be absorbed by astrocytes or simply diffuse away out of the cleft.

It means what it says: clearance of neurotransmitters from the synaptic cleft. In case of DA it's mediated by DA transporters. They are there to shorten the response of DA, making the synapse ready for another signaling cycle. It also regenerates DA in case the transporters are located in the presynaptic neuron.
Reference
Ciliax, J Neurosci (1995); 75(3): 1714-23


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does life make or break?
Ok, this question seems like it may be impossible to answer, but would be interesting to see if anyone has an idea.
Throughout the course of a human life, do we make more molecular bonds than we break, or vice versa?

Metabolism ≈ Anabolism + catabolism
Metabolism is the set of all chemical reactions happening inside a living body. These reactions can either breaks down big molecules and build up big molecules. The set of reactions the breaks down big molecules is called catabolism. The set of reactions that build up big molecules is called anabolism.
Energy
Generally speaking, anabolism cost energy and catabolism yield energy. The molecule that is directly used to transfer this energy is Adenosine triphosphate (ATP).
Any energy transfer is coupled with some loss of energy from the system (see Energy conversion efficiency).
Entropy
For any chemical reactions, there is always an overall increase of entropy. As a consequence, a living organism increases the entropy in its surrounding. In other words, it breaks more than it builds.
Your question

does life make or break?

Life does both! But on average, it mainly breaks things up (just like any other chemical reaction).
Want to learn more?
The concepts of energy and entropy are studied in physics and chemistry but not so much in biology. I cannot really give you a good source of information.
Khan Academy offers a very good introductory course on metabolism (here), you should have a look!

that's a great answer, thankyou. But if the breaking of molecular bonds is endothermic, and life 'mainly breaks things up', does that mean life is negative entropy? http://www.masterorganicchemistry.com/2010/10/28/the-marriage-may-be-bad-but-the-divorce-still-costs-money/

My guess would be that, as complex organisms, we make more complex molecules than we break ---> net exothermic ---> entropy


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Describing trait evolution across a very small phylogenetic tree
I am very new to phylogenetic comparative methods but I want to explore the evolutionary patterns of a number of quantitative traits I have across a small sample (5) of closely related species (between .45mya and 4.3mya divergence). I am confident in the structure of the tree, but I only have phenotypic data for a small sample of the tree. I want to measure how correlated the evolution of the traits are across this small phylogeny and test the traits to neutral evolutionary models.
Should I even attempt this?  I know that there will be limits for what I can infer about evolution of these traits, but I’m not sure where to start in terms of identifying the specific weakness. I know it will depend closely on my trait measurements, some traits display notable divergence and others do not change much across the phylogeny.
Are there any approaches that would be useful for describing the evolutionary patterns for this small sample?  What references would be useful for convincing me to hold off until I have a larger phylogenetic sample?
Thanks in advance for any advice!

Welcome to Bio.SE! It's early in the morning for me and I'm having a little difficulty understand the question. You have 5 species and you want to build a tree. If there is a clear progression of the phenotype through the divergences then you could infer the history of the phenotype and maybe pin it down at a genetic level? I don't see why there would be any problem with this as a preliminary study whilst you wait for larger datasets.

Are you saying that you have phenotypic data for 5 species in a much larger phylogenetic tree? This will clearly limit the types of conclusions you can draw, and all conclusions will be extremely uncertain. As a first step, it would probably be useful to estimate the phylogenetic signal in the different traits (Bloomberg's K, Pagel's lambda), to see what you have to work with. Plotting the traits on the tree is also useful, but I assume that you've already done this.


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How long does a spiking signal last?
It is surprisingly hard to find information about the timing of neurons, in particular how long an action potential can contribute to the summation of a neuron. Is it on the order of milliseconds or rather seconds, i.e. for a neuron to fire, do many of the presynaptic neurons fire about at the same time?

I can answer the first part but I don't quite understand how your second part "do many of the presynaptic neurons fire about at the same time?" relate to it. Can you elaborate or clarify?

My thought was that if the falloff of the activation is very quick, then it would matter than many neurons have to fire within a brief time window to surpass the activation threshold.

Effective integration time of a typical neuron is in the order of 10-100 ms. You might want to look into this classic paper (read it with a critical mindset):

Shadlen, M. N. and Newsome, W. T. (1994). Noise, neural codes and cortical organization. Curr. Opin. Neurobiol., 4:569-579.

Or some biophysics book like:

Biophysics of Computation by Christof Koch

What is effective integration time? and what is a typical neuron? Do you mean a physical one or a modeled one?

@nico good questions. I should expand this answer at some point...

