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Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?
To be specific: Assume chromosomes A and B are homologous. They've both replicated into A1, A2 and B1, B2 and have formed a tetrad at the equator (synapsis). Most textbooks show either A1 and B1 OR A2 and B2 exchanging genetic material, but I've never seen an experiment/paper proving that this is actually the case, and now I've come across this figure showing both A1, B1 and A2, B2 crossing over https://web.archive.org/web/20160314020121/http://www.uic.edu/classes/bios/bios100/lecturesf04am/lect16.htm
see ("crossing over" under meiosis)

So which version is correct, or do we simply not know for sure? Thanks in advance.

Welcome to Biology.SE. You might want to correct. It is sister chromatids and homologous chromosomes (not homologous chromatids).

In the case of meiosis genetic material is not being exchanged between sister chromatids, and to simply say that crossing over happens between homologous chromosomes doesn't really denote which of the two cases listed in the question is happening. I dunno what else to call this :/

Yes, it is perfectly possible for both pairs of non-sister chromatids to cross over in a single tetrad. The "standard textbook" depiction is a simplification, true tetrads can sometimes be very complicated and the nested crossing-over would be difficult for entry-level textbooks to cover.

This microscope image clearly shows two chiasmata occurring on two sets of chromatids, with both of the "blue" chromosome's chromatids undergoing crossing over.
In fact, even more complicated chiasmata complexes can form during meiosis. For example, this slide depicts many chiasmata occurring in a single tetrad. More examples can easily be found by searches.

One or both pairs of homologous chromosomes could exchange genetic material during the process of crossing over.  The number of cross-over events depends on the number of chiasmata. There are also ways for meiosis to occur with no exchange of genetic material between homologous chromosomes.
The image you reference at uic.edu is incorrect.  The purple arms and red arms would not be "swapped" like that until anaphase of first division. The sister chromatids are bound together prior to anaphase of first division.  Many textbook and internet depictions of this are incorrectly drawn.
At diplonema of first division, sister chromatids A and A (and B and B) have axial cores holding them from separating.  There are chiasmata holding the bivalent (all four chromatids) together that end up being cross-over sites. For each chiasma (singular) two of four strands are affected.  There can be multiple chiasmata per bivalent.  Humans average two chiasmata per tetrad (four chromatids).  Without at least one chiasma, fertility would suffer.

Can you provide references for your claims?


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How are subspecies defined, in contrast to species?
When should a taxon be considered to be a subspecies of a certain species, and when as a different species? Are there some general guidelines how to assign a specific taxonomic status to a taxon?

This Q is more similar to What is a subspecies?, and should be closed as a duplicate to that question.

Also see the questions http://biology.stackexchange.com/questions/26105/what-is-difference-between-breed-variant-subspecies-and-species and http://biology.stackexchange.com/q/14414/3624

source: Stack Exchange

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Are nucleotides at the ends of DNA stripped on aging?
I had the following understanding (now after reading a popular science article seeming wrong understanding):
DNA in (regular) cells (in human and some other organisms) are protected by telomers. Telomeres are shortened at each division. When telomeres reach zero size, nucleotides of the ends of DNA become "stripped" so that the DNA shortens a little. The shortened DNA does is not fully functional. This leads to aging of the organism.
But in a popular science article I've read that telomeres however shortened seem not to reach zero length. So the DNA nucleotides at the ends of DNA are never stripped. However shortening telomeres leads to the cell to become not divisible or even death of the cell.
So two related questions:

Are coding/regulatory nucleotides (not just telomeres) at the ends of the DNA ever stripped as a result of aging?
If they are not stripped and so the DNA itself is not damaged, how shortening telomeres may lead to aging? That is how aging can be caused by just shortening telomeres which however do not reach zero length?

There seems to be a slight confusion. Telomeres are made of nucleotides. Telomeres are not adds up at the end of the chromosome, they are the end of the chromosomes.  Telomeres are repetitive sequences. For example the repetition of the sequence TTAGGG is commonly found in telomeres in vertebrates.

I suppose you might want to rephrase your question to ask whether the chromosomes are sometimes shortened enough so that coding sequences or regulatory sequences get stripped.

Also, could you post the article you read?

@MarchHo https://med.stanford.edu/news/all-news/2015/01/telomere-extension-turns-back-aging-clock-in-cultured-cells.html

The Stanford article that you read is correct, in the sense that telomeres do not need to be completely removed by cell division before deleterious effects occur and cells start undergoing senescence.
This Nature article describes an experiment in which the minimum length of telomeres (beyond which chromosomal fusion occurs) was determined:

The critical telomere length was 12.8 repeats (of six base pairs)
  long, they found — any shorter and the chromosomes began to fuse
  together at their ends (R. Capper et al. Genes Dev.
  doi:10.1101/gad.439107; 2007). Baird suggests that without
  sufficiently long telomere caps, the cell may perceive the chromosome
  ends as broken strands of DNA and attempt to piece them together.

Therefore, we can conclude that while it is not impossible for non-telomeric nucleotides to be stripped from chromosomal ends, this generally does not happen, since cellular defense mechanisms such as non-homologous end joining (NHEJ) and microhomology-mediated end joining (MMEJ) would activate before that point, and start joining chromosomal ends together. This would then lead to issues during mitosis, which would likely halt further cell divisions.

Are you sure that the research was replicated? From what I am familiar with, human telomeres usually require somewhere between 2kb-4kb of TTAGGG repeats to prevent senescence. I thought it had to do with the ability for the telomere to loop over on itself and form a T-Loop with strand invasion into the D-loop. I thought that that chromosomal architecture is what imposes the limit, and you can get much shorter than that as still form the T-loop.

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Are cortical columns restricted to somatosensory cortical sections?
From this previous question, it seems like evidence for the minicolumn organisation of the neocortex seems to be primarily based off observations around the sensory parts of the cortex, such as the primary visual cortex and the barrel cortex. Have column-like organisation been observed in non-sensory regions of the neocortex?

Cortical columns (also called minicolumns) are not limited to the somatosensory cortex. As shown in this paper (which discusses how the miniucolumns change in response to aging), it is also present in the associative cortex.
However, it should be noted that "minicolumn" in this paper is defined as neurons that are close together and form a minimum spanning tree, as shown below.

Connectivity doesn't seem to be analysed, probably because connectivity information is really painful to collect, but I'm not sure given I'm an amateur when it comes to neuroscience.


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Differences among competent cells?
What are the differences among the following competent cells DH5 alpha, Nove blue, and BL21? Why some of them are for cloning and others are for protein expression?
Any references where I could find the answer?

There are a lot of differences, you can check the companies that sell competent cells for guides on how to choose (NEB, Sigma Aldrich). But there are only a few things that matter for the really common uses of competent cells.
The most important part of selecting your cells is choosing cells suitable for protein expression or for plasmid preparation.
The cells meant for plasmid prep carry certain mutations like endA that inactivate nucleases that would otherwise degrade DNA. Typical choices here would be DH5$\alpha$ or XL1-Blue.
Cells meant for protein expression have some proteases mutated, and can often use different promotors like T7. A typical example are BL21 cells, and BL21(DE3) which can use the T7 promotor.


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Mechanisms and Assumptions of the Species-Area Realtionship
I would like to choose a model to use to describe a species area relationship based on plant species richness data that I have collected.  Rather than choosing the power model a priori, I am considering all options (eg. exponential, untransformed, etc).
Does anyone know of any good recent synthesis work on how to choose the best model?  Of particular interest are the assumptions behind each model, and the ecological mechanisms that each model might imply.

Disclaimer: I am NOT an ecologist! What do you mean species-area relationship? Do you mean number of species, or presence/absence of a particular species. I don't understand what the "species" variable is.

@Remi.b It's referring to the relationship between the species richness of a particular region/site and the area of that site. Such plots often follow a power function (i.e. linear on the log-log scale)

Dengler 2009 would be a good start.

I'm sure this paper, his citations and papers citing Dengler's paper will get you well on your way.


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Do we actually know the molecular dynamics of any enzyme?
That is right, is there a limitation, say Heisenberg's uncertainty principle or something that limits our understanding of machinery of enzymes at atomic level? Can we know how do they actually work?
As far as I can tell, there is no explanation of actual design and working principles of any enzyme at atomic scale. Even the nobel prizes are given to discoveries not related to molecular details but rather pathways in which enzymes are not the primary concern, they are just represented as simple geometric shapes.
PS: I know that we have the exact molecular structures of some enzymes discovered using crystallography techniques, but even then, do we know which parts execute which function and how?

MD simulations.
Molecular Dynamics algorithms like Gromacs and AMBER aim to simulate atomistic mechanisms of biological macromolecules.
This video shows a good example of a resulting video from such a simulation for the CmAAT1 Enzyme, CmAAT1-Hex-aCoA complex. Much more data such as energy values and electrostatic interactions is available from the simulation, but that's not as pretty as the video!

