text:
Why are the genomes of Humans 99.5% the same?
Human's DNA sequence is said to be roughly 99.5% equal. As far as I understand, this means that if I walked up to you and compared our DNA, the sequence of base pairs would be 99.5% the same.
My question is: Why is there only 0.5% variation in our DNA? I can think of two reasons:

For some reason, the other 99.5% (roughly) is locked in place. These sections, if changed, either result in us not being 'human', or simply get some sort of genetic disease and so aren't very good mutations.
There hasn't been enough time. I remember hearing that all humans have a common ancestor some long time ago. If that's the case, perhaps over time only about 0.5% of our DNA has had time to randomly mutate, and if we wait a really really really long time, more and more of our DNA will mutate, and we will become 'less like each other'.

Or am I completely misunderstanding the situation? I didn't take biology in high school so answers should be simple please.

A complete answer will need to go quite in depth into the field of population genetics and it will take time to give the introductory knowledge necessary. But shortly, the answer is definitely not 1. and is pretty close to 2 :)

@Remi.b Thanks for quick insight, would you happen to know where I could get online resources to start learning about population genetics? (or anything that might help me understand this better)

It is a little frustrating to receive as answer "just learn more", but you can find book recommendations in population genetics here. You might first want to follow an introductory course to evolutionary biology such as Understanding Evolution (free online ressource).

@JoshuaLin I am not sure if you are notified to edits to answers. I made some substantial additions to my answer to provide more detail, to hopefully address different details of your question,

In a genome that is 3 billion base pairs, a difference of 0.5% works out to a difference of 15 million bases. When a single base change can change the amino acid sequence of a protein, that can add up to a huge amount of diversity, which is what we see over the nearly 8 billion humans on the planet, and the 99.5% sameness is why we are linked together so closely as a species.
How can the lack of diversity be explained?

Nothing in Biology Makes Sense Except in the Light of Evolution.

The above quote was made by the evolutionary biologist Theodosius Dobzhansky. What this basically means is that you need to take a look at your question from the perspective of evolution and natural selection.
The first thing you need to note is that there is evidence to suggest that modern humans went through a population bottleneck. What that means is that at a certain point in our history, there were very few individual members of our species alive and this can account for the "lack" of diversity that we see in our genome. The number that is quoted is as low as 10,000 individuals left alive after the supereruption of the Toba volcano about 75 thousand years ago.
That means that there were very few mating pairs left, and that significantly reduced the genetic diversity of our species. This is known as Founder Effect.

Founder effects
A founder effect occurs when a new colony is started by a few members of the original population. This small population size means that the colony may have:

reduced genetic variation from the original population.
a non-random sample of the genes in the original population.

So if we use an average of 20 to 25 years per human generation, we are only looking at about 3,000 to 4,000 generations since there were maybe only a few thousand breeding pairs of humans. Contrast that with bacteria which can go through three to four thousand generations in less than a week, and you can begin to get a feel for why there is so much sequence homology (sameness) in the human genome. See Bottlenecks and founder effects at UC Berkley's Understanding Evolution site for more information.
You also should understand that any changes that are deleterious will be under strong selective pressure. This may not mean that the organism may not survive to reproduce, in may just mean that on average, they may be less successful; fewer offspring that have fewer offspring in comparison to the rest of the population. At some point that lineage may go extinct, either because the change makes it very difficult to survive, or the offspring make less desirable mates and eventually don't get the opportunity to reproduce.
Any changes that disrupt a vital gene will likely be fatal and will lead to spontaneous abortion or if the mutation was sustained in a sperm, then the inability of that sperm to survive to fertilize an egg, so the sperm that was heavily mutated may just never make it to the egg. The average number of sperm in a single human ejaculation is about 250 million. And yet only a single sperm makes it to fertilize the egg, and that is assuming that a fertilization event takes place. There is an incredible amount of selection that goes on in the act of procreation, even before we get to development.
Why the 99.5% to 0.5% figure might be misrepresentative of the population as a whole.
Another thing that you will want to think about is how the 0.5% to 99.5% number was arrived at. The referenced in the question links to a Wikipedia article Human Genetic Variation. The reference provided for this was from a New York Times article about J. Craig Venter, In the Genome Race, the Sequel Is Personal - Wade, Nicholas. September 4, 2007. The quote that is references in Wikipedia is:

Biologists had estimated that two individuals would be identical in 99.9 percent of their DNA, but the true figure now emerges as much less, around 99.5 percent, Dr. Scherer said.

The 0.5% figure is provided as a quote from Stephen W. Scherer, who was a coauthor of this paper, The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007. DOI: 10.1371/journal.pbio.0050254. From that paper the following quote is found:

Inclusion of insertion and deletion genetic variation into our estimates of interchromosomal difference reveals that only 99.5% similarity exists between the two chromosomal copies of an individual and that genetic variation between two individuals is as much as five times higher than previously estimated.
- The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

So at the very least, the statement was made in a peer reviewed article. However there are some problems with this.
The first is the method of the paper. It looks at a single human genome, that of Dr. Venter, and is used to draw the conclusion of 0.5% difference between any two individuals. And the comparison is made based on the analysis of differences between Dr. Venter's maternal chromosomes and paternal chromosomes. Let's look at what the problems might be here:

It is a huge leap of statistical faith to assume that a single genome is representative of the nearly 8 billion genomes out there.
Dr. Venter's genealogy is English on both parental lineages. We have to remember that there was another population bottleneck in middle ages Europe caused by outbreaks of cholera and the Black Death. This fact may imply that Dr. Venter's lineages are genetically close and that if his lineage were more diverse, say Indigenous Oceanian and English, they may have found a much higher percent difference between maternal and paternal chromosomes.

The donor's three-generation pedigree is shown in Figure 1A. The donor has three siblings and one biological son, his father died at age 59 of sudden cardiac arrest. There are documented cases of family members with chronic disease including hypertension and ovarian and skin cancer. According to the genealogical record, the donor's ancestors can be traced back to 1821 (paternal) and the 1700s (maternal) in England. Genotyping and cluster analysis of 750 unique SNP loci discovered through this project support that the donor is indeed 99.5% similar to individuals of European descent (Figure 1B), consistent with self-reporting.
- The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

Dr. Venter is male. The Y-chromosome was problematic to sequence, and you cannot really do a comparison between it and the X-chromosome. How would the genome of a woman compare?