The length of an action potential (or spike) varies depending on several factors: refractory period, type of cell (interneurons tend to be faster) and where in the brain you are recording (in cortex both area and layer are important). Wikipedia page says something about 1ms for sodium based and 100ms for calcium based spikes.I never saw a 100ms AP, usually I record from cortex where I find AP in the range of ~1 to ~5ms.
The length of the integration however depends on too many factors, length of the dendritic tree, spatial location of the synapses, number of those synapses, strength, spine clustering, affinity and time constant of receptors, amount of Calcium, etc... the Shadlen and Newsome paper @Memming referred to is a good start. In general I'm always weary of magical numbers, if its a measurable phenomenon it's just what it is if not everithing comes with a lot of assumptions...

Thanks for this answers. Since you know about neuronal measurements in the cortex, you might perhaps also know an answer on this question on neural firing rates. Thanks again!


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What causes spontaneous muscle twitches?
Sometimes a small region of my body starts shaking, without any reason and then stops abruptly. Apparently this is a common phenomenon (source: NIH).  I researched its cause for a bit and came to know that it is because of nerve excitation.
Why do those nerves get spontaneously excited in the first place, without any conscious, voluntary, internal stimulus being presented?

Short answer
Spontaneous muscle twitches are thought to be caused by spontaneous activation of motoneurons controlling the muscles.
Background
Spontaneous muscle activity (twitching) is referred to as muscle fasciculations. Most commonly, they are benign, but they can be associated with certain pathologies too, such as ALS.
Fasciculations are thought to originate due to spontaneous activation of muscle fibers due to processes in the motoneurons. At the axonal endings there are synapses that junction onto the muscle. The axonal tips of motoneurons are thought to be highly sensitive to depolarization (electrical firing), which is what triggers acetylcholine release and muscle contraction.  The complicated process itself takes a small fraction of a second.  If any of this happens involuntarily, then the muscle fiber contracts spontaneously (source: ALS Association).
Specifically, it is thought that spontaneous depolarization of motoneurons are the cause of fasciculations. This decreased firing threshold can be the cause of disease, disrupted ion homeostasis in the body, fatigue, drugs and other causes (Blum & Rutkove, 2007).
Note that spontaneous / random activity in neurons is not only possible, it is quite common. Especially in neurons close to firing threshold, such as the motoneurons responsible for muscle activity, slight perturbations in ion concentrations inside or outside the cell can trigger an action potential. Further, channel opening is a stochastic process, meaning that even voltage-gated Na+ channels can open without a depolarization being present; although the chance is slim that will happen, it can statistically still happen. Stochastic processes like this can cause neurons to fire spontaneously, without a stimulus being present.
Reference
- Blum & Rutkove, The Clinical Neurophysiology Primer, Springer (2007)

So how does it happen involuntarily? Where do they get that stimulus from?

@Polisetty - There is no verifiable stimulus, inherent to spontaneous phenomena in general

@Polisetty - Some neurons happen to cross threshold for non-apparent reasons (local irritation causing surrounding tissue fluid electrolyte imbalance, for example.) Neuronal membranes do not always work predictably (unlike, say, gravity.) It happens all the time, all over the mody, and mostly it goes unnoticed because we become habituated to these minor glitches.

@Polisetty - I totally agree with anongoodnurse and I have added a paragraph to my answer. I hope this helps.


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What happens if there is a blood incompatibility during pregnancy?
There are possible combinations of blood types with the rH factors:

Rh factors are genetically determined. A baby may have the blood type and Rh factor of either parent, or a combination of both parents. Rh factors follow a common pattern of genetic inheritance. The Rh-positive gene is dominant (stronger) and even when paired with an Rh-negative gene, the positive gene takes over.
If a person has the genes + +, the Rh factor in the blood will be positive.
If a person has the genes + -, the Rh factor will also be positive.
If a person has the genes - -, the Rh factor will be negative.

I am aware that an infant receives one gene from the father and one from the mother, but what happens when the mother's Rh factor is negative and the newborn's is positive? What happens if the mother is O and the infant is A or B?
What happens within the placenta and to the maternal blood poles which are connected by open ended arterioles into intervillous spaces? Will the chorionic villi be "demolished" and exchange of materials isn't as possible?