Implicative mechanisms.
There are also telltale signs of active regions of crystal structures. Software like Consurf can show conserved residues. This implies possible biochemically important features like key structural or enzymatic residues, areas of a protein. The image below is from the consurf gallery and is based on the crystal structure 3COQ. Pink is areas of conservation. It therefor appears that those residues are involved in binding DNA.

Consurf is only one of many tools for identifying key residues. After these residues are identified, mutant knockouts of the protein can be made to see exactly how the function of the protein is altered. From that, a fairly good mechanistic model can emerge.
Uncertainty

"Can we know..."

The word "know" is a philosophically ambiguous word and I've gathered that scientists generally tend to avoid it. This is particularly true when it comes to the simulation side of things. It is generally best to regard MD simulations as an approximation of what happens.

Thank you! I am thrilled by all that new information. So currently is this the borderline about molecular dynamics studies? And here is a follow-up question if you wish to answer: why conserved regions are the regions that get the job done?

One more thing sir, why scientists try so hard to visualize molecular interactions which requires a lot of computational power and sophisticated algorithms? Are these MD simulations used somewhere other than fancy scientific presentations? I mean, this is just an approximation, as you stated. Even though these algorithms follow some physical and chemical properties, could they be used in pharmaceutical studies? I believe no, it must require an excellent precision to design or find a fitting key for enzymes.

And I think simulation is absolutely not the right way to discover underlying principles of molecular dynamics. Think of it sir, a bulk of atoms(composed of electrons and a nucleus to emphasize unconsciousness) organized in such a way that they, as a whole, can manipulate organic compunds. This absolutely requires an unbelievable manifacturing process at an unprecedented precision level. With obviously underlying excellent design details which should be our actual purpose of research. Not the redundant, fancy visuals of these enzymes. What are your thoughts sir? Thanks..

@m1clee I've responded to your points in the chat. http://chat.stackexchange.com/transcript/message/26824047#26824047

@m1clee The folk from the Shaw lab in NYC who built the Anton MD HPC came to our lab the other day to show us their recent MD simulations. They are probably the world leaders when it comes to MD. Check out their work if you want to learn more https://www.deshawresearch.com/publications.html.


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cell specialisation and their location
When we create new cells, how come they are of the 'right' type at the 'right' place?
For example, when I make a new cell on my lips, it's obviously not the same as a new one in my kidneys.
Is the differentiation done by using a different part of the DNA each cell has?
How does the mechanism of growing specific types of cells at a specific place work?

Yes differentiation is primarily about using only a portion of the genome as you pointed out. However, differentiated cells possess a kind of "memory" which enables the daughter cells to continue the usage of the same set of genes. This "memory" is enabled by epigenetic mechanisms which leave inheritable "marks" on the DNA such as methylation (I won't explain further as this would take an entire book).
About the place: each part of the body can produce cells locally (except for some tissues). For example the epithelial cells in your lips will arise from your lips. What signals the division of cells in response to a signal such as lets say injury is again a broad question. One simple mechanism is this (not an independent mode but just one aspect of a complex process): cells generally divide but stop dividing if there is no free space i.e. the cell is surrounded by other cells. This is called lateral inhibition of growth.
I would suggest that you pick up some good cell biology and molecular genetics books to understand these processes.
Cell Biology:

Molecular Biology of the Cell - Bruce Alberts et al.
Molecular Cell Biology - Lodish and Baltimore

Molecular Genetics:

Molecular Biology of the Gene - James Watson et al.
Genes - Benjamin Lewin

so, if I understand, the 'specialization' gets replicated as well, so a 'lip' cell will only make another 'lip' cell; is that correct?

@Thomas it is correct, 'specialization gets replicated' in epigenetic forms to daughter cells, and normally lip cells will only produce lip cells. However, if one tinkers with cellular mechanisms, he can get other specialized cells(e.g. kidney cells) through induced pluripotent stem cells (IPS cells). This is the aim of the research for which Shinya Yamanaka won the Nobel Prize in 2012 Medicine.


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Why does the proportion of transposable elements vary so much across species?
Intuitively, transposable elements (TEs) are harmful as they may cause genome instability. However, some people argue that TEs are also sources of variations, especially regulatory sequences[1].
If TEs are harmful, then their proportions may be low in most species. And if they are beneficial, then their proportions should be high. Either case leads to the conclusion that their proportions should stay close to each other. However, the fact is that the proportion varies greatly across different species:

Maize: 85% [2]
Human: 45% [3]
Arabidopsis: 10% [4]
Plasmodium: absent [5]

Why is that? Is there other factors that influences the proportion of TE, such as evolutionary pressure?

Reference
[1] Rita R, et al. 2012. Transposable elements: an abundunt and natural source of regulatory sequences for host genes. Annu. Rev. Genet 46:21-42
[2] Schnable PS, et al. 2009. The B73 maize genome: complexity, diversity, and dynamics. Science 326:1112-15
[3] International Human Genome Sequencing Consortium. 2001. Initial sequencing and analysis of the human genome. Nature 409:860-921
[4] Arabidopsis Genome Initiative. 2000. Analysis of the genome sequence of the flowering plant Arabidopsis thaliana. Nature 408:796-815
[5] Biemont C, Vieira C. 2006. Genetics: junk DNA as an evolutionary force. Nature 443:521-24

I can think of two factors that would influence this, but there are probably more.
1) How do transposable elements (TE) get into the genome in the first place?  The answer is both vertically and horizontally.  Vertical transmission needs no explanation.  Horizontal transmission of TE has been documented in several cases.  In some cases, infectious agents can transfer them between species individuals, for instance, viruses can package transposable elements in addition to their own DNA.
http://www.cell.com/trends/ecology-evolution/abstract/S0169-5347(10)00123-0
2) How efficient can the TE replicate?  For example, in the human genome there are a variety of different types of retrotransposons, but only the L1 element can replicate.  Others like Alu and SINEs parasitize their replication machinery and therefore replicate also but at much lower frequencies.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884099/
So, the difference between species has to do with both of these and probably other factors.  I would imagine in the 2nd case, the selective pressures put upon a given species at any point in time, due to infections or inter-species competition, would surely impact the efficiency of TE replication because they are so important to genomic evolution and adaptation.


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Do chromosomes uncoil in interphase II?
During interphase II, there is no S phase in which DNA replicates. However, in this stage, do the chromosomes remain wound? Or have they unwound into chromatin form, and recondense during prophase II?

In many cases the chromosomes do undergo some dispersion, they do not reach the extremely extended state of the interphase nucleus, this all happens in telophase -I. It would be correct to refer to the stage between two meiotic divisions as interkinesis which is generally short lived.
The prophase-II is initiated immediately after cytokinesis, usually before the chromosomes have fully elongated.

According to the diagram found on this site, chromosomes do unwind during Interphase II of meiosis.
Sparknotes, although it's not necessarily a reputable scientific source, seems to concur:

Once the nuclear envelope has re-formed after the first meiotic division, the cell enters a short interphase. This interphase is not as specific as mitotic interphase; during meiotic interphase, chromosomes may decondense as the cell waits to proceed with meiosis.

Finally, this website provides a clarification in stating that there is no true "interphase" between meiosis I and II (I guess true interphase would be marked by replication of DNA which, as you state, does not occur):

The period between meiosis I and meiosis II is sometimes called "interphase," this is confusing because it is not a true interphase such as that seen between rounds of mitosis because no synthesis occurs (all chromosomes have two chromatids throughout this stage).

Interestingly, the very own existence of an interphase II between meiosis I and meiosis II is highly questionable, and a search on Pubmed found an article by Vernet et al., according to which interphase-II exists only in male meiosis.


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Where can one find completed and processed Hi-C datasets?
I and a statistics graduate student at UCR, and I am working on Optimal Binning schemes and peak detection in Hi-C data analysis (a dataset that conveys information about proximity of a DNA strand with itself within the nucleus).  I am not a bioinformatician, so I am looking for someone that already has some complete data, or a website that may have these available for download.  The more datasets, the better.
Can anyone help me?  If you provide the data yourself, I will be sure to mention you in the foreword to my dissertation.
Thanks!
P.S.  If someone can find data generated specifically by the program "Hi-C Pro" with "allele specific analysis," I would be doubly grateful.


text:
Why do we have two brain hemispheres?
Is there any explanation why we have two brain hemispheres? Is there any advantage of having two in contrast to having one (or three / four)?
From what I've read so far (not too much; I'm not a biologist) each half can take the job of the other half when it comes to injuries. Is that correct?
Are there animals which have more than two hemispheres?
edit: I have seen What was the evolutionary reason for cross lateralization of the brain?, but that question seems to be about the question why the left hemisphere controls right body parts and the right hemisphere controls left body parts. My question is why there are two hemispheres at all.

Possible duplicate of What was the evolutionary reason for cross lateralization of the brain?

You will probably want to read Do the Left Brain and Right Brain have different functions? too.