The Y chromosome is 59% covered by the one-to-one mapping due to difficulties when producing comparison between repeat rich chromosomes. In addition, the Y chromosome is more poorly covered because of the difficulties in assembling complex regions with sequencing depth of coverage only half that of the autosomal portion of the genome. The X chromosome coverage with HuRef scaffolds is at 95.2%, which is typical of the coverage level of autosomes (mean 98.3% using runs). However it is clear that the X chromosome has more gaps, as evidenced by the coverage with matches (89.4%) compared with the mean coverage of autosomes using matches (97.1%). The overall effects of lower sequence coverage on chromosomes X and Y are clearly evident as a sharp increase in number of gaps per unit length and shorter scaffolds compared to the autosomes (Figure 3). Similarity between the sex chromosomes is another source of assembly and mapping difficulties. For example, there is a 1.5-Mb scaffold that maps equally well to identical regions of the X and Y chromosomes and therefore cannot be uniquely mapped to either (see Materials and Methods and Figure 3). From our one-to-one mapping data, we are also able to detect the enrichment of large segmental duplications 10 on Chromosomes 9, 16, and 22, resulting in reduced coverage based on difficulties in assembly and mapping (Table S3).
- The Diploid Genome Sequence of an Individual Human, Levy, et.al. PLoS Biology; September 4, 2007.DOI: 10.1371/journal.pbio.0050254

There is another thing that you need to remember and that is the history of the Human Genome Project. Dr. Venter developed a new method of sequencing and became a commercial competitor to the International Human Genome Sequencing Consortium project. While the International Human Genome Sequencing Consortium project beat out Dr. Venter's enterprise(8), it's approach, to use an amalgamation of the DNA of many donors, some of whom had their DNA included and some who did not, to preserve anonymity, Dr. Venter circumvented this by performing the sequencing on his own DNA. When his team was beat out by the International Human Genome Sequencing Consortium, he doubled-down, invested more time and effort and came up with the sequence put forth in this paper, which had a higher degree of resolution than previous efforts. The paper is making an argument for the value of their technique over the techniques being used by the International Human Genome Sequencing Consortium and is trying to make a claim of the superiority of their method. The data being presented is likely factual, but because of this history you have to look at the paper, the methods, and the motives behind it.
It is only 15.5 years since we had a full draft of a Human Genome Project produced by the International Human Genome Sequencing Consortium. In order to sequence that genome samples were taken from a few hundred individuals. Small stretches of the DNA were sequenced and then all of those pieces were put together in computer. That means that there was a lot of averaging that happened. So by default, the most prevalent base in the population of volunteers at every position was chosen. That means that that should be representative for the rest of the population as well.
When we make statements about comparisons in datasets as large as the human genome, more often than not we are looking at known, small subsets of the genome, and we are extrapolating by statistical methods based on that fact. One thing you learn as you read science papers, and not just science news articles, is that you always need to look at their materials and methods to determine how they arrived at their data and headline numbers. It is often quoted that we have only a 1.5% difference between Humans and Chimpanzees, however when you look at those papers the comparisons were done only on areas of the genomes that lined up well. That isn't to say that there isn't a remarkable degree of similarity between us and our nearest living evolutionary relative, it is just that there is more to the story than the headline.
Also, we don't have that many full genomes sequenced to compare to one another, as a percentage of the 8 billion people alive today. While we have representations from most a vast majority of the ethnic groups identified, we may be missing families with novel lineages.
Another thing that you need to think about is that many of the areas in the human genome are repeats and structural elements that do not encode for genes of affect gene expression. Things like telomeres, which protect the ends of chromosomes, and centromeres which are the attachment points on chromosomes that make sure that the are distributed properly into newly divided cells. These elements tend to stay the same because the proteins that bind to them require that sequence specificity in order to function properly, so those are regions were almost every ones DNA will be the same, and not just between humans. These elements often are very similar in most vertebrates.
We also need to consider structural RNAs. These molecules have functions within the cell that require that there sequences be highly conserved (unchanged). Ribosomal RNAs, Transfer RNAs, Small Nuclear RNAs all rely on their specific sequence to fold properly in order to perform their task in the cell. A single base change can change the folding of these elements and as a result they will loose their function, which means those cells won't be able to produce proteins properly which means that the cells will die. If this is happening in germline cells, then they are not going to be involved in fertilization so any mutations there will be passed on.
I could go on and on, but the take away is that it isn't surprising that there is very little sequence diversity on a percentage bases within the human species, but there are many caveats to that fact as well.
Edit: Significant edits to add relevant, referenced information to back up answer.

I want to create more accounts so I can upvote this answer more.

@Nathan I appreciate the sentiment, I am simply glad you found it informative.

I would like to comment that out of the 150 million differences only a tiny fraction change protein sequence in a meaningful way. First, because protein coding sequences are 1.5% of the genome. Second, a random amino acid change in a protein is very unlikely to have a functional effect. Third, because changes that affect function may potentially be selected against. So the actual number of functional differences much smaller (I am guessing ~100000 or less).

@Bitwise I think you should read that paragraph again. I don't say that it leads to 150 million changes, I say that because only a single base change can change an amino acid sequence, that can add up to a significant difference. The point was that you need very few differences to come up with a large amount of variety between individuals. What you are saying about functional change isn't quite right. You can have a "Silent" mutation in a gene, but if it is such that the tRNA is encoded at a factor of 10 or 100 less that the original tRNA, then you can kill the protein even with no aa change.

@AMR I did not say you are wrong, I just wanted to clarify for readers that even if there are 150 million differences, only a very tiny fraction are actually meaningful. I considered proteins because that is what you mentioned, but there are many other types of changes that can be functional (e.g. in regulatory regions). Still, even if you consider all of these, the vast majority of differences will not have any effect.

@Bitwise The OP is a High School student that hasn't taken Biology. I agree that there are many more places such as promoters and enhancers, splice donor / acceptor sites that can affect functionality, but as we don't usually teach that to first year undergrads, I was only pointing out what someone with a casual understanding may know. Their question is from the perspective that 0.5% is not a lot of variation, they use "only", and I was trying to say to them that that is more than enough to provide uniqueness to 8 billion individuals.

@AMR: It's some time ago, but why would you bring up a sentence like "You also should understand that any changes that are deleterious will be under strong selective pressure." after talking about bottlenecks? After bottlenecks selection (be it purifying, positive or balancing) in general is quite weak and has low efficacy in reducing deleterious variants. Of course both purifying selection and drift reduce variation (and therefore contribute to the low genetic diversity among humans) , but this might still lead to misinterpretations ...


text:
Regression to the mean and evolution
I don't have a strong biological background but, in studying statistics, I met the idea of regression to the mean. e.g. children of tall parents tend to be shorter than their parents, and so on.
Does this interact with evolution ?

Interestingly, statistics have evolved quite significantly in parallel of evolutionary biology. Galton, Pearson and R. Fisher are important names that contributed to both biology and statistics.

Have a look at Wikipedia > Heritability > Parent-offspring_regression.

When you talk about "regression toward the mean", do you refer to the modelling of data (linear regressions) or do you refer to the natural tendency for extreme values to be less extreme in a future measurement (origin of the term regression but rarely used with this meaning today)?

answers to this question are related: Is it possible for a child to grow taller than their tallest parent?