Search erythroblastosis foetalis on Wikipedia

Little harm comes from ABO incompatibility (that would have been a major problem with reproduction.) Rh incompatibility is more dangerous, though.
If a fetus is Rh+ and the mother is Rh-, when there is mixing of maternal-fetal blood (at birth, but sometimes before that), the mother will form antibodies to the blood cell surface antigen. It doesn't usually affect the first baby (not sufficient antibodies), but if a subsequent baby is Rh+, there can be major consequences, which are multiplied with repeated exposure. Those maternal antibodies - which cross the placenta - can attack the fetal red blood cells and cause destruction of many of them (called hemolytic anemia) which, if severe enough, can be fatal to the fetus. It was a not-uncommon cause of fetal demise before Rhogam (Rh immune globulin) injections.
The immune globulin shots are given to women who are Rh- with Rh+ mates at a period before birth (before blood mixing), and immediately after birth if the child is Rh+. The antibodies bind with Rh+ antigens and "mask" the antigen from the mother's immune detection, so to speak, preventing the mother from making antibodies that can be used against subsequent pregnancies.
The major risk is to the fetal blood cells, not the placenta. The placenta isn't attacked. But with anemia, the fetus struggles, for example, without enough blood, the fetus can go into congestive heart failure and die.
It's also possible to form anti-Rh antibodies from blood transfusions. If an Rh- female has had a blood transfusion prior to her first pregnancy, maternal antibody levels will be drawn earlier during the pregnancy.
What Is Rh Incompatibility?

Thank you for your answer, the details you posed are very interesting. As a follow up question, is the Rh immune globulin injection affected by maternal sensitization? Would it be possible for anyone to be impervious to the Rh Shots?

I'm sure there are cases where the usual Rhogam shots were insufficient to protect against the formation of maternal antibodies, but that usually involves massive amounts of maternal-fetal blood mixing, not what would be the case with the vast majority of pregnancies. Rhogam has changed the outcome of literally countless pregnancies and is very, very effective, so I would not say anyone is "impervious". It's more a case of "has the mother enough antibodies to cover all the antigens she has been exposed to?"


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Are males taller than females in humans?
Is there any scientific evidence that in humans males are taller than females? And if so, what is the reason that they are taller (please include genes or hormones that accounts for human growth and how they are affected in males and females)?

I assume that you are talking about humans only, and would suggest to edit the question accordingly - I do not think this is entirely clear from the wording of the actual question. This is relevant, as in many other species, females are taller/bigger than males.

@Gerhard the question was migrated from the health website. My questions is comparing human males and females.

Ah, that explains it ;) But I'd suggest to edit the question anyways, eg. by using "women" and "men" instead.

Are males taller than females?
Best data I could find come from the Statistical Abstract of the United States (1999) > Section 3. Here is a table reporting the percentage of the male and female population which height is lower than a given threshold

Note that this data collection was done among students in US universities and is therefore not representative of the whole world or even the whole country.
Does height follow a bimodal distribution?
A difference in height between males and females is often used as a classical example in introductory statistic class to exemplify a bimodal distribution as seen in this picture

and on these (a priori fake) data

However, Schilling et al. 2002 argued that while the difference in mean height between the sexes is real, this difference is too small relative to the variance in height within each sex to be clearly depicted on a graph.
Note that I found this non-peer-reviewed paper which shows real data that display a truly bimodal distribution of height.

Genetics of height
The question why are they taller? is very broad. I will just focus to give you some hints about the genetics of height in humans. First, you want to make sure you understand the concept of heritability.
Evoy and Vissher 2009 report a heritability coefficient of 0.8. This estimate is impressively high - only a few phenotypic traits have such high heritability. They also review articles discussing that 50 loci are correlated with variation in height (actually, today, more than 500 loci are known to contribute to height, see the link in AlexDeLarge's comment to this answer). However, these loci are not sufficient to explain the whole heritability observed (common missing heritability issue). Yang et al. 2010 provide evidence that the remaining heritability is due to incomplete linkage
disequilibrium between causal variants and loci of weak effects. In short, height is a highly polygenic trait.
Related post
You should have a look at Is there a genetic reason explaining the difference of the height of male and female? for more information.

+1 for the answer to the first part of the question, but the second needs work; differences in height due to sex are probably primarily due to development rather than genetics (males and females are fairly well-mixed populations...). This paper describes one developmental mechanism (sex-based differences in GH-dependent STAT5b regulation of IGF-I expression): http://www.ncbi.nlm.nih.gov/pubmed/15506072. It also discusses selective pressures for sexual dimorphism in humans versus other species, which could be another part of the answer to the "reasons" part of the question.

@shnisaka: You might also want to take a look at my answer to this question about the genetic basis for height difference in human males and females.

@AlexDeLarge Thanks for the link. I added it to the answer.


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How's the membrane potential restored to resting state after hyper polarisation?
I have known for so long that Na+/ K+ pump restores the membrane potential. But as it pumps in 2 K+ for every 3+ Na+ moving out how can it make the membrane potential less negative when the net result is one positive charged ion moving out?