Bilateral symmetry evolved to be the predominant body plan. According to Wikipedia it accounts for about 99% of all animals. And while this is pure opinion, it kind of makes sense when you consider that almost everything starts from a single cell and we divide in two. And as the genes that control body plan are highly conserved in most organisms, then the simplest way to form a multicellular body that starts from a single cell and grows by dividing in half many times is to have two sides.

"From what I've read so far (not too much; I'm not a biologist) each half can take the job of the other half when it comes to injuries. Is that correct?" The brain does have plasticity, but there are limits, and if you have passed certain developmental targets, then it becomes very difficult to compensate. Over long periods of time and a lot of occupational therapy, some people have recovered some of the functionality, but it depends a great deal on where in the brain the damage was done.


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Problem: What is this pattern of inheritance?
The following question was on a pretest of mine, and I'm trying to figure out the answer using what we've learned about Mendelian and non-Mendelian patterns of inheritance. I'm struggling quite a lot with this question; I'm not sure if that's because of me or if the question itself is poor/confusing.
I don't know what the answer actually is, as there was no answer key to go along with the exam. My best guess is that the pattern of inheritance is Incomplete Dominance based on the Red x Yellow cross and the fact that neither allele was dominant over the other in the resulting progeny. But is it even possible to state this with full confidence? What about the other crosses?

In a plant species, plants may produce red, yellow, or orange flowers. The table below shows the results of crosses between the plants that produce each flower color.

Based on this information, which pattern of inheritance controls flower color in this plant species?
(A) Codominance
(B) Complete dominance
(C) Incomplete dominance
(D) Multiple alleles

The answer is incomplete dominance.
It can't be codominance, because codiminance involves both phenotypes being expressed in different parts of the organism: you would end up with red and yellow spotted flowers.
It obviously isn't complete dominance, because the red x yellow cross produces orange flowers.
Knowing that it has to be incomplete dominance or multiple alleles, we can examine what we would expect to see in either of these cases.
Multiple alleles
In the case of multiple alleles, each individual plant has two alleles out of a possible three. These alleles will also express some sort of dominance pattern over each other. Let's say, hypothetically, that the dominance pattern goes Red > Orange > Yellow.
In this case, all of the yellow flowers would have a genotype of yellow/yellow. The orange flowers could be orange/yellow or orange/orange. Red flowers can be red/orange, red/yellow, or red/red. When performing the crosses between red and yellow, you would then expect some mixture of offspring, probably mostly red. If the dominance pattern was different, you would still expect to see some mixture of offspring. But instead we see only orange offspring.
Incomplete dominance
In this scenario, homozygote red individuals have a red phenotype, homozygote yellow individuals have a yellow phenotype, and heterozygous individuals have the mixed orange phenotype.
In this scenario, you would expect red x red to produce only red offspring, and the same goes for yellow x yellow, because both parents have to be homozygous. Orange x orange would produce offspring in a genotype ratio of 1:2:1, as is the case when you self-cross heterozygous organisms. Orange x red and orange x yellow will produce offspring in a 1:1 genotype ratio, as is the case when you cross a heterozygote with a homozygote. These are exactly the patterns we see, so we can conclude that the answer is incomplete dominance.

Thanks so much for your thorough response, this question was bothering me. But I see how one would arrive at that answer now.

Are you saying that for the answer to be multiple alleles, each phenotype needs to be represented my an allele? So one Red, one Orange, and one Yellow? Is that the technical definition of multiple alleles for inheritance? It seems like that is a bit of a confusing answer choice, as there have to be different alleles for red and yellow, at a minimum.

@AMR Yes, that's the definition I'm using. I guess the wording is a bit confusing

@CactusWoman But according to my textbook, "multiple allele" refers to inheritance involving a single gene that has 3 or more alleles, such as the gene that codes for blood type (which has alleles I^A, I^B, and i). What would be the difference between, say, blood type and the flowers in this case?

@AleksandrH That is what we are saying. In your flower example multiple allele would mean there is a Red allele, an Orange allele, and a Yellow allele, however, in the example of the questions, there is no Orange Allele. A Red/Yellow Heterozygous will have an Orange phenotype, but there is no actual Orange allele, only an Orange phenotype.

Ah, I see what you guys mean now. So the fact that a Red + Yellow cross can produce Orange implies that there is no "orange" allele, correct? Rather, the orange flowers are produced as a result of incomplete dominance between the Red and Yellow alleles?

@AleksandrH Correct, the orange phenotype is the result of the heterozygous red/yellow genotype.


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How does Australia fit into 'New World' / 'Old World' dichotomy?
How are places such as Australia and New Zealand classified when differentiating geographic areas based on 'New World' and 'Old World?'
My understanding is:

New World = North America + South America (+ Central America)
Old World = Europe + Asia + Africa

This is biologically relevant via biogeography:

Ex: neotropical vs. paleotropical (comparable to New and Old World Tropics)

I've seen online sources group Australia / New Zealand in both New and Old World (or in neither). So what's the right answer?
Reputably cited answers only please!

Please comment as to why you down voted

I do not see any reason to downvote this question either. +1

I downvoted the question because it's not biologically relevant. The concept of Old and new worlds reflects only the history of European exploration and colonization. As for biology, there may be more differences between north and South America than between North America and Asia.

@IMil - makes sense and thanks for sharing. It's basically my answer :-)

@IMIL but it IS relevant for biology. I gave a direct example demonstrating so (and see Christiaan's new world primate example below). Just because it's not about cells, cancer, or microbes doesn't mean it's not part of biology. Biogeogrpahy is a prominent and legitimate sub-field of biology. Further, the relative difference between N & S are irrelevant to the validity or relevance of this question. New World and Old world may have originated in a more historically dated context, but that also does not disqualify a question pertaining to their use. (Besides, they are still often employed).

...Your comment is equivalent to downvoting a question that asks for clarification, for example, about the historical taxanomic kingdom of "Monera". Yes it has older origins (and actually is now defunct), but that doesn't mean that studying or understanding the concept of the Monera kingdom (typically through questioning) is irrelevant. I fully disagree with your approach to judging biological relevance.

First off - this is an answer without citations. I looked for them, but couldn't find any. The terminology is undoubtedly described in reputable sources, but it is unlikely a paper is dedicated solely to explain this terminology, making literature searches tricky. Having said that -
I discussed this question with an anthropologist and she agrees with my idea that the terminology Old and New World is a historic and Euro-centric one, dating back to the colonial times when Europe viewed itself as the center of the world.
The Americas were discovered relatively early, around 1492. It was designated the New World. Australia wasn't found until around 1606. By that time the New World was already a century old and very likely already solidly associated with the Americas.
The New World, in a biological context, is often used to describe groups of closely related species found in the Americas and not elsewhere, such as New World monkeys. In certain areas of expertise the terminology is baked in in the jargon, .e.g,  monkey and ape behavioral research areas. New World monkeys can be referred to by the Cebidae, as per the Linnaeus's classification. However, due to practical reasons geographical clustering of species can be more convenient.
The term New World means different things in a biological context or in the context of wines, for example (Americas versus Americas + Australia - admittedly Australian wines are pretty good).
In all, I think the terminology 'New and Old World' is confusing, rooted in historical considerations. Australia as well as Antarctica don't fit in this terminology.


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Unmyelinated long axons in the sympathetic nervous system
I was recently looking over some textbook material (pdf) which claimed post-ganglionic fibers of the sympathetic nervous system are unmyelinated.  This was surprising to me, since I had previously thought that long distance transmission of an action potential required myelin (I can even remember being told that myelin was essential for large life forms, because the nerves otherwise could not have controlled distant body parts).
First, is the textbook correct?  Second, assuming it is true that post-ganglionic fibers are not myelinated, is there some advantage to this arrangement?  At the very least, I would think it would be far more energetic to send a signal in a unmyelinated axon.


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What is the definition for vitamins?
I have found the following definition on Wikipedia:

An organic chemical compound (or related set of compounds) is called a
  vitamin when the organism cannot synthesize the compound in sufficient
  quantities, and it must be obtained through the diet;

That doesn't seem to exclude essential amino acids and essential fatty acids though, and those are also organic chemical compounds that by definition can't be synthesized in sufficient amounts.
So is the definition incomplete?

Generally speaking, bulk essential nutrients (e.g. amino acids, fatty acids) are used stoichiometrically to form macro cellular structures and are 'baked in' to the structures or compounds they are used to make. Once those structures are destined for degradation, sometimes the bulk essential nutrients can be recovered and reused in the synthesis of other structures or compounds, but catabolic elimination from the organism is always an option that yields useful energy.
Vitamins, on the other hand, are usually used catalytically. Vitamins are not 'baked into' the compounds they help make or process; vitamins transiently participate in the reactions required to make or regulate a compound or structure, but don't ultimately get 'used up' by that process.
Ultimately, vitamins don't have a bulk energetic value to a cell. For instance, once vitamin E (α-tocopherol) is oxidized, its only fate is to be excreted as waste. Fatty acids and amino acids, once destined for degradation, have their remaining chemical energy extracted prior to excretion of their downstream waste products.
It is philosophically interesting to remark on the diversity of bulk biomolecular building blocks that are still necessary for some organisms to obtain from their environment. Not all of them get called vitamins.