Actually i was referring to the tendency of values to be around the mean on the normal distribution curve.

"the tendency of values to be around the mean on the normal distribution curve". What do you mean? Do you mean the tendency of extreme data points to regress toward the mean in future measurements? If yes, then please let us know how it could affect evolutionary processes as it is not obvious for me. Also, your example does not match this. I am voting as unclear.

TL;DR answer: Regression to the mean doesn't always occur (children can be taller than either parent, as can be easily observed at any high-school basketball game), so it doesn't affect the theory of evolution through natural selection.
The observation of regression to the mean was of great concern to Darwin and early thoughts on natural selection (don't confuse "evolution", which is the observed phenomenon, and "natural selection", which is one of the theories proposed to explain evolution).  The problem has been effectively resolved since the rediscovery of Mendel's genetic work at the end of the 19th century.
"Regression to the mean" is inevitable if inheritance works through blending of features.  That was how everyone believed inheritance to work in the mid-1800s, and Darwin understood that it presented an insuperable obstacle to his theory.  That is, if blending inheritance was true, then natural selection could not be true.  Darwin puzzled over this quite a bit, and came up with some unsatisfying suggestions to overcome it, but at the end of the day, one of the predictions that his theory of evolution through natural selection made, was that blending inheritance could not be true.
Of course, blending inheritance is not true.  Mendel showed that in fact inheritance is quantal, not blending.  We now know that many traits of interest look, superficially, as if they're blending (which leads to regression to the mean), but are actually the result of multiple traits interacting.
With blending inheritance, the variation that is required for natural selection to work is lost, generation after generation; regression to the mean in an inevitable consequence.  With gene-based inheritance, variation (can be) preserved generation after generation; regression to the mean is a common but not inevitable consequence, because the variation in the original population is still present and can be re-created given appropriate selection pressure.

Interesting read on how Mendel was mostly wrong.

Mendel wasn't wrong on the key point that inheritance is not blended, which is what's relevant here.

That's true, I should have been more specific. I was just mentioning the article as possible interesting reading for those whose understanding of Mendel's work didn't go beyond high school biology. Your answer is actually pretty decent.

There is a concept known as "heritability" which essentially is a measure of how much of the variability in a certain trait that is due to genetic factors. This is closely related to regression to the mean. Now for length the heritability sometimes is estimated, by measuring the lengths of many parents and their offspring, to be around 0.7. This means that if your father is ten centimeters taller than the average man in your population and your mother is ten centimeter taller than the average woman in your population you are expected to be around three centimeters shorter than your same sex parent but still seven centimeters taller than the average for your sex in your population.
A heritability of 0.7 is very high so if it were a clear evolutionary advantage for an individual to be taller or shorter than the current average height the length of the population will be expected to change rather fast.
There are other traits, for instance the tendency to have one-egg twins, where the heritability is believed to be basically zero. This means that even if you are a one-egg twin and being a one-egg twin constitutes a clear evolutionary advantage the relative amounts of one-egg twins will not increase in the population because there is no heritability.
You could say that the higher the heritability, and thus the lower the regression to the mean, the faster a trait will change in a population in a certain direction if there is evolutionary pressure for it to do so.

source: Stack Exchange

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

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

sort: votes


text:
Does urea at different concentrations (5 or 0.5M) have different effects on proteins?
The problem is to explain why each additive gives rise to the distribution of the protein (RMAS) as shown in the Western blow below:

In each case, the homogenates were subjected to high-speed centrifugation and the supernatant/pellet fractions were resolved separately by SDS-polyacrylamide gel electrophoresis. The gels were blotted and probed with an antibody raised against RMAS.

I am specifically stuck on explaining the effect of the 0.5M urea vs 5M urea on the soluble and insoluble proteins represented by the pellet and supernatant respectively. My thinking is that at low urea concentrations (0.5M) the pellet protein is destabilised by urea and solubility increases showing a band. However, soluble proteins are denatured and show no band. However, at 5M urea, the pellet proteins are reversibly soluble and therefore do not show as a band whereas the soluble proteins are OK and so show a 'normal' band. I don't know if this is the right explanation, so could someone please explain it to me??

What you need to do is compare the relative amounts of the protein in the insoluble (pellet) fraction to the soluble (supernatant) one. This way you can determine how soluble the RMAS has become through the effect of the indicated compound.
DTT breaks disulfide bonds, but does nothing else to solublize the protein, so it's all in the pellet, with none detectable in the supe. NaCl is a salt that increases the ionic "strength" of the lysis buffer, but doesn't really do anything to solublize the protein, so again all of the target stays in the pellet. On the other hand, detergents like Triton and SDS free the protein from the insoluble fraction and move most of it into the supernatant, leading to the pattern you see for them. Depending on the exact subcellular localization of the protein of interest, and the amount and combination of detergent(s) used, you may see essentially no protein at all in the pellet, as it has all been solublized.
Urea and guanidinium hydrochloride are chaotropic agents, disrupting hydrogen bonding, van der Waals forces, and weakening hydrophobic associations, causing the protein to denature and separate from other proteins in the pellet, thereby putting it into the supe. This effect is generally seen at relatively high molarities (e.g. GuHCl is often used in the 6-8 M range), which explains the difference in effect seen with 0.5 and 5 M urea. At low concentrations, there is just not enough urea present to effectively denature the protein. I am a little surprised that nothing showed up in the 0.5 M lane, however, this is just a simulated Western showing ideal results - in real life things are almost never quite this cut-and-dried.

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


text:
Life after decapitation?
I saw a video where an ant lost its head and was still walking for some time.
If this is possible for an arthropod, what keeps it from working with a vertebrate? (Humans, especially)

Cockroach bodies can survive without a head for up to two weeks. You cannot really physiologically compare an arthropod to a mammal, for many reasons.

Why? I just want to learn why this happens. I dont care if it is mammal, artopod, fish etc.

Arthropods. Segmented bodies, hemolymph, very simple nervous system. Mammals, unified body, blood, Central Nervous that is removed with head that controls many of the organ systems, endocrine system with hormones originating in the head and throat, organ failure from loss of blood....

So, you say that arthropod because they have different nervous system they can survive without head? Then why they have their brain??

https://en.wikipedia.org/wiki/Arthropod

@Orphee You probably want to replace your title by walking after decapitation or can a human walk after decapitation or motor activity after decapitation. The concept of life is very different from the concept of  walking.