If you see a normal AP curve, you would be able to appreciate that the membrane potential is generally brought back - which is around -70mV. So the potential doesnt matter much since its restored by the ion fluxes. What matters most is the ion composition on either side. You might see that after depolarization, Na+ came in (it generally satys out) and after hyperpolarization K+ came in. The potential is safe but the distribution is altered. This is what the pump takes care of, not the potential (although slightly electrogenic)

The Na,K-ATPase restores negative membrane potentials.  When a cell is hyperpolarized, leaky K+ channels take care of that. Leaky K+ channels are always open. Generally, K+ has the tendency to diffuse back out of the cell along its chemical gradient through leaky K+ channels, after been pumped in, making the cell's inside more negative. However, in the reverse situation, where the cell is hyperpolarized, they may flow inwards, along the electrical gradient.
Note that while the Na,K-ATPase is indeed the driving force behind the membrane potential, it is not the direct consequence of the ratio of Na+ being pumped out and K+ being pumped into the cell. It is the leaky K+ channels that determine the membrane potential largely, together with the Na+ channels being permanently closed, except when an action potential is generated.
Suggested further readings
- What keeps the resting potential of neurons constant at -70 mV?
- If the average resting potential of a neuron is -70 mV, why is there such a high ratio of potassium ions inside relative to out?


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Why is it always Sodium that we talk of in blood pressure?
Why is that we emphasize so much on sodium in blood pressure? I understand that it is a major extracellular ion, but, it also is tightly regulated. So when something is that tightly regulated, won't small concentrations of the potassium matter? And what about the chloride and bicarb? They are all there in the blood in comparable quantities but we never talk of their osmotic importance. Sodium retention and blood pressure - why not chloride retention?
Is it not required (like calculating sodium includes them too)?
or is it that they actually don't matter?
Also aldosterone, we conserve the sodium but aren't we pushing out potassium? Potassium also is an ion with oncotic activity right? Why is Natriuresis so important why not say, Chloriuresis?
So all in all, why does sodium steal the limelight?

The key is in fluid compartments and osmotic activity. For the purposes of this discussion, let us say that there are two fluid compartments the ExtraCellular Fluid (ECF) and IntraCellular Fluid (ICF). Only the ECF contributes to blood volume and blood pressure.
Na is not only the major ECF ion, but it is also confined there. The ICF concentration of Na is much lower than in the ECF, and it is continuously, invariably and actively kept out of the ICF. In other words, the vast majority of ingested Na ends up in the ECF, and drag the associated amount of water (ie volume, thereby increasing blood pressure). It is the opposite for K, which is mainly in the ICF. As for Cl, it is more or less equal in the ICF and ECF, and is allowed to move freely between them, meaning that you need to ingest twice as much as a given amount of Na for a similar effect on volume distribution. Bicarb is a minor ion, and moves freely between compartments. These are the reasons why, clinically, if someone is hypovolemic (ie dehydrated, losing blood) they are given a sodium based fluid or a protein based fluid (colloid), because both will drag volume and stay in the ECF.
As for the other part of your question, isn't it tightly regulated? Yes, but extra sodium takes some time to get excreted (much less than 1% of sodium that goes through the kidneys is excreted). In other words, any extra sodium (i.e. extra volume as we have established) will stay there for some time, and if you are continually having high sodium meals, every day, you will walk around with extra sodium most of the time. Therefore, your blood pressure will be higher than it would be, if your diet was lower in sodium.
So, no, sodium is not stealing the spotlight from anyone when it comes to ECF. But the other ions have their glory under other spotlights.


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Does Alzheimer affect more than day-to-day memory?
I know that Alzheimer's damages a part of the brain called the hippocampus, which has a central role in day-to-day memory.
But, could it affect also on things in other memory centers, things such as taste and moves?

Oh, yes, though short-term memory loss is often an early sign.
"For many, decline in non-memory aspects of cognition, such as word-finding, vision/spatial issues, and impaired reasoning or judgment, may signal the very early stages of Alzheimer’s disease."  from https://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet.  Warning: grim.
Whatever your brain does, Altzheimer's eventually undoes.  For more details:  http://www.alzheimers.net/stages-of-alzheimers-disease/

"For more details:www.alzheimers...". Just in case the link goes dead, could you summarize those details.


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Is Zika suspected of causing birth defects only if contracted during pregnancy?
There seems to be growing evidence that a recently spreading strain of Zika virus is in fact linked to microencephaly and other birth defects in newborns (see here, here, and here for examples).
I understand that this is currently an active area of research and a number of questions remain unanswered. However, even given the current uncertainties, I feel any discussion about when a mother gets infected has been largely ignored by all of the news/media/science outlets I've seen.
My question is: does the virus lead to birth defects only if the mother gets infected during pregnancy, or can a previous (or latent) infection lead to similar birth defects? If the former, does timing of infection during different trimesters matter?

sources suggesting support for either case would be nice, too, in the absence of yet published rigorous support...