It's just naming convention. We recognize, officially, the 13 vitamins based on activity, but we intentionally classify amino acids, etc. as such instead of as vitamins. It's just one of those things that people stick to so that it's standard, such as beverages as a blanket term for certain drinks but not for every type of fluid. (maybe that's a bad example, but hopefully you get the idea)


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Are two eyes necessary for 3D vision?
It has always been my understanding that humans have two eyes so that we can have 3D vision: the left eye sees more of the left side of an object than the right eye and vice versa. This helps us to estimate depth among other things.
Now when I close one eye, I still am able to perceive depth. I assume this is because my brain fills in the blanks For how long does this work? Do people eventually lose the depth perception (or at least it diminishes significantly) when they lose a single eye?
If so, how low does it take? If not, clearly we are capable of perceiving everything with one eye. Why do we then have two (besides redundancy and a larger field of view)? What is considering the evolution of man better in having two eyes as opposed to one or three, or four,..?

Here's an open-access article on monocular stereopsis that might be interesting: https://www.researchgate.net/publication/253334388_Seeing_in_3-D_With_Just_One_Eye_Stereopsis_Without_Binocular_Vision .. Being said this may very well be more suited on cognitive science SE.

@Kendall +1 for neat article. But I disagree about migrating the question.

I guess distance can be perceived with information from lens focal length, but that is not sufficient for 3D vision.

Try getting a friend to throw a ball back and forth with you. Then attempt to close one eye while continuously tossing the ball. I think you will be surprised by the results if they are the same as mine.. It does in fact, from my experience becomes extremely difficult to make the judgements needed for the task with only one eye.

I can accurately understand 3-d structure of an object in hand, from various perspectives when I see from 1 eye. Isn't it normal?

It seems like you suffer from a misconception. "The left eye sees more of the left side of an object..." is not how distance perception works. Otherwise we wouldn't be able to estimate the distance from flat objects, such as traffic signs and shooting targets.
The actual mechanism is parallax estimation, or Binocular disparity. In a nutshell, the closer an object is to your eyes, the bigger the difference of its position on the left and right eye's retina will be.
You may perform a simple experiment: find a place where several parallel wires hang in the air: a train line or aerial phone/power line. Look at the wires normally, and they will appear just as black lines in the sky, with no distance perception. Now tilt your head to the side, and you will instantly gain a feeling which one is closer, and which one is further away. Why the difference? Because any shift of a horizontal wire gives the same picture, meanwhile for vertical wires the difference is obvious.
When you close one eye, your brain loses the ability to estimate parallax. However, it is left with several options:

Visual cues. If one object overlaps another, it's obviously closer. If two objects look the same but one is smaller, it's probably further away (or a child). If you know the expected size of an object (a mountain/a horse/a fly), you may get the feeling of distance as well.
Focusing distance. When you focus your eye on a near and far object, the feelings are different.
Memories. You remember what you've seen with two eyes.

Of these, only (3) depends on previous binocular vision. (1) and (2) are available even to those who were born with one eye. However, parallax estimation is much faster and more precise. With a single eye you will be able to hit a fly on the wall, but catching it in the air will be extremely difficult.

Actually, there is 4. moving your head (or the whole body) in order to get different viewpoints. Human brain is perfectly adapted for this approach and computer graphics frequently "abuse" it, because the 2D screen cancels any binocular vision or focusing distance cues. That's why 3D object are frequently presented slowly rotating.

As someone who is blind on one eye I can confirm an option 1 works pretty well under most circumstances and option 2 covers a lot of the others. they don't work well on quickly moving objects though.

Edit01 (here and scattered throughout)

[Not meaning to be antagonistic… but admittedly somewhat defensive.]
Insofar as the following is a citation of an existing work, it is the below Martin and Foley item, pp165-185 (with a noted exception) — noting again that I read this years ago, and did not consult it (nor anything else) when writing the below… and (again) that I consider that, although this can be studied as a science, most of the root knowledge is innate (of course) and implicit and could be rendered explicit by any adult who did not already have it so (as in the following example).  (It is of course theoretically possible that I have read other sources on the same material.  As far as I am concerned, most modern adults would consider almost everything here neither insightful nor controversial, with the exception of brightness (for which I have no source), height cues (which I did not mention) and kinetic depth effect (which I did not mention and which is not obviously and certainly relevant to the question).)
Atmospheric colouring is an exception in that one can use this to work out that air is blue (as opposed to needing to know that air is blue to make sense of an apparent phenomenon).
Brightness is an exception in the case of which indeed I should have supplied a reference… except that, as noted, I can not see it in the noted text book, and thus have no idea where I heard it (noting that I do have a memory of the excitement of learning this (or possibly working it out)).
More citation anomaly and disparity as noted.
End — Main Body of  Edit01.

Original, with references in “[]” added.

Going from memory, since no one else has covered this… .
This is more a psychology question (as below).
3D vision utilises about seven different mechanisms.  Binocular vision accounts for only two of these.
• Occlusion — each eye sees slightly different areas of a partly occluded object.  [(“Occlusion” suggests also the monocular topic “interposition”, below.)  As a binocular phenomenon, Martin and Foley (p183) label this “binocular disparity”, which is [from a quick look] actually about the image from the same object falling on “different” — I would say “non-corresponding” — areas of the retina (as a function of being closer to, on, or further from, the focal distance).  [From a quick look] they do not seem to cover the fact that one eye will actually see more of a partly occluded object (which means I have no idea where I heard it (and I am thinking that I might well have worked it out myself)).
• Focus — you have to focus both of your eyes on an object to see it not-fuzzy; your system knows about (relative) eye positions and subject distance.  This includes both focusing the lens in the eye [“accommodation” [p167] is lens shape] and pointing both eyes at the object [“convergence” [p182] is the eyes turning towards each other].
Binocular occlusion information only works out to about (from memory) 2m [“10 feet” Martin and Foley p183].  This would be increased by having the eyes further apart.  (Focus works out to a much greater distance; I am not sure which of the above two aspects is more useful, but I am guessing it is lens shape (and that they are of roughly similar usefulness).  [Martin and Foley mention “10 feet” (p167), citing Hochberg (1971) for accommodation (lens shape)… but appear to have chosen this as immediately arbitrary.  Their point is that it yields “rather weak” distance information.]
Other (monocular) 3D vision cues include the following.
• Object size — many objects have a standard size [“familiar size” p167], and almost all objects have different proportions (such as leg thickness) according to how big and heavy they are [which Martin and Foley do not cover; the source is me]… and an object that is further away will have a smaller image size.  [pp167-169 “size cues”, “relative size”.]
• Brightness — any given object will reflect less light into the eye from further away (because the eye is a smaller target further away).  (This is more useful and important than one realises.)  [From a quick check, this one does not appear to be in the noted text.  I do not think (particularly) that I worked this out for myself, but if it is not in that text, then I have no idea where I heard it.]
• Perspective — many types of object (e.g. road, path, wall, river) have a stable width, or similar or analogous, and this will have a progressively smaller image size with greater distance.  [“linear perspective” p170.]
• Texture — many objects have a known texture (or (assumptively) a regular texture), and the image size of the detail of the texture will decrease with distance.  This works for groups of animals, and leaves, and the like, as well.  [pp169-170.]
• Air tinting — the further away an object is, the more it is tinted blue by the interposing nitrogen.  [“atmospheric perspective” p170.  Martin and Foley also say that more distant objects appear “blurr/y/”.  I would say that that is largely because we have less visual acuity for an object that is further away (because the image size is smaller); Martin and Foley put it down to interference by air particles.]
• The physics of movement — speed and acceleration can be informative.  [Martin and Foley treat this area on pp174-176.  I was thinking of… what I said.  M&F mention “motion cues” (the class), “motion parallax” (which involves the subject moving laterally, and multiple stationary objects), “motion perspective” (which involves the subject moving towards or away, in any environment) and “kinetic depth effect” (which is about apparent 3D-ness in rotating objects, and is ostensibly not about distance).]
[Other monocular items that Martin and Foley mention… .  • Shading [p170] — objects can cast shadows on other objects.  I would say that this is primarily not about distance perception.  • Interposition [p167] — the nearer object obscures part of the further object (or not).  • Height cues [pp173-174] — my take on this is that, on flat ground (and because the viewer is above the ground), an object that is further away will have its base closer to the horizon and thus visually higher… and, for objects in the air, I would say here only that it is more complicated.]
Focus is very valuable for (for instance) catching a ball, whereas a task like driving [with one eye] has much more 3D information available.  [Source:  I worked this out using thinking.  …So it’s me.]
As for having more than 2 eyes… having eyes spaced apart vertically (as well as having the existing horizontal spacing) would give additional occlusion information, but the gain would be minimal.  [Source:  I worked this out using thinking.  …So it’s me.]
Source

The source is a custom book — that is, “Custom Book”, which is, “a compilation of chapters from… [existing] Pearson Education Australia titles.”  The publisher logo “Prentice Hall” appears, but only as a logo, and not on the cover.
The Custom Book is “PSYC236 Cognition and Perception”, ©2001, Pearson Education Australia Pty Ltd.  It is “Sourced from:  Sensation and Perception 4th Edition”, ©2001, Martin and Foley.
The cited material is from a chapter numbered 6, which appears to be its number in the original/source book; ditto for the page numbers.