If someone walks, then he is alive (eg if u see a walking animal you will automaticaly understand that it is alive).


text:
Why do my muscles move slowly when cold?
When my hands are cold, e.g. outside in the winter with no gloves for a while, their muscles begin to move slowly (assume I'm otherwise comfortably warm, e.g. dressed well but gloveless).
I don't seem to lose strength or endurance really, only maximum speed. Coordination is difficult and rapid repetitive movements are impossible, attempts instead lead to a continuous contraction (like normal, but the threshold is much slower). Of course normal function returns when the temperature is brought back to normal.
Why is this so? What is the correlation between lower temperatures and slower muscle response? Is it something with the neurons, something with the muscle tissue, or both? Is it related to blood flow (like when my hand "falls asleep" when circulation is cut off) or is it a property of the tissues themselves?

Both innervation and muscle activity are long chains of complicated biophysical transformations with thermodynamic kinetics -> that is your link to temperature. It's like the main perk (and the sole purpose) of being homeothermic.

@Eli Is the implication that this question is too broad?

This is that type of questions that have a two-word answer (i.e. thermodynamic kinetics). And as long as you understand that the processes involved happen to be complicated interactions between many molecular machines, those two words are sufficient. Yet, if you don't understand those things the question becomes too broad and you'd be better off reading some "Kinetics/Biophysics/Thermodynamics for dummies" textbook.

Damn. It's like that video of Feynman explaining magnetism. Guess I'm that guy.

This, while requiring some prior knowledge, will get you started. Refer to wiki for additional information while reading the paper.

As Feynman said, though, it is a great question. He wasn't disparaging the guy, he was teaching him. But yeah, the answers are looking and involved. For edification, you might want to scope out the freezing and thawing of frogs.

In fact, Feynman has inspired me to come up with an answer.

Sorry for the delay, I was low on time and didn't want to post a poor answer. Let's get into it step by step. The most important thing here is to understand that every single thing you do is a combination of many highly complicated biochemical and biophysical reactions/processes that slow down as temperature gets lower. Since any chemical reaction is a physical process I won't differentiate physics and chemistry any further. The speed of molecular processes is explained by thermodynamics. And in thermodynamics, all other things being equal, things slow down as the temperature gets lower, because temperature is a measure of thermal motion. Why? We will get to that later.
Now, what are those processes we are talking about? I'm not going to list every single molecular cascade in a eukaryotic cell that has something to do with muscle contraction (there are many, believe me). Instead, I'll give you a beautiful example that is directly related to movement. That is innervation. Everyone knows that neurones use axons for long-range transfer of electric impulses. Although people tend to portrait axons as wires, they really are nothing like metal wires, because the resistance is so high any biologically feasible electric signal won't travel for long. So how do axons work? Let's look at one:

Imagine a chain of Wi-Fi base-stations that retransmit a signal and you have a very good analogy. Any axon is mostly covered by glial cells, forming an isolation-coating (myelin sheath), but there are regular coating-free patches (Ranvier nodes). These nodes are the "base-stations". When a neurone sends a signal, it triggers the depolarisation of its cellular membrane by opening various ion-channels. The first Ranvier node senses the change in the electric potential and opens its own potential-sensitive ion channels, so the signal travels from node to node. In order the neurone to transmit a signal again, it has to recharge all the nodes (obviously, it takes time). The process is done by special active ion-pumps that use energy (ATP) to move ions against the concentration gradient. Now, let's list some thermodynamic processes:

Something senses the change in electric potential and changes its conformation. This is work.
The movement of ions along the concentration gradient. This is diffusion.
Something senses that the membrane is depolarised and triggers recharging. Once again, work.
The movement of ions against the gradient. This is done by molecular machines that require ATP. So here we have at least 2 reactions: 1. an ATPase transforms ATP to ADP; 2. an ion-pump works. Hey, what is work after all? ;)

In fact, a similar list of processes can be given for the actin-myosin system that actually performs the muscle contraction, when the cytoplasmic concentration of Ca ions increases after they are set loose from the intracellular Ca-storage facilities (the reticulum) in response to a neuronal or mechanical signal. It's just another charge-shoot-sharge cycle.
Now let's return to thermodynamics. First, consider diffusion. Diffusion depends on the speed of the molecules. The speed depends on temperature. So this is clear and simple (if you don't want to know, why it does). Now, let's consider reactions. Any reaction/process is probabilistic. We call reactions "fast" when the probability is so high there is no lag between individual events. Where does that probability come from? Although details, such as free energy distribution model (e.g. Maxwell distribution in ideal gases), depend on the medium you analyse, the basic idea of any reaction is to reduce the potential of a system. Aside from concentrations, there are 3 basic things to consider: 1. the starting free energy, 2. the activation energy, and 3. the resulting free energy. Let's look at a picture.

The higher the difference between 1 and 3, and the lesser the difference between 1 and 2, the higher the probability. Okay, this doesn't completely explain why this stuff is probabilistic. The thing is that the starting free energy of reagents forms a distribution, hence only a fraction of molecules have the energy to break the activation barrier. Any time two molecules (that could possibly react) meet, you play a game called "can we make the jump or not". The game is clearly probabilistic. When you lower the temperature, you shift that distribution, reducing the fraction of molecules that can make the jump.
Now we can go further into details, but I feel like this is already enough to give a sense of why things slow down as you lower the temperature.

There is nothing like electromagnetic potential. It is electric potential. People seem to like telling it that way since it sounds a little more fancy. However it is a huge misconception.

@m1clee although there is such thing a electromagnetic potential (four-potential), I do agree with you that I was supposed to write electric potential. I'm sorry for not double-checking the terminology.


text:
Cancer cells and their ability to avoid the immune system
Since cancer cell retain their ability to trigger the immune system from their pre-cancerous state and any condition that causes an auto-immune reaction in a specific area of the body will attack any cells in that area then could an auto-immune reaction actually attack any cancer cells in that area also?
Noting that regular human cells are not able to avoid 'attacks' by an auto-immune response so the normal cells can not pass on any 'strategies' for avoiding an auto-immune disease attack to any cancerous cells they 'turn into'.. Is all this possible?

There are several types of cancer immune evasion.
Such as releasing immunesupressive cytokines, downregulation of MCH and comprising mutiations which are not immunogenic.
If the cancer at a tissue is evading immune system by immunosupressive cytokines it may not be affected from auto-immune attack.
However if the cancer is not attacked by the immune system just because it is not "different" enough from the nearby healthy tissues, then at this time auto-immune attack to the tissue may technnically attack the cancer also.

Has there been instances where an auto-immune reaction has attacked tumour cells?