Related http://biology.stackexchange.com/questions/43050/how-long-do-viruses-such-as-zika-stay-in-the-body

As you mentioned, there is evidence that mother-child transmission of Zika virus causes congenital anomalies like microencephaly.
Now your question, if a cleared infection before the pregnancy could affect it? In principle, no. Once the virus is cleared, it should not reactivate, unless there is reinfection. Here's a quote from the Zika article from Uptodate.com:

Women of childbearing potential — It is uncertain how long women of childbearing potential should wait between Zika virus exposure/infection and conception. Most pregnant women with Zika virus exposure give birth to normal infants [111]. Zika virus usually remains in the blood of an infected person for a few days to a week, and thus far there is no evidence that a fetus conceived after the virus has cleared from the blood would be at risk for Zika infection [94,112]. However, information regarding the persistence of Zika virus following infection is not known. It has been suggested that infection due to other flaviviruses such as West Nile virus may persist years after initial infection [113-115]; these data are controversial. Pending further study, healthcare providers should encourage women to make such decisions based on their individual circumstances, values, and preferences.
Daniel J Sexton, MD
  Editor-in-Chief — Infectious Diseases Section
  Editor — Bacterial Infections
  Professor of Medicine
  Duke University Medical Center

Citing whole sections is discouraged.

@Christiaan Except all of it is relevant, and answers directly the question

There are citations to unmentioned sources and its better to synthesize an answer rather than reproducing it. The info is good,  it's just the way it's presented.

Could you also provide a link to the article and expand on points it makes

@rg255 I would like to, but the article is not accessible for free, I can only access it because of my University affiliation. But here's the link: http://www.uptodate.com/contents/zika-virus-infection


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Does the species of snake that eats Amphidromous inversus have chiral dimorphism?
From what I read at Schilthuizen and Davison (2005), Amphidromous inversus is a species of snail that occurs in 2 forms that are nearly mirror images of each other occurring in nearly equal proportions. I don't see any way that could be evolutionary stable if it was only eaten by snakes with a symmetrical jaw because then the snake species would evolve to be ambidextrous and then the snails would lose the selection pressure for being the rarer form but retain the selection pressure for the more common form. I can't find the information anywhere on the internet of what the snake species that eats that species of snail looks like. Have observations shown that that species of snake has a chiral jaw and occurs in 2 forms that are mirror images of each other in nearly equal proportions?

I don't know much about this particular species of snake but here are some info that may help.
What do we mean by right-handed snakes?
I doubt that in this context a snake could be ambidextrous. What they call handedness in these snakes (Pereatids) concerns the density and size of teeth on each side of the jaw (pictures from Hoso et al. (2010))

This asymmetry helps them to forage on snails.

Here is how they describe the snake feeding behaviour.

The Japanese pareatid, P iwasakii, strikes an exposed soft
  part of a crawling snail from behind at a determined leftward angle
  to grasp the ventral shell surface with the upper jaw and the soft
  body by inserting the mandibles into the aperture. The snake then
  extracts the soft body by alternately protracting and retracting the
  asymmetric right and left mandibles.

On the figure below, the individual on the left is sinistral and the individual on the right is dextral. Note by the way that snails of different chirality have a hard time to mate together.

"Right-handed" snakes can easily forage on dextral snails (the most common and ancestral form), while they have a hard time to forage on dextral snails. Hoso et al. (2010) reports a survival probability of 0% for dextral snails and 87% for sinistral snails.
Left-handed snakes
Hoso et al. (2007) report that "left-handed" snakes have never been found in south-east Asia. This is surprising as noted by Hoso et al. (2010). Even in areas where sinistral snails are relatively common, all snakes were "right-handed".
They do not suggest any potential explanation for this lack of "left-handed" snakes but one could speculate that "handedness" in snakes might be under other selection pressures than those related to foraging. It is also possible that intermediate forms are deleterious and that mutation of large enough effect are rare. It is possible that the genetic variance for handedness is just not present. It is possible that even if in some areas there are more sinistral species of snails than dextral species, the abundance of dextral is still higher and therefore, there is no selection for switching to being right-handed.


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Coagulation of blood in small intestine due to trypsin
Trypsin is secreted in the small intestine to convert proteins into dipeptides i.e. to carry out digestion of proteins. However, it is also a coagulating agent which coagulates blood by hydrolysing fibrinogen into fibrin. My question is, why doesn't the blood in the small intestine coagulate?

Remember trypsin is an intraluminal enzyme, and is not normally in contact with blood.


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What are calories and how to burn them?
What exactly is a calorie? When burning calories, do we always lose fat?
I have tried many apps to measure calories, do they give exact amounts? How many calories should be taken a day?