But the question is based on a misconception or reversal of causality. "humans have 2 eyes so that we can have 3D vision" is backwards.  We have 3D vision because we have two eyes.  We have two eyes because, like all vertebrates (and insects &c), we are bilaterally symmetric and have two (or pairs) of just about everything.  But starfish, for instance, with 5-fold symmetry, have 5 eyes.

Welcome to Biology.SE! While this could be part of a good answer, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus not appropriate for this site. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!

@jamesqf Eh, I do think the OP has a bit of confusion about that, but I think their question is more along the lines of "why can I still perceive depth with only one eye". "We have 3D vision because we have two eyes" isn't true - there are several monocular depth cues that give us 3D vision as well. People physically missing an eye or with amblyopia still see in 3D. Additionally, many other mammals have poor stereoscopic vision despite having 2 eyes, our quality of stereo vision is an adaptive trait shared with other mammals like other primates and carnivores (and non-mammals like raptors).

In summary, I think this answer perfectly answers the question that was asked, it's just missing references as noted in the banner and pointed out by tyersome.

@Bryan Krause: True, and also binocular stereopsis only works for relatively close objects.  For instance, ever noticed the exaggerated 3D effect of viewing a fairly close subject with good binoculars?

That the following 3D vision cues are available is necessarily true (given gravity et al.):  occlusion, lens focusing, eye focusing, object size, brightness, perspective, texture, air tinting, acceleration physics (which is, of course, all of them).  Any text book on the psychology of vision will mention these.  (I can dig mine up if this would actually help?)  I do not think I ever read any attempt at explaining how the human vision system utilises this information.

Theoretically, I could do a huge search for mention of experiments that show that we use them?  However, I think a reasonable person could accept {the fact that the items in the list belong there necessarily} as sufficient.  …So I am taking this as yet another personal slight.

The ability of seeing in 3-D is an emergent quality of the brain. Yes; at a certain level, all perception is based on emergent qualities of our brains.
That being said, when I was sleep deprived for almost three full days, I began to see in 3-D using only one eye. Somehow, my brain ‘unlocked’ an ability that had previously been limited to seeing with both eyes. Even more astonishing 2-D printed photos and 2-D computer images appeared in 3-D as well.
Anecdotal? Yes. But genuine and real to my perception as anything else I experience. Go figure!
See definition of ‘neural reality’. I believe this allows a sneak peak behind the curtain of human perception.

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text:
Why do I see different hues of colors between each of my eyes?
Frequently, I see colors with a slightly different hue when looking through my eyes individually. The right eye is more red-tinted ('warmer' hued) and the left is typically more blue-tinted ('cooler' hued). However, sometimes I can't notice any difference in hue between the eyes (even when closing the other) and on a very rare occasion the warm/cool differentiation is switched (left is warm hued, right is cool hued). Numerous others have confirmed they've experienced similar patterns.
My questions:

What causes this differentiation between eyes?
What would cause the hues from being sometimes clearly noticeable and other times non-existent? Is the cause potentially environmental, behavioral, physiological, chemical, etc?
I wonder if this is occurring at the eyeball level (e.g., cone physiology) or somewhere in my brain (e.g., PVC in the occipital lobe)?

Red + Blue is what gives me 3D vision!! :p

If I had to guess, I would say maybe it's related to cone fatigue/neural adaptation, with each eye experiencing slightly different stimuli and ending up with different temporary adaptations.

@CactusWoman seems like a fair guess,  but I've never heard of this effect influencing perception of color hues. Further, the difference in hue perception can last for hours, even under changing visual stimuli

This is an interesting phenomenon which I have been aware of for several years, but I haven't yet come across any official description of it or explanation for it.
Nonetheless, the phenomenon is easy to explain. It is a result of light adaptation in your retina responding to different levels of light being received by each eye.
Background
The level of ambient light present over the course of the day varies by as much as 10 orders of magnitude, and our visual systems have evolved to account for this. The human retina and later visual processing centers have a number of ways to adapt to the light level present in the environment. They are constantly doing this, but these adaptation mechanisms take a little bit of time to adjust to a different light level, usually on the order of fifteen seconds to a few minutes. This is why when you step out of a dark room into the sunshine, you are momentarily blinded by the (relatively) bright light.
Some of these adaptation mechanisms are color-specific, such as those that occur in the cone cells themselves.
Explanation
TL;DR-ers, just read this section
Most of the time, both of your eyes experience roughly the same levels of light intensity, both in general and for each color of light. But this is not always the case.
If you have one eye covered for a period of time, such as when you've been laying down, then your two eyes will be adapted to two different sources of light. If you then uncover that eye, then for a short period of time that eye will perceive the world to be brighter than the other eye. If the light level present in the environment has a tint to it as well, then the just-uncovered eye will perceive that tint more strongly than the other eye.

DIY Science Time
You can verify this yourself, like I have been doing over the past hour, with nothing more than a makeshift eyepatch and nothing better to do.

First, check your initial state by closing one eye and then the other and switching back and forth rapidly while looking at something white. If you've been awake and active, the images from each eye should appear to have roughly the same hue and intensity.
Cover one eye completely (without pressing on it) for a period of about five minutes, while leaving the other eye open.
Then, remove the eyepatch and alternate closing each of your eyes again.

If my hypothesis and explanation is correct, the previously-covered eye should see the world as slightly brighter and more strongly tinted than the uncovered eye does (the hue of this tint should depend on your light source).
If you guys actually do this, you should report your results in the comments, especially if your results demonstrate a flaw with my hypothesis. Let's do some science, people.

I appreciate the effort you put into writing your answer and the enthusiasm you have for running your experiment, but I'm ultimately looking for existing evidence cited from one or more reputable sources. If you have any such source(s), please add them . Thanks! :)

Your crystalline lenses are different colors.  You are developing cataracts.
I have noticed this too.  I assumed it was early cataract in the yellow eye and this is the opportunity to do the back reading.  A cataract is the lens of the eye which has yellowed and to some degree opacified with age.
from http://vsri.ucdavis.edu/research/psychophysics

Changes occur slowly and so unless you compare one side to the other you don't perceive everything is getting yellower.  But after cataract surgery everything is much bluer.  The squares in the image below show regular white light and then how yellow it appears through a cataract.  Same source.

I assume your red tinted eye is the cataract eye.  But do not be worried.  Cataract surgery is not a big deal.
I do not have an explanation for the switching back and forth / normalization.

Thanks for the interesting post. However, I would think cataracts is certainly not the culprit in this case given the switching back and forth.

@theforestecologist I wouldn't be so quick to dismiss this. The key finding here is the fact of a difference. The subjective experience of an occasional switch in hue could certainly occur at the cortical level. Cataracts are extremely common.

While cataracts is a possible explanation, the much more likely explanation is this answer about light adaptation.
There's a significant amount of literature about perceptional hue shifts with varying adaptation to brightness. While these experiments were not done with monocular variants, it's reasonable to believe that the effects measured can affect eyes individually.
Stabell et al. 2003 describes the effects of light and dark adaptation of rods on specific hue thresholds:

Specific-hue threshold as a function of absolute rod threshold was measured with long-, middle-, and short-wavelength monochromatic test lights presented 17 deg extrafoveally. The measurements were obtained both during the rod phase of long-term dark adaptation and under conditions where the rod receptor system was gradually light adapted from a dark-adapted state by a scotopic background field of increasing retinal illumination. The results show that change in specific-hue threshold with change in absolute rod threshold is not, in general, identical for light and dark adaptation of the rod receptor system.

Ambler 1974 also describes a similar effect linked to brightness adaptation:

Rod interference is a possible factor contributing to the elevation of chromatic threshold in peripheral vision. It was found that light adaptation lowered peripheral chromatic thresholds. This result was interpreted as being due to the lowering of rod sensitivity. It was also found that light in the photochromatic interval appeared blue, indicating that rods may add a blue component to peripheral color vision.

Additionally, the Purkinje effect can also contribute to shifts in the hues observed when the eyes are differentially adapted to brightness. This effect has also been shown in Wolfe et al. 2015 to affect monocular vision, further supporting the hypothesis that perceptional hue shifts can be caused by light adaptation.