I haven't read about such case.  But it is more like  "Has there been a car  accident which treated cancer by removing the cancerous tissue (skin) "? Even if there is not known case, it does not make such "treatment" impossible.  If normal immune system doesn't attack cancer just because it recognize cancer as "self" then when auto-immune disorder starts it will attack to "self" so to the cancer which is same as that "self".  However if immune system already recognized  and poised to attack the, but inhibited by inhibitory receptors and ligands, then  autoimmune may fail to attack the cancer

PS: could not edit the previous comment for grammar correction.  the last sentence should be "However if immune system already recognized and poised to attack the cancer, but inhibited by inhibitory receptors and ligands, then autoimmune may fail to attack the cancer"

Mostly wrong, yet not a bad notion.
Most* (*all? Been too long.) forms of cancers turn off the natural identification scheme (self-MHC or major histocompatibility complex) as well as the limits on replication. This is because there is a self-kill switch attached to that system.
A cancer would need to release the stand-down signal in a timely fashion, which it cannot do if it is spending its resources on rapid growth.
This means most* cancers are already valid targets without needing an auto immune disorder.
At least one targeted anti-cancer treatment operates by turning MHC back on, causing them to die.
There may be some sorts where the ability to target native cells would help. Doubt it, but could be.

Could a benign virus cause an auto-immune reaction in a persons right knee say and therefore cause all the cells in the knee to be attacked by the immune system including any cancer cell that are there ( even though they can avoid the 'regular' immune system attack??

By normal definitions of "benign", no. You describe an infection that causes indiscriminate damage to the body.

That said, histamine causes a localized region where the body goes killing, taking out native cells as collateral damage. (That's not terribly exotic stuff, but that also makes it that much more believable.) A parasite is more likely to trigger the effect you want than a virus.

So could a mild histamine or a parasite ( that doesn't cause 'unrecoverable' damage) cause all cells in a certain area to be attacked? What causes an auto-immune reaction anyway , is it genetic?

Histamine triggers all sorts of nasty cell reactions. It is quite destructive, so it's fairly localized. It does real harm. A parasite would work by triggering that reaction and, potentially, by eating the cancer cells. Whether or or not that damage is recoverable is contingent on extent, much as with surgery.

Auto immune reactions are often genetic, but that doesn't always mean heritable. Some forms can be triggered by expression errors like in MHC. There are chemical agents that can wreck the body's ability to trigger an immune response. Not totally sure how selective immunity restores itself, but there is some form of coordination between cells and immune system when the self MHC codes are set, so there is likely something that can hack that and change what's read. (This is a really involved topic, though, and better asked over on biology, methinks.)

I mean the questions about immunology with that last bit, there.

Can expression errors in MHC be caused artificially?

Theoretically, since transcription errors can naturally cause this, it should be possible via some form of DNA manipulating enzymes. (a retrovirus, say.) I assume it's possible other ways, too.

So could something like a retrovirus cause an auto-immune reaction in the area where the retrovirus is injected?

Yes, that's theoretically possible. It would need to encode the changes directly or indirectly. (The enzymes to alter that gene expression region or the control signals to create those enzymes or force a situation that otherwise causes this.) I've no idea if that's a phenomenon actually found in nature.


text:
Inbred mice has no severe phenotype outcome?
Why does 20 generation of inbred mouse have no particular strange phenotypes, but on the contrary, when on purposely inbreed dogs or tigers for specific phenotype cause severe deformation of the bone structure or cranial structure?

Depends on what strain of mice you're talking about. Many of the "wild-type" strains I've worked with have some sort of issue or another, such as shortened lifespan, propensity to develop diabetes, etc. Then there are the strains that are bred specifically for a certain phenotype. Additionally, not all dog breeds have severe defects. Basically, it's hit-or-miss.

The danger of inbreeding come from increasing the frequency of rare, negative, recessive alleles to the point of producing individuals with two copies of the bad allele.  If a population lacks such alleles (due to past genetic bottlenecks) inbreeding isn't inherently dangerous.

@AdamC that is possible, though the individuals that are fittest to survive the bottleneck may lack fitness when conditions improve, as is suggested by the obesity and diabetes epidemics we are seeing in developed nations with abundant agriculture. It also leaves out that the genetic diversity that random sexual reproduction produces. Lab strains are one thing, but considering the constant host pathogen arms race that goes on keeping the gene pool diverse gives a species a better chance against its pathogens.

@AMR I don't disagree with what you're saying (though I'm not sure how obesity and diabetes are related to a genetic bottleneck) but what does your comment have to do with the question?  The question covers several topics so one could certainly answer it from a number of different perspectives.  Why don't lab mice experience inbreeding depression? or Why do negative traits appear in dogs when other traits are selected for? or Can you take inbred lab mice and, through artificial selection, produce negative traits like seen in dogs?

Thanks Adam C, you phrased my question perfectly. Still.. I am not completely satisfied with all the answers... I'd love to hear some answers that's more in detail.

@AdamC (and OP): It isn't that they don't experience inbreeding depression: they definitely definitely DO. Inbred lab mice have many negative traits. A large percentage are blind (and not just albinos, there is actually a specific mutation common to many inbred strains that casues total blindness by ~1 month age). Several strains have hearing difficulties. Many strains have issues with tumors (you see this especially with rats).

Some information on inbred strains of laboratory mice:
https://en.wikipedia.org/wiki/Inbred_strain
http://what-when-how.com/molecular-biology/pure-line-molecular-biology/
A relevant quote on the consequences of inbreeding:

Inbreeding in allogamic organisms bring the deleterious recessive alleles to homozygosity; the immediate consequence is an increase in the frequency of defective offspring, or, in another words, an increase in the genetic load of the population. This phenomenon is called inbreeding depression or inbreeding degeneration. As inbreeding continues, the deleterious alleles are selected out and eventually disappear. The original heterozygous populations are often more fit than the resulting pure lines because they profit from heterosis and balanced polymorphisms; the main advantage of pure lines is the quick production of many individuals with the same well-adapted genotype, while the allogamy continuously generates new genotypes.

In other words, inbreeding is harmful because it makes it more likely that offspring will have two copies of bad recessive alleles, meaning those alleles get expressed, meaning the organism gets the bad consequences that wouldn't show up if they had only one copy. This is what happens over a single generation however; over many generations the bad alleles are selected against, precisely because they are harmful to the organism so it reproduces less, and after enough generations of inbreeding you hit a point where all individuals are genetically identical and have all the "good" alleles (if they were lucky; otherwise they die out or stay stuck with some bad-but-not-fatal alleles). They still may be worse off than their more diverse ancestors, but they're not completely messed up like their unfortunate great-aunts and uncles who didn't make it either.
The big difference between inbred mice and dogs or tigers is the "for specific phenotype" aspect. Laboratory organisms are inbred so that you get a large pool of genetically-identical individuals, meaning they're much easier to experiment on. The aim is the inbreeding itself, not any particular phenotype. For example if you look at the page for the most popular strain of laboratory mice, C57BL/6, you can see it has many different properties and is used for many different things.
On the other hand, dogs aren't inbred for the purpose of inbreeding or of being genetically identical; the aim is to get desirable phenotypes, and inbreeding is just an efficient way of achieving that aim. It also isn't obvious that many of the problems purebred dogs have is inbreeding (i.e. lack of genetic diversity, high levels of homozygosy) per se, but the fact that the traits being bred for are just plain unhealthy for the dog, or part of a bell curve that include bad outcomes at the edges. For example, Syringomyelia in the Cavalier King Charles Spaniel:

Some researchers estimate that as many as 95% of CKCSs may have Chiari-like malformation (CM or CLM), the skull bone malformation believed to be a part of the cause of syringomyelia, and that more than 50% of cavaliers may have SM.* It is worldwide in scope and not limited to any country, breeding line, or kennel, and experts report that it is believed to be inherited in the cavalier King Charles spaniel. CM is so widespread in the cavalier that it may be an inherent part of the CKCS's breed standard.