I'm voting to close this question as off-topic because  the latter part of the question is off topic (try sports or health SE) and the first questions show no research effort, and calorie is chemistry, - read on calories and ask about what you are unsure of.

A calorie is a measure of energy. In nutrition, we usually mean the kilocalorie (kcal), which is the same as about 4.2 kJ (kilojoule). A average person needs about 2,000--2,500 kcal per day, but this of course varies quite a bit between people, depending on size (muscle mass, particularly) and level of physical activity (physical work, exercise).
Nutrition guidelines found on the labels of food products give a pretty good summary of the amount of energy they contain. I'm not sure what applications you have been using, but they most likely rely on the same basic data, so the values should be similar. You can use these values to figure out roughly what your calorie intake is, and to spot very calorie-rich foods. But counting calories exactly is actually quite difficult --- you need to carefully weigh everything you eat and keep track of lots of numbers, and it's easy to make mistakes.
Burning calories does not always mean burning fat. Fat is a long-term energy storage form in the body. When exercising, the body tends to burn stored carbohydrates (glycogen) first, and turns to burning fat when carbohydrates are exhausted. Therefore, prolonged, low-intensity exercise like long walks are usually better for burning fat than short "sprint" type of exercise. The body also burns fat during normal daily activity if your energy intake is lower than the daily need (when dieting). But it is also possible that some muscle mass is degraded (to amino acids) and used for energy as well.
See also Wikipedia articles on food energy and exercise. Please note that "how to burn calories" is a heavily debated issue, there is an entire industry of weight loss methods, and various claims about "easy" methods or products to lose weight quickly are generally not true. The only reliable method to lose weight is to reduce food intake and increase exercise, for a long period of time.


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Could You Boil Water from Blood?
According to Wikipedia...

About 55% of blood is blood plasma, a fluid that is the blood's liquid
  medium, which by itself is straw-yellow in color. The blood plasma
  volume totals of 2.7–3.0 liters (2.8–3.2 quarts) in an average human.
  It is essentially an aqueous solution containing 92% water, 8% blood
  plasma proteins, and trace amounts of other materials.

Does this mean it would be possible to boil water from blood for consumption? For example, in The Walking Dead, Rick and the gang are dehydrated and without water. When a pack of wild dogs confronts them, they kill them and cook them for consumption. Could they have collected the blood, boiled it, and used some sort of contraption to catch the clean, vaporized water?

It seems possible, vaporization can work for this.

This question doesn't make sense. Any substance that contains water can be vaporised and the water later distilled.

@MarchHo I agree with you, but I am still impressed by how Zulfe could think about this disgusting but interesting topic ;)

I'm voting to close this question as off-topic

Seems ok to me. It's framed properly in a biological context

This question is rather about chemistry and methods to seperate water from other liquid. Distillation is probably the solution indeed.


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Is dextrocardia congenital?
Dextrocardia is displacement of human heart to the right side. Does it occur during the life span of a human being or right from birth?

A simple google search gives your answer "Dextrocardia is a rare heart condition in which your heart points toward the right side of your chest instead of the left side. Dextrocardia is congenital, which means people are born with this abnormality."

Oops... never knew this.... thanks for telling me....

As the comments pointed out, this is not a hard question to answer with some research, but I'll add a few more details.
Dextrocardia is congenital. The human heart normally actually isn't so much on the left side - it's more pointed towards the left. In dextrocardia it points more towards the right side. This develops within the first few weeks of embryonic development, as the heart is one of the first organs to develop.

Source
It occurs in about 0.7 percent of live births and 2.7 percent of stillbirths, indicating that there are health problems in the fetus associated with it. After birth, it's possible that the heart functions perfectly fine, but often there are other heart defects associated with dextrocardia.
Dextrocardia with situs inversus is a condition in which the heart and visceral  organs are reversed. As for the cause, it's genetic and follows a recessive inheritance pattern, meaning both parents need to be carriers, but don't necessarily have the condition.


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Why is DNA double stranded and RNA single stranded?
Why is DNA present as a double helix structure and RNA as a single helix? What causes the difference between them? What are the practical physiological differences between dsDNA and ssRNA? How are the key biophysicochemical features responsible for those differences? What is the role of these differences? Also, why is DNA preferred over RNA as the genetic material?

where is your question?

why the DNA double helix and RNA single? What make the difference between them? why they are not the same? what the role of the differences?

Though these are too many questions, and these are all too basic, I will post an answer. Please edit your question to make it easier to understand.

I don't have any problem with answer of question all them perfect. thank you

answer of this question I wanted (Why is DNA preferred over RNA as genetic material?) and you answer

I have added this also in my answer.

Though this is a basic question (a few google searches will provide all answers) and you have asked a lot of questions, I shall answer them one-by-one.