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text:
How do microbes develop resistance to anitmicrobial peptides?
I would like to better understand how bacteria use the "strategy" of alternations to lipid A and membrane proteins in order to resist antimicrobial peptides of the immune system?
It is my understanding that the by altering its lipid A, the bacterium makes its membrane less hydrophobic, increasing hydrophilicity, resulting in an increased amount of fluidity for the outer membrane.
This should then inhibit the hydrophobic portion of antimicrobial peptide embedding into the lipid membrane of bacteria.
Is this accurate? Is there anything I am missing about these alterations than confer resistance?


text:
How much genetic divergence must there be to yield two different species?
I read that humans are a few percent Neanderthal. So how much difference between egg and sperm is needed for there to be no offspring. That is, for there to be two different species? Is this a measurable quantity or just a random genetic mismatch?

The 'no offspring' barrier is a bit arbitrary, I'm afraid. Consider pizzly/grolar bears, who are perfectly fertile. And yet grizzly bears and polar bears are considered two different species.

Could you please add a reference to where you read something. It helps to give a frame of reference to people trying to answer your question. An article in the Daily Herald, is different than one that you read in Popular Science is different that one you read in Nature.

Try reading this first, Reproductive Isolation , and then if this still doesn't answer your question or if it raises other questions, please feel free to edit your question.

Besides "species" being an ill-defined term, the required genetic divergence isn't appropriately characterized by "how much" genetic change, but rather what precise genes have changed in what ways to prevent population mixing. A single gene or two might cause it, if it affects a critical function, say having to do with sperm/ovum compatibility.


text:
How old is the oldest intact DNA?
DNA fragments are known from bone fragments from the Mesozoic, but these don't count. I'm guessing the oldest DNA is recovered from permafrost, but how old exactly?

This sounds like an interesting question, but I'm not sure why your example doesn't count. Can you expand on that?

Well, the oldest intact DNA found is actually 419 million years old, and it belongs to (not surprisingly) bacteria. Samples were extracted from surface-sterilized salt of different geological ages (23, 121, 419 million years of age, MYA).
But as you mentioned, these are fragments. Studies on the half-life of DNA suggest that even under ideal circumstances, DNA sequences older than 1.5 million years will be too short to be readable.
The oldest genome known to date, though, is 700,000 years old, and was recovered from samples from a horse leg bone. You were correct, the leg was in permafrost. That's a considerable jump from mastodon and polar bear fossils which were about 50,000 and 110,000 years old.


text:
how to change format of ent file into PDB format?
whenever i download files from Protein Data Bank(PDB),they are downloaded in .ent format. How can i convert them into PDB format??

Just rename the file to .pdb - in other words, .ent files are PDB format:

The archival PDB files will be distributed with the reserved conventional names, in the form pdbentry_id.ent, where entry_id is a PDB 4-letter code, e.g. pdb1abc.ent, for PDB format entries; rentry_idsf.ent, e.g. r1abcsf.ent, for X-ray experimental data; entry_id.mr, e.g. 1abc.mr, for NMR experimental/constraints; entry_id.cif, e.g. 1abc.cif, for mmCIF format entries; and entry_id.xml, e.g. 1abc.xml, for canonical XML format entries.

From http://www.wwpdb.org/about/faq

nothing happened..:/ still it's a ENT file

Not sure what you mean, sorry. If you open it in a text editor you should see that it looks the same (I think). I can't seem to access the pdb's ftp server at the moment, sadly.

@HayaDar Open the file fresh in notepad, file > Save As > file types: all files and change the whole thing to filename.pdb


text:
Can a hormone be absorbed into the body digestively?
Obviously, to act most hormones must be present in the bloodstream. What happens if a hormone or hormone-containing food is consumed normally? Is there any way for the hormone to reach the bloodstream?
A related question is whether hormones are destroyed by digestive enzymes and chemicals, which include hydrochloric acid and bile salts. If hormones are destroyed by these chemicals then it may be impossible for them to enter the blood stream.

Yes, some hormones can be absorbed from the digestive tract. Birth control pills are a perfect example.

@MattDMo Well in that case the drug is encapsulated a special "enteric coating" that protects it from stomach acid.

@ImprisonedRhesus peptide hormones (e.g. growth hormone, insulin, pituitary hormones, etc) are denatured by stomach acidity and digested by proteinases - as MattDMo says above the steroid hormones (testosterone, estrogen, bile salts, etc) can be absorbed by the GI tract

This entirely depends on the kind of hormone. Hormones can be chemically completely different things. For example, estrogen is a steroid hormone and is chemically very stable so that it can pass the stomach without being harmed by the acidic conditions (even without enteric coating. AFAIK enteric coating is only used in emergency contraceptives, not in regular ones. And for the emergency contraceptives it is used in order to reduce side effects such as vomiting). As such, estrogen in your food or drink will have an effect on your body and there are many studies suggesting that this is a reason for reduced fertility in men.
On the other hand, insulin is a peptide, which would be digested and its hormone function completely inactivated when swallowed.
There is even the notion, that the gas nitric oxide may have a hormone function. In that case, it could reach the blood stream even through inhalation.
In summary, whether or not a hormone can be active after ingestion entirely depends on the kind of hormone.


text:
Symmetry of species
I've got a silly question, sorry for that. I know, that we probably have no the right answer and the current answer could be "that's evolution, external conditions". I'd like to speculate, why most of mammals (for ex.) and people especially are symmetric?
I know, that we are not completely symmetrical, but anyway.
Thanks a lot.

When I get back home, I'll try to find a book that I have about this ("Fearful Symmetry: Is God a Geometer?" by Ian Stewart) which tries to address the question of why organisms have the symmetries that they do. If no one else has answered by then, of course...

Not entirely a duplicate or subset of the linked question. -- IF one were to see this question by dshulgin as asking: Why are Chordates still symmetrical? There are two additional considerations not clearly addressed in the linked question. -- 1) Fundamental distinctions in organisms are unlikely to change via Neo-Darwinian Evolution -- 2) Bilateral symmetry is a very good proxy for genetic fitness and therefore a symmetrical member of your species is a better mate selection. -- These two considerations are not relevant to the linked question but do apply to @dshulgin's question here.

There's really two answers to the question.  The first is overall symmetry: mammals, like all tetrapods, are bilaterally symmetric.  This comes from a distant common origin with other bilaterally symmetric organisms.  Organisms which evolved from this common ancestor often have organs in pairs, probably evolving as a re-use of regulatory genes.
The other answer is the high degree of symmetry in external appearance.  While internal organs are roughly symmetric, there is some asymmetry.  However the external appearance of most bilaterally symmetric organisms is highly symmetric.  This suggests a different force at work.  In fact, there is some evidence for sexual selection for bilateral symmetry.  Mate choice is driven by indicators of health, and bilateral symmetry is a common indicator of health.

It is, of course, not just mammals, but nearly all animal life is symmetric. Even plants are usually symmetric in some degree. There are exceptions here and there. For example, one interesting exception is that of the fiddler crab which has one claw larger than another. In general, when a single appendage is present on an animal it is nearly always on the center line of the animal. For example, the horn of a rhinocerous or the central horn on a triceratops, or a human's nose.
The symmetry is generally enforced genetically, not environmentally. For example, if you hold a paper up to your face you will find that the left side of the face is different than the right side, or at least that is the way it is for most people. Thus, once conceived, the two sides of the face grow differently, a phenomena that geneticists call genetic "expression". For example, your fingerprints are "expressed" traits, not genetic traits, and for this reason the fingerprint on your left thumb is different than the fingerprint on your right thumb.
Even genetically, however, many parts of the body are not symmetric. For example, the heart is on the left side of the body, but the liver is on the right.
The evolutionary logic for symmetry probably is because it makes locomotion easier and more effective. If an animal is not symmetric, they may have difficulty moving efficiently.

Although not a biologist, Steven Pinker notes that bilateral symmetry evolved in organisms to allow them to move in a straight line. For a bilaterally symmetrical animal to move, they simply alternate movements between one half of their body and the other. This is true for fish, snakes, insects, mammals, etc.  There are exceptions, for instance, flying and hopping, but those creatures evolved from ancestors that first locomoted by alternating limbs.
If you look at jellyfish, for example, they are radially symmetric, and their manner of locomotion is to swim in a sort of spiraling shape.
Probably after it arose, bilateral symmetry became a sexual selection criteria, because it is costly to perform during growth, as Pinker goes on to explain.


text:
curly braces in sequence motifs
what do curly braces in sequence motifs stand for?
e.g. in
RTCRYBN{4}ACG
what is N{4}? moreover, i notice that in TRANSFAC matrix notation the N{4} is completely omitted:
NA  Abf1p
XX
DE  RTCRYBN{4}ACG
XX
P0  A     C     G     T
01  0.500 0.000 0.500 0.000 R
02  0.000 0.000 0.000 1.000 T
03  0.000 1.000 0.000 0.000 C
04  0.500 0.000 0.500 0.000 R
05  0.000 0.500 0.000 0.500 Y
06  0.000 0.333 0.333 0.333 B
XX
P1  A     C     G     T
01  1.000 0.000 0.000 0.000 A
02  0.000 1.000 0.000 0.000 C
03  0.000 0.000 1.000 0.000 G

moreover the MEME suite's transfac2meme completely ignores the second chunk of the matrix after the P1 row.