(emphasis mine)
Same thing for that spine malformation that's related to selecting for corkscrew tails. The genes that make the tail corkscrew also mess with the spine.
In other words, the issue isn't inbreeding or not but whether the genes themselves are harmful. When organisms are selected for traits that are directly harmful in their extreme, or are associated with harmful genes that just happen to be next to those that are selected for in the chromosome, then the harmful consequences will spread through the population. Inbreeding is only a problem insofar as it allows the process go faster (more offspring per generation have the desired trait). On the other hand when you're just inbreeding with no specific focus on phenotype, or not phenotypes that have obvious harm associated (i.e. no lab would select for a frivolous trait that also causes harm. They're either selecting for the harmful trait on purpose, or they're selecting against it, because they'll want animals that are as healthy as possible except for the one variable they're interested in), then you'll end up with populations that are fairly normal except for some of the direct consequences of genetic uniformity.
It should be noted that most purebred dogs probably aren't inbred strains the same way many laboratory animals are; those are genetically identical, so the whole point is that their offspring will be like they are. So while they may be less fit than a non-inbred version of them might be, their offspring won't be any less fit than they are. And this is not what's observed with purebred animals like dogs and horses; individuals aren't identical, and looking at the page on Syringomyelia it seems the problems are getting worse.

Because we have selected particular inbred strains that seemed "normal", at least superficially, and mostly for strains that produced good litters and didn't often bite the researchers. However, inbred strains of mice and rats have many deleterious mutations. In some cases they probably survive only because they are held in cages with ample food and water, so they are not subject to the same selection pressures as wild mice would be.
For example, many common mouse strains have the rd1 mutation (see: Jackson labs). This mutation leads to complete degeneration of photoreceptors by about 1 month of age. Note that these are not typically albino mice, so this is different from the vision deficits of albinos. These are mice that appear mostly normal, but they are totally blind.
The most common mouse strain used in research is the C57BL/6 mouse, sometimes called "black 6". Again, see Jackson Labs for some of the phenotypes observed in this strain. I'll list just a few here: hearing loss, high preference for alcohol, dermatitis bad enough to occasionally result in self-mutilation and death, susceptible to obesity, sensitive to atherosclerosis, small kidneys, susceptible to several tumor types, high rate of developmental issues with the lens of the eye, and on and on.
Given that this is the strain often considered "most normal" I think you can see that it isn't at all correct to think of inbred mice as not having any severe phenotypes.


text:
Is eradication of the Common Cold possible?
This is a thought experiment, but everywhere I've read seems to say that colds ALWAYS come from someone else. There's no mention of a cold arising in someone without it coming from another infected being.
So my question is, if everyone in the world stayed out of physical contact and air space with everyone else for 2 weeks (or until every cold virus would have completely disappeared), would all variations of the cold virus then be extinct leading to a world without colds?
Or is there somewhere else that colds can arise from?

@rg255 I disagree that this is not of interest to biologists. If eradication of other diseases can be done, then it is perfectly valid to theorise about the eradication of diseases such as the common cold.

You'd think there would be numbers of papers on this. I have two references but they're not great.  The answer is not really.  Many people carry cold viruses asymptomatically.  This can be either a natural immunity, or that their body has beaten it down but not entirely eliminated it.  Cold viruses do not survive long outside of the body as you stated.  The only way they've made it this far is some survive inside the body until they are spread to other people.  In essence we are the reservoir.  So you could isolate everyone for two weeks, but that won't cause a problem for the viruses that are just tagging along.  There may be other reservoir animals as well for many of the viruses.  But even those that only affect and are carried by humans would survive.
The group of cold viruses is just too varied and different to eliminate them.  Also the cost of such an effort would not really be justifiable given the typically mild symptoms.
Natural Reservoir


text:
Are platyhellmintes and annelids segmented?
Are the organisms of platyhelminthes unsegmented worms or segment? And what about those belonging to annelida?
I guess Platyhelminthes are unsegmented and annelida are segmented but i am not sure about it?

Welcome to Biology.SE. A title should be a short version of the content and not just the field of interest. You should use the tags to indicate the field of interest. Also we expect from an OP some effort to answer its own question. Your question is answered by the first sentences of the respective wikipedia articles. I edited your question. Feel free to roll back if you don't like the edit

Here are the first sentences from the wikipedia articles for platyheminthes and annelids:

The flatworms, or Platyhelminthes, Plathelminthes, or platyhelminths (from the Greek πλατύ, platy, meaning "flat" and ἕλμινς (root: ἑλμινθ-), helminth-, meaning "worm")2 are a phylum of relatively simple bilaterian, unsegmented, soft-bodied invertebrates.
The annelids (Annelida, from Latin anellus, "little ring"),2[n 1] also known as the ringed worms or segmented worms, are a large phylum, with over 17,000 extant species including ragworms, earthworms, and leeches.


text:
A question involving immunoprecipitation to identify interacting proteins?
Using recombinant Flag-tagged Dcr-2 and His-tagged protein X, pull-down assays were performed to determine whether protein X and Dcr-2 interact directly. The recombinant proteins (either alone or in combination) in binding buffer (150 mM NaCl, 1 mM EDTA, 50 mM Tris pH 7.5, 1% Triton X-100) were pulled-down by Flag antibodies coupled to Sepharose beads. Following extensive washing, the proteins were eluted from the beads with SDS buffer, and duplicate sets of samples were analyzed by SDS PAGE. Samples were also taken of the proteins before they were used in the pull-down assay and these were run on the same gel (input lanes in Figure 2B). One gel was stained with Coomassie blue dye (Figure 2A), and the other was transferred to nitrocellulose for Western Blotting. The membrane was probed with a His-antibody (Figure 2B).

The question asks: Do Dcr‐2 and protein X interact directly?

My reasoning is that they DO interact directly. In Fig 2B: the intense bands on LHS shows that Dcr-2 interacts with protein X-that is bound to anti-His. In Fig 2A: the protein X interacts with the Dcr-2 bound to antibody FLAG. I feel I'm not explaining this very though...Could someone please explain their reasoning? Thank you

If the answer doesn't satisfy you, it would be great to tell me the problem in a comment, so I can possibly improve it. Thanks.