Why is RNA single stranded (and not double stranded like DNA)?

dsRNA is less stable than dsDNA.  See this: http://en.wikipedia.org/wiki/RNA#Structure. An important structural feature of RNA that distinguishes it from DNA is the presence of a hydroxyl group at the 2' position of the ribose sugar. The presence of this functional group causes the helix to adopt the A-form geometry rather than the B-form most commonly observed in DNA. This results in a very deep and narrow major groove and a shallow and wide minor groove. A second consequence of the presence of the 2'-hydroxyl group is that in conformationally flexible regions of an RNA molecule (that is, not involved in formation of a double helix), it can chemically attack the adjacent phosphodiester bond to cleave the backbone.
RNAses are very common.  Most critically, in biological systems, the presence of dsRNA is a signal of viruses and active transposable elements, so ssRNA is an easy way for the host cell to distinguish foreign elements.  Yes, that was an oversimplification and ignored functional dsRNA, but even then, dsRNA likely evolved from systems to foreign elements.1

Why is DNA double stranded (and not single stranded like RNA)?

Firstly, the 'information' part of DNA is the nitrogenous base, as opposed to the pentose sugar or the phosphate residues. In a single-stranded molecule, this important part would be exposed to the cellular environment, providing more opportunity for it to be mutated by the various chemicals there. In a double-stranded configuration, however, the two nitrogenous bases are locked within the complex, facing each other in the centre of the molecule. This organisation helps to safeguard them from local mutagens.
Secondly, having two complementary strands facing each other fundamentally means having two copies of the same thing placed right next to each other. This allows for proof-reading. George C. Williams summarised this beautifully in his pithy passage (from "The Pony Fish's Glow" (1997)) (recall that adenine [A] on one strand should always bind to a thymine [T] on the complementary strand, and visa versa; likewise cytosine [C] always binds to guanine [G], and vice versa i.e. Charagaff's rule).2

Source

What is the difference between DNA and RNA?

A complete table of differences can be found here (sadly I can't create a table in markdown) along with this image:

How are roles of DNA and RNA different?

RNA has several different functions that, though all interconnected, vary slightly depending on the type. There are three main types of RNA:

Messenger RNA (mRNA) transcribes genetic information from the DNA found in a cell's nucleus, and then carries this information to the cell's cytoplasm and ribosome.
Transfer RNA (tRNA) is found in a cell's cytoplasm and is closely related to mRNA as its helper. tRNA literally transfers amino acids, the core components of proteins, to the mRNA in a ribosome.
Ribosomal RNA (rRNA) is found in a cell's cytoplasm. In the ribosome, it takes mRNA and tRNA and translates the information they provide. From this information, it "learns" whether it should create, or synthesize, a polypeptide or protein.

DNA's genes are expressed, or manifested, through the proteins that its nucleotides produce with the help of RNA. Traits (phenotypes) come from which proteins are made and which are switched on or off. The information found in DNA determines which traits are to be created, activated, or deactivated, while the various forms of RNA do the work.3
EDIT- As you've asked another question in comments, I will add it here:

Why is DNA preferred over RNA as genetic material?

DNA offered several advantages over RNA so was chosen by natural selection to represent higher beings:

DNA was chemically more stable than RNA so it was possible to maintain greater length of DNA in comparison to RNA. RNA has hydroxyl group (OH) present on the 2’ carbon. This hydroxyl group invites hydrolysis reaction and so it was not possible to maintain long length RNA molecule. This hydroxyl group was absent in DNA leading to stability of DNA molecule.
DNA was more capable in handling self-repair during replication process due to the presence of Thymine instead of Uracil. It was due to the fact that often cytosine was changed into uracil due to the deamination. Now in case of RNA it was impossible for cell to know if uracil should be present there or not but in DNA since Uracil is not all present so it was quite easy to identify the error and rectify that.
DNA also offers more information security because of the double helical structure.4

A comparison of molecular structure of DNA and RNA from here

References:

https://www.quora.com/Why-is-RNA-single-stranded-in-general-and-not-double-stranded-like-DNA
http://medicguide.blogspot.in/2008/07/why-is-dna-double-stranded-but-rna.html
http://www.diffen.com/difference/DNA_vs_RNA
https://www.quora.com/Why-was-DNA-chosen-to-be-the-genetic-material-instead-of-RNA
http://www.atdbio.com/content/2/Molecular-weight-and-mass

Thank you and But I'm wondering Wallis There is a big role for the Commission in the DNA of synthetic significant role in storing information more than the RNA

yes it help me.  I want the exact image, Does DNA structure advantage in the information stored than the RNA?

I'm sorry about my language

dsRNA is less stable than dsDNA..Not really true.. in fact, dsRNA hybridizes more strongly. RNA, in general is chemically unstable. Nothing specific to dsRNA.