I'm voting to close this question as off-topic because this is about the computational aspect of Bioinformatics. While questions on interdisciplinary subjects like bioinformatics are welcome, they must focus on the biological part of the subject.

@AMR I would not consider this as off-topic because it is about understanding data from a bioinformatics repository. It is not about programming or any other software issues.

@WYSIWYG It is not asking about the biology in any way. You could just as easily be looking at astronomical data. If they had asked how can I determine if a DNA binding protein will bind to this sequence or how can I determine if this is an enhancer site, then that is a biology question. This is purely from the technical side. Also mdperry's answer answers it, so there is no point in keeping it open anyway. It also shows no research effort, because all that is needed is to Google bioinformatics nucleotide codes and the first entry gives the answer. It could be closed for several reasons.

@AMR This question is about analysis of bioinformatics data, which is on topic (akin to bioinfo data formats).. I have worked in bioinformatics a bit and I can vouch that it is not some kind of an obvious thing.. Experienced people may look at it and know, but not everyone... AFAIK we made it clear that this may not be not one of the close reasons..

@AMR your comments are unfair -- i have tried to answer this question myself. your googling suggestion does not answer my question as i already knew what 'N' stands for but not the {4} bit.

N is the IUPAC code for any nucleotide, so in DNA sequence an N signifies any one of the four bases could be in that position.
The {4} means 4 of the previous character in the pattern, or NNNN. In Perl regular expressions \d{4} means match 4 digits in a row, so the notation is quite similar.

thank you for your answer. i knew what N stood for but i couldn't find what curly braces meant. i guessed that could mean NNNN but then it doesn't explain why the TRANSFAC matrix for the motif ignores these nucleotides. moreover there are motives like TNNCGTNNNNNNTGAT in the same document. why isn't the same notation used here? i.e. TNNCGTN{6}TGAT?

As to why some people prefer using curly braces vs. expanding the characters and printing them all, I have no idea (or why some programs or databases prefer one or the other). I have not used TRANSFAC very much at all; as I recall it requires a licence(?). I think what is important to keep in mind is that using a consensus sequence (the IUPAC codes) is generally not going to be as sensitive as using a Position Frequency Matrix (PFM) or a Position Weight Matrix (PWM). That matrix you show is not a real PFM/PWM--it is a PFM derived from the consensus sequence motif.

it's a TRANSFAC formatted file in the Yeastract database which is open to public; and it just seems that they are being inconsistent with regards to their notation in the same document then. okay, i didn't realise i was using something that was't a real PWM. when you say 'less sensitive' do you mean using it for binding site predictions won't be as accurate as using the real PWM?

Let's say that there are between 10 and 100 known Abf1 binding sites in the Yeast genome. By lining them up (aligning them to each other, and summing up the number of each nucleotide at each position, and then dividing that number by the number of sequences in the alignment) we get the PFM. A simple way to create a PWM (circa 1990) is to multiply the value at each field in the matrix by the log(base 2) of the number, (m x log2(m)). (there are probably much more sophisticated transformations available now). Now you have a way of calculating the bits of information at each site in the matrix

With a PWM you can use a program to scan along an entire chromosome, giving each site a score. If you do this (make a PFM and a PWM) do you get the matrix from TRANSFAC? If you do, great, but if you don't then you might well get more 'hits' with the real PWM. Keep in mind that without experimental confirmation of some sort none of these predicted binding sites are necessarily real binding sites, they are just sites that score above some arbitrary threshold.

apologies for a slow response -- many thanks for your clarifications! i think a PFM should be sufficient for my needs; i have used them to identify potential binding sites and got 2.5k (at 0.05 q-value) using the FIMO software. knowing even putative binding regions should be enough.


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Is there a formal definition of signature of natural selection?
I’ve searched for a definition of signature of natural selection. Unfortunately, I haven’t found any formal definition of it.
The signature of positive selection on standing genetic variation. I found this post that links to an article measuring the signature with an Fst and a Linkage Disequilibrium test.
Are we looking at only some frequency of alleles in different populations? Is the signature only a fixation of alleles in a population where this allele was positively selected?
Another article says:

A single beneficial substitution can be detected in polymorphism
  data, so long as it occurred recently. The fixation of a favorable
  allele in a population distorts patterns of variation at linked
  sites, thereby leaving a distinguishing signature that lasts up to
  about 104 generations in humans or about 106 in Drosophila
  melanogaster (Przeworski 2002). In principle, targets of positive
  selection can therefore be identified by searching polymorphism data
  for regions that harbor this signature (Nair et al. 2003; Wright et
  al. 2005).

Is it always in linkage disequilibrium?

Here is how I would personally explain what a genetic signature is:

A genetic signature of a certain type of evolutionary history (type of selection or demography) refers to the effect that this specific type of evolutionary history has on genomic properties of populations today.
We are interested in understanding such signatures because knowing the association between a number of evolutionary histories and their genetic signature allows us to reconstruct the evolutionary history of a population just by looking at the genomics of this population.
For example, recent selective sweep, population expansion after a recent bottleneck and/or linkage to a swept gene are all causing negative Tajima's D. Balancing selection and/or sudden population contraction are causing positive Tajima's D. In this example Tajima's D is a statistics that is used to measure this so-called signature of the different process.

The above was NOT a citation. I am NOT aware of any publications defining rigorously what a genetic signature is. I think it is not so uncommon for authors to use a term without strictly defining it. As long as the unclarity of the definition does not yield to limit cases and misunderstanding, then it is totally fine.

Do you have a reference to this? I mean, is this a quote? Is it like the gene signature or the genomic signature?

Nope I don't! Feels like we already had this discussion on another post $\ddot \smile$ This is why I said I would explain... and I am not aware of any publication defining rigorously what a genetic signature is. I tried to make this point even clearer.

Haha! Thanks a lot for your contribution! I'm going to continue the research until I find something. This concept is, most of the time, used with selective sweep, right? For instance I found Nielsen, R. 2005. Molecular signatures of natural selection and Hohenlohe, P. A., P. C. Phillips, and W. A. Cresko. 2010. Using Population Genomics to Detect Selection in Natural Populations: Key Concepts and Methodological Considerations with nice figures (fig 1 and 4 respectively) Seems that these images could represent a "signature".


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Are there any predators without camouflage?
Are there any predators that don't use camouflage?

If your question is related to "natural" camouflage, i.e. camouflage that is the result of genetic programming, then Humans would be a good example of predators that do not posses natural camouflage.

Raptors are also good examples. Eagles and hawks, are not really camouflaged, although their ability to be able to stalk their prey at altitude may make them unseen to their prey, unless they are hunting other birds such as pigeons.

Birds of prey, chimpanzees, bats... there's a lot of things that don't appear to use camouflage - but it's difficult to really say definitely, e.g. I imagine a neon pink chimp would be less successful at hunting than the dark furred chimps we see in nature, so one could argue that chimps are camouflaged... Most predators will benefit from avoiding detection for as long as possible, this could constitute colouration camouflage, but also behaviours to reduce detection (e.g. stalking slowly through bushes). Wikipedia say camouflage is "the use of any combination of materials, colouration..." ...

Could you therefore clarify/refine your question, perhaps ask for examples where colouration appears to make no effect on hunting success. E.g. that could be evidenced by studies showing no relationship between the colour variation in a population and the success of hunting.

As the answers show, the answer is definitely 'yes', but without a definition of 'camouflage' I think this should be closed as opition-based. What effectively counts as 'camouflage' depends on the the perception of the interacting species (prey) - so a species can be camouflaged against one species but not another one - and it can include multiple types of colouration or behaviours.

Poison dart frogs have aposematic colouration, making them the exact opposite of camoflaged.
They are also predators, since they feed on ants, termites and beetles.

What is a predator?
As discussed in the comments by @MarchHo and @AMR, there is discrepancy between the definition of predation in the biology literature and in the every day use.
Population definition
From the Oxford dictionary

predation- The preying of one animal on others; the behaviour of a predator (predator n. 2); (also occas.) an instance of this

Under this common definition, the answer is "Yes".
Scientific definition
From wikipedia (who uses the scientific definition)

In ecosystem predation is a biological interaction where a predator (an organism that is hunting) feeds on its prey (the organism that is attacked)

Under this scientific definition, predators describe whichever organism that feed on other organism. There exist no animals that do not predate (Elysia chlorotica is a quasi exception). So, the question boils down to "Are there any animals that are not well camouflaged?" and the answer is always "Yes".
Examples
The Lilac-breasted roller (just to name a nice colorful species) is very poorly camouflaged and feeds on various insects

Zebras do not camouflage (for predation purpose) when they predate grass (grazing).