First: You are right with your reasoning that Protein X (X) and Dcr-2 interact directly. Lets go through the blots: In the input you check for the proteins loaded into the setting and stain unspecifically with Coomassie.
This part of the blot shows you no unspecific input, and both proteins of interest present. This also shows that Dcr-2 is much bigger than X which allows an easy identification of band patterns.
In the eluate you will only see proteins which are bound directly in the reaction or which interact with bound proteins. Dcr-2 is Flag-tagged so it will directly bind to the beads and can be eluated from them. This is shown in the coomassie part of the blot. Dcr-2 alone binds and can be eluated, while X alone does not bind and therefore gives no signal. Dcr-2 and X together give two bands, sind Dcr-2 binds to the beads and X is interacting with Dcr-2.
This binding is also shown with the anti-His antibody which only recognizes Protein X. The protein shows up in the input where X is added. It also shows up in the elution lane (where Dcr-2 is also present) showing that X is an interaction partner for Dcr-2.


text:
How chameleons change color?
Well, I was watching a video about chameleons and I saw that their cells can change color. Can someone explain me how is this possible?

https://en.wikipedia.org/wiki/Chameleon#Change_of_color

When it comes to displaying color, most organisms use chromatophores. Chromatophores are pigment-containing and light-reflecting cells, or groups of cells. Chromatophores reflect the color that they look like.
Chameleons also use chromatophores. The outermost layer of the chameleon’s skin is transparent. Beneath this layer are the chromatophores. The deepest layer contains melanophores, which are filled with melanin. Above that layer are cells called iridophores, which have a blue pigment that reflects blue and white light. Layered on top of those cells are the xanthophores and erythrophores, which contain yellow and red pigments, respectively.
For a chameleon to change color, it must expand or contract certain chromatophores depending on the signal of the nervous system. The expanded chromatophores block the contracted ones and the color of the expanded chromatophores determine the color of the chameleon. For example, to make the chameleon green, the iridophores and xanthophores must expand, and melanophores and and erythrophores contract.
Reference
WIRED - How Chameleons Change Colors
More to read
This Nature article provides a detail description and explanation of how this occurs - Photonic crystals cause active colour change in chameleons


text:
Why are belly buttons on the stomach (why does the umbilical cord end up attached to the stomach)?
Belly buttons are at the site where the umbilical cord was attached to us as we developed inside our mothers. The same is true for all placental mammals.
Why are belly buttons on the stomach? Why didn't the placement end up somewhere else like the chest, the back, the head, etc.? Is it optimal for the umbilical cord to be near the intestines?

While it doesn't answer your specific question, a really good book for this kind of question is Your Inner Fish, by Neil Shubin.


text:
How much should one smoke in order to prevent Parkinson's?
There are studies who claim that nicotine has a neuroprotective effect against Parkinson's(such as this: http://www.ncbi.nlm.nih.gov/pubmed/11772120)
What would be the minimum amount of nicotine(cigarettes smoked) and frequency in order to prevent Parkinson's, at the same time not to damage his health by becoming an addicted smoker?

The closest thing to an answer you can find is probably in the paper you linked. Did you read it?

@Remi.b I've read only the abstract, I also tried to obtain the full text(as they described here: http://www.ncbi.nlm.nih.gov/guide/howto/obtain-full-text/) and I didn't manage to find it. Do you know how to obtain it by some other means?

@Flowryn I am not too sure about this claim. Yes, nicotine may effect dopamine release to some extent but there is no clear consensus on this issue. See the newer articles that cite this paper. In fact this J.Neuroscience paper says that nicotine free tobacco and decaffeinated coffee can also have neuroprotective effects.

You will not prevent parkinsons by smoking/nicotine consumption, you may see a slight reduction in risk of parkinsons but the effect will be relatively minor and likely outweighed by the negative side effects of smoking/nicotine

You should probably weigh in the total risk of getting Parkinsons (the German Wikipedia names a prevalence between 1,5 and 2%) compared to the risk of getting lung cancer from smoking which is a lot higher.

@Flowryn perhaps you can edit your question to remove the emphasis on smoking because eventually people will tell you a lot more about how smoking is bad instead of how nicotine may possibly help Parkinson's patients. You can instead add a note that nicotine can be administered as inhalant, patch or some oral formulation like gums.

I'm voting to close this question as off-topic because the one paper cited is from 2001, and there is a body of research that shows that COPD, a risk factor from smoking, can be a risk factor in the development of Parkinsonism.


text:
What is membrane-partitioning free energy? Can it be simulated?
Firstly, is there a strict definition of the "membrane-partitioning free energy"? It is banded around in membrane biology, but I have never seen it strictly defined. The only non-scholarly site that google shows is this Q&A on quora, and the answer there even has ambiguity in what is defined as partitioning in the membrane. This seems wholly unclear.
Furthermore, is it possible to study free energy changes upon partitioning in GROMACS, or with any other molecular dynamics simulations? If not, what are the methods I would need to use to determine the free energy of partitioning?
Links and citations for further reading on this topic are encouraged.

Welcome to Bio. Could you add some bacground to your question? The sources for the terms would be of help. For example, what membranes are you talking about? What are the purposes of the methods you are looking for? Good answers can only be generated to clear questions.

When you refer to membrane partitioning, are you referring to the invagination of the membrane during cytokinesis or do you have something different in mind?

In the biological context, membrane-partitioning is usually referring to the stage in which the transmembrane-destined region of a protein moves from interacting with the water, to interact with the interface of the membrane.
In the diagram below showing a four step thermodynamic cycle, the partitioning free energy can be referred to as-is ΔGwiu in terms of free energy where w is water, i is the interface, and u is unfolded. The image comes from the same paper that introduced the famous Wimley and White octanol-interface scale from 1999.

Note that in a more recent 2015 article, they comment that the partitioning phase ΔGwiu is generally the only experimentally accessible step. With that in mind, simulating ΔGwif where f is the folded helix becomes necessary. This 2014 Nature Comms paper use folding-partitioning molecular dynamics simulations to estimate the free energies that are experimentally inaccessible. They used Gomacs 4.5. In fact, a study using a simulation from 2005 suggests that folding isn't necessarily required for insertion of the helices.

Note that all the information here is behind a paywall. Feel free to ask me for clarification or expansion in the comments.

James, pm me. Would love to hear more from you in this subject.