@wysiwyg oh I actually meant dsRNA being recognized by RNases. Seems like I mixed two points up. I'll edit it when I get some time :)


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Are there any major noticeable limitations to genome sequence compression methods that use reference templates?
Recently, I have been researching about big data analytics in biochemistry, and started wondering about how genome sequence compression could affect analysis.
Of all the method listed on the Wikipedia page, the reference template method is my favourite as, it not only seems effective, but also was the idea that popped into my head before I did any study regarding this topic.
But, before I implement it in a project I am working on, I wanted to know if there are any common and obvious drawbacks/limitations that the bioinformatics industry faces quite often when using this scheme.

This question is possibly a better fit for bioinformatics.stackexchange.com

I’m voting to close this question because it isn't about biology as defined in the [help], isn't clear (what compression method), and shows evidence for a complete lack of prior research.

The biggest drawback is that reference template cannot address the question of genome sequence compression. It addresses variant information compression.
Granted, a lot of the interest in genomics has been addressed towards variants, basically because they are easier to analyze than actual whole genomes. Additionally, when many people say "genomics" or "genome sequence" what they mean is "human genomic variation", basically because there is more money to be made with human genomics than with other genomes; and therefore most people are really talking about human genomic variants when they talk about "genomes".
Even in the variant case, templating approaches stop working very well when you have structural variants of the genome, or at least they become extremely complex. More recent advances like genome graphs can address some of the biggest issues, such as structural variants, but they still have not very well defined (AFAIK) limits in terms of how divergent the genomes can be before they break down.
But leaving that aside, any two sufficiently divergent genomes cannot be compressed by the reference template method or by graphs. The number of differences becomes so large that it is ludicrous to record the differences between the genomes, as that information can end up being larger than just recording the two full genomes and compressing them independently. This becomes clear if you consider trying to compress a Drosophila and a Saccharomyces genome together, or even very closely related genome sequences such as human and chimpanzee, which have: "...approximately thirty-five million single-nucleotide changes, five million insertion/deletion events, and various chromosomal rearrangements."
At that degree of divergence, it is much easier and almost certainly more space conscious to just separately represent the two genome sequences and compress them independently. For a review of tools in this space, you can see here.

The most obvious drawback of the reference template method is that if you use it, you've already analysed data.
Usually, you get data from wet biologists. They sequence samples and upload sequences to a server. Often an uploading process is already automated. If you sequence in-house, the data is already on your server. If not - biologists do not want to do an extra job. Moreover, if it is not a big project you do not have that much data that transferring and storing it is the problem. So you'll get the data as *.fastq.gz files.
Then you make QC, align reads and make an SNV-calling or expression analysis or whatever you want. Aligning and SNV-calling could be painful, complicated (Copy Number Variation, heterozygosity etc) and time-consuming. It is the problem. Resulting data usually is stored as Variant Call Format (VCF). Under the influence of CRAM and 1K Genome Project which uses it, VCF has been developed.


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Why does our body regulate metabolic processes using the thyroid hormone?
People with hypothyroidism do fine when taking medication containing their daily dose of thyroid hormone. This means that the signaling function of the thyroid hormones is, in principle, unnecessary. If a constant signal would do, then there is no need for that signal in the first place, as you could just by default switch on whatever process is now switched on by the thyroid hormone. So, what's the whole point of regulating metabolism via the thyroid hormone, especially considering that it predisposes us to thyroid disease?

Because it evolved that way, and there was not a significant evolutionary pressure to change it?  And possibly not a mechanism to allow the change, once humans' distant ancestor had evolved a proto-thyroid.

@Count I disagree slightly with "...the signaling function of the thyroid hormones is, in principle, unnecessary..." Thyroid hormone (T4 - aka "Thyroxine") has a half-life of 4-5 DAYS. It is essentially a constant level in the circulating plasma that is important - this is why patients with hypothyroidism that take exogenous T4 do fine. It doesn't have anything to do with T4 not being important biologically. If you take exogenous thyroid hormone away from someone with hypothyroidism or who has had their thyroid removed surgically, once their plasma T4/T3 is gone they do horribly.

The answer is in special situations, where a trade-off has to be done between thermogenesis and energy saving. This applies to hibernation of animals as well as to critical illness in humans.
This kind of adaptation is referred to as TACITUS syndrome (thyroid allostasis in critical illness, tumours, uraemia and starvation), NTIS (non-thyroidal illness syndrome) or ESS (euthyroid sick syndrome). In this situation, total and free T3 are downregulated, and, in special cases, TSH and T4, too. See an open review article by Wajner and Maja, which is available from http://dx.doi.org/10.3389/fendo.2012.00008 , for details.