@RoshanShrestha Ping me in the biosphere, or via twitter (@jbkr_). There is no PM function I'm aware of here.


text:
is there a difference in meaning between the terms "bone architecture" and "bone structure"?
I'm wondering whether "bone architecture" and "bone structure" mean the same thing, or whether they refer to two different concepts.
In this article - http://rheumatology.oxfordjournals.org/content/48/suppl_4/iv3.full - bone microstructure and bone microarchitecture are mentioned in the abstract in a way which makes them sound like they are the same thing. Also, they seem to be used as synonyms in the rest of the article.
This website - http://www.doitpoms.ac.uk/tlplib/bones/structure.php - discusses cortical vs cancellous bone under "structure and composition of bone" while other sites often discuss the same thing under the heading "bone architecture".
So am I right in thinking that the architecture of bones and the structure of bones are synonyms and that either term can be used when referring to osteoporosis? Thanks.


text:
Can somebody be deaf to voices of some people only?
The voice of females is generally of high frequency, while that of males is generally of low frequency.
Also, as we age, we gradually keep losing the ability of hearing sounds of high frequencies.
So, can such a situation occur when a person is not able to hear voices of females, or maybe of certain people, while he can hear the voices of other people? I tried searching about it, but found nothing.

I think it's unlikely, while female voices may be relatively higher in frequency than male voices, I think the frequencies lost with age are much higher

I can confirm that the wife's voice demands far less attention from me than do the childrens' voices. That said, she would argue that I give her far less attention that I do the the children...

Although you loose the high frequencies in your hearing with age (20kHz and below), this is highly unlikely. The frequency spectrum of our voice is pretty much limited, which is also shown by the fact the for normal telephone, the spectrum transmitted is located between 300 and 3400Hz and the spectrum band between 300 and 3000Hz is named the "voice band". See here for some details.
According to reference 1 the "voice fundamental frequency" for men is between 85 and 180Hz (depending on the reference) and for women between 165 and 255Hz. These frequencies are close enough together to rule out specific hearing of male or female voices. Furthermore the frequencies even overlap.
What happens in age-related pathological hearing loss (also termed Presbycusis) is that voices generally get muffled due to losses in the spectrum and hearing intensity. See the Wikipedia link and also reference 2 for more details.
Reference:

The frequency range of the voice fundamental in the speech of  male
and female adults
Presbycusis

Sensorineural Hearing Loss (SNHL) can reduce the ability to hear faint sounds even when the sounds are clear and audible. Tone deafness in contrast affects a person's ability to learn music, but not the ability to perceive or recognize speech.


text:
Why do we have two eyes?
Humans, animals and birds all have two eyes. Why? In addition to why two instead of one, why aren't there more than two?

Two eyes are important for 3D vision.

First, it's not true that all animals have two eyes. For example many spiders have four, six or eight eyes whilst worms have none, but all are animals.
In simple terms, the reason typical mammals have two eyes is probably similar to the reason that cars usually have four wheels, the reason houses keep out the rain and why coffee cups have handles. It's because that's what works.
Each time an organism develops, there is a high chance that the genetic information that built it will include something new. When that happens, most often the phenotype (essentially, the organism's appearance, such as how many eyes it has) does not change. The organism looks the same as its parent(s) did. If something significant does change, it is most likely to be bad news for the new organism. The chances are the organism will not survive and the particular genetic information that built it will not used again. Hence, organisms don't tend to be that different to their parent(s). Dogs don't give birth to cats.
But just rarely, this new combination produces something different and useful - useful enough that the organism is particularly successful and a good fit for its environment. In that case, simply because it can, the organism has more offspring and more of those offspring themselves survive to have offspring of their own. The genetic information that built the organism is thus used to create more, similar organisms.
So, the first eyes were produced by accident. When eyes turned out to be useful, subsequent generations from the first organism with eyes were more likely to have eyes themselves. As it turns out, analysis of genomes shows that eyes have evolved like this multiple times.
We can only assume that since mammals typically have two eyes, either the random genetic accident that would produce different numbers of eyes in mammals has never happened, or if it did happen, the result was not a good fit to the environment.
Why not no eyes? Human beings are occasionally born without eyes and the cause may be genetically inherited. One might reasonably imagine that for much of human history such a child would be unlikely to survive into adulthood and thus pass on this mutation.
Why not one eye? One reason in the case of primates is that two eyes are useful for estimating distance, which is difficult with one eye. A two-eyed animal has an advantage against predators, making it more likely the next generation is going to have two eyes.
Why not more than two eyes? Perhaps a larger number of eyes requires a larger head making childbirth impossible, or perhaps it requires too much energy to sustain. Who knows? What we observe today - humans typically have two eyes - means that, if that mutation for more than two eyes did happen at some stage, then more than two eyes wasn't optimal for the environment in which the resulting organism found itself, so it didn't get passed on to the next generation.

Please answer questions here with facts, preferably supported by citations. Hand-waving and conjecture are generally not welcome here.


text:
What test to apply to detect genomic signatures of selection?
I would like to ask you for your sugestions for selecting a test to detect signatures of selection in the following mouse model:
We have three groups: animals exhibiting trait A, trait B and controls. These animals were selected over the last 4 decades (controls were mated randomly and do not show any of the traits). That is total 170 generations (~4 generations per year).
We want to detect the genomic signatures of selection for trait A and B.
I am new in population genomics, but according to this paper (http://www.ncbi.nlm.nih.gov/pubmed/21218185), showing a desition tree (fig 1). I should apply a the Fst and a Linckage 'Desequilibrium test, given that the time scale would be short (40 years, 170 generations) and there are multiple populations.
Could you corroborate if this is the correct approach?
Thanks

Do you assume you know what loci are affecting the trait? What kind of data do you have? There are a number of different approaches. Here, here and there are some papers that should help you.

Thanks. I have no clue about the loci affecting the trait. The purpose of the study is to define that. We will do resequencing.

Ok. You really have a number of different existing algorithm for that. I am not able here to make a good list and comparison of these algorithm but the aforementioned papers should help. One other set of question, you must ask yourself is "Do I know in which environment the individuals are selected in?", "Are the individuals occurring over a continuum of environmental gradient or are they occurring in either of two different environments?".

I hope I got the question right: The mouse lines have been artificially selected in the same lab facility. From a founder population, animals were grouped by trait A or B. Within this groups, animals were mated over ~170 generation, avoiding inbreeding. A control line was kept, mated randomly and does not exhibit neither of the traits.

Where is the selection process? Only the separation according to their trait value?

Yes, they were separated according to their trait value. Trait A and B increased steadily over the ~170 generations.

I am assuming in this answer that you do not have any information about what environment is affecting the selection pressure so that methods like Bayenv2 can't be used.
The standard algorithms are:

Lewontin-Krakauer test
fdist
BayeScan
FLK
PCAdapt

Whitlock and Lotterhos 2014 showed that most often FLK and Bayenv2 perform better than the the three others. A number of articles (Meirmans 2012, Bierne et al 2013, De Mita et al 2013 and Fourcade et al 2013) have also shown that fdist and BayeScan suffer from high false positive rate. I would therefore recommend to go with FLK but I am probably not good enough to give very good advice.
Note that you should learn a bit about how these algorithms work and not using them blindly.