Anteater do not camouflage (for predation purpose) when they predate ants

The Mandarinfish is also poorly camouflaged and predates on harpacticoid copepods, polychaete worms, small gastropods, gammaridean amphipods, fish eggs and ostracods.

As @AMR suggested in the comments, humans are poorly camouflaged too.

Not sure if this answer is intended in jest, but zebras are disruptively camoflaged

They do not camouflage for predation purpose at least. One could draw millions of other examples of this kind of course.

I like your answer +1, especially for defining predation (which also applied for microscopic organisms).

@MarchHo Zebras are camouflaged against their predators but not as themselves being predators. That is a different issue that plants don't have vision.

And you added birds and humans after I had commented on it. It is generally customary to attribute that.

@AMR I also thought at first that predators implied carnivores, but it is also used in the context of herbivores by scientists. I agree on the issue of attribution, though.

As @MarchHo said, predation have different meaning in the scientific literature than it its everyday use. I will add a word about that.

@AMR I added the bird and human example mostly in reaction to MarchHo 's answer. I also wanted a colourful species and I wanted to state the obvious. Took me a while to see where you commented on it. I am not sure who said it first though, we both said it 15 hours ago. I don't cite hawk an eagles so I'll have a hard time to give you credit for that but I will be happy to give you credit for thinking about humans first and I will edit my post.


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What nocturnal animal sound am I hearing in the trees in Maine?
Every year, during late summer nights (usually around 9:00 pm) in Maine, I hear a noise coming from high up in the trees. The trees I hear it from are mostly maple or conifer, but where I live there are few trees that are not. It sounds like a cardinal's chirp (fourth sound down in link), but longer, scratchier, and lower pitch. The sound starts and ends abruptly. There are three to six chirps in a row from the same tree, and then silence for a few minutes. Sometimes I will hear it again after a few minutes from the same tree and sometimes from a different tree. The skies are usually clear when I hear it. No one else in my family can hear it. I live in a suburban area, but when I go to a more densely forested area I hear it more frequently. Does anyone know what this is?

I think this question might be better fit for The Great Outdoors SE. There might be some people there who are more familiar with bird calls than the people here in Biology SE.

@AleksandrH I did ask it there a few months ago, but no one has answered it.

Do you have a recording of the actual sound itself? 2. What time of night do you hear the sound? 3. Have you noticed what the weather is like prior to and during the time you hear the sound? 4. How high up in the tree is the sound?

What kind (i.e., species) of trees are you hearing the sound from?

https://groups.google.com/forum/#!topic/maine-birds/nvlvEqggNjo

@theforestecologist That sounds like my situation, except the sound I am hearing is definitely not a spring peeper.

@IOWF ok so please answer some more questions or provide more info

Do you typically hear what sounds like one individual, or a couple "talking"  back and forth,  or does it seem like there are many making the sound?  If many, how many (dozens, 100s?) and do they overlap in making the sound?

@IOWF Did you want an answer to this question? You've neglected to provide additional necessary info (i.e., answering any of the questions proposed to you in the comments) for over a year now. I see you're still active on the site, so please respond if you're interested in getting a positive ID or if you have any updates. Thanks.

I have been hearing this sound all summer after dark, I live in southern Maine. I just got home from work (December 2nd) and I'm hearing it again. Must be something nocturnal to be out this late! (10:30pm) I will try to record it.

since you don't have a recording of the sound you might be better off on a birding site where thy will have samples of songs you can listen too, just going from your description it could be anything even a tree frog.

My initial guess (knowing almost no information) is that it's a Northern saw-whet owl (Aegolius acadicus). These owls live year round in Maine but also increase in number as some migrate from Canada through Maine for winter. You can hear their advertising song here.
Northern Saw-whet Owls have a distinctive too-too-too call -- an insistent series of whistled notes on roughly the same pitch, given at a rate of about 2 notes per second. Males calling to advertise their territory can be heard up to half a mile away. Other males respond with a softer, faster, lower version of the call.

Thanks, but its not the one. The noise I hear is similar, but scratchier and less frequent.

Darn. Ok. Please provide more info so that we can try to figure this out. Please answer my questions in the comments under your question.

You still deserve a +1 :)


text:
Relationship between body size and damage done by electricity
We all know that if a person gets stunned by a 2000 volt stun gun, he/she may be knocked unconscious, but he/she is still alive and apparently no damage done on his/her body.
But what could happen if that 2000 volt is applied to a snail whose body is way smaller than that of a human being?
Will it create a lot of damage into the snail's body?
Or the same effect as that of humans.

Certainly it will be more. When a person gets stunned by a 2000 volt stun gun the electricity spreads into whole body. If the target is large the damage would decrease (as you see in humans it has no serious damage) but if the body is smaller, the damage will be greater.


text:
Non-descriptive gene nomenclature
I formally come from a physics/physical chemistry background, but I have begun to specialize in the area of the biomedical sciences and biomedical engineering. I found myself reading an article which talks about using leukocytes as carriers for targeted cancer drug delivery. One of the frequent adhesion molecules that comes up in the paper is E-selectin, whose wikipedia page I looked up to learn more about the molecule.
On that wikipedia page, it says that E-selectin is encoded by the SELE gene. Now, I can see that the gene is called "SELE" as it abbreviates "Selectin E", but my question is: how did this become the "official" name for the gene? Why doesn't the official name reveal anything about the actual nucleotide sequence of the gene? If someone had never heard of E-selectin before, how is he/she supposed to learn anything about the gene just from the name "SELE" ?
Sorry if this is a very nit-picky question. It's just that most of the substances talked about in chemistry have official names that reveal information about the structure, even if there is a more commonly used "nickname."

Biology names, especially proteins have been a free for all. The investigator that discovered it would usually name it, but there wasn't really any standard. Some named them by molecular weight, such as p21 or p53 which were 21 and 53 kD respectively. Even worse is that people studying different organisms would discover a protein and name it and it was only much later on that it was realized that the molecule had homologs in other organisms with different names. That is how you can get the Son of Sevenless or Sonic hedgehog genes or more descriptive names like DNA ligase or Katanin.

Often times we knew the proteins long before we determined the genetic sequence. With alternate splicing, you can end up with different proteins with different functions originating from the same gene. We estimate there are over 100,000 different human proteins, but only 20 to 30 thousand discrete genes. That means that some of this proteins are fusions of multiple gene products are the result of alternately spliced DNA. So the gene may have been named for a different protein and it was only later discovered that a different protein was a different splice form of the same gene.

Welcome to Biology.SE.
To my knowledge there is no good rule on how to name genes. The first person to name a gene or an allele is free to just pick up a that (s)he finds easy to remember and eventually intuitive. Sometime the author just picks a funny name. Here are a few examples from Drosophila melanogaster data base:

bag of marbles: involved in oogenesis, spermatogenesis.
breathless: involved in development of trachea.
buttonhead: regulates segmentation of the head.
dissatisfaction: involved in many aspects of sexual behavior.
hobo: a mobile genetic element.
Indy: for "I'm not dead yet"; this mutation makes the fly live twice as long.
windbeutel: German for "cream puff".

Did you suggest to name genes based on their sequence? Would be quite painful! One cannot name a gene based on its sequence as the sequence is way too long. The median gene length in humans  is 24,000 base pairs (Fuchs G et al. 2014). You just need to refer to a database to match a sequence to a gene name (see BLAST for example).
How could we improve this system?
Do you have any suggestion on how we should name genes? Should they be named in relation to the phenotype they affect or to the biological pathway that are involved in or maybe something else? The issue is that we often annotate and name a gene before knowing much about its effect.
Note that some genes have several names which is indeed confusing. Would be good to solve this a little bit.

Thanks for the detailed answer! I wasn't suggesting that each gene by identified by its sequence because I know the lengths that we're talking about here. I was just hoping that a kind of "language" would be developed, where sequence could be conveyed in a few letters. I can't think of any good ideas off the top of my head, but let's look at a chemistry analogy: take for instance diethyl ketone. It would be cumbersome to specify an origin position and then provide coordinates for each atom. However, those 13 letters are enough to tell you it's (C2H5)2C=O. That's what I was talking about.

To add to this... there is a transposon in Drosophila called Baggins and a gene called Smaug.. Both these are characters from the novel -The Hobbit

@MuhammadKhan Biological macromolecules are hundreds to thousands of amino acids long Genes can be a few hundred to well over a million nucleotides long, and they are interrupted, meaning that there are long stretches, introns, that get spliced out of the mRNA that makes the protein.   You are asking more of an information theory question in How can we compress the sequence into a form that is manageable but can be decompressed into the full sequence, and that would be difficult. Just take a look at the protein FASTA sequence for SELE and you will get an idea of the challenge.

This is an example of a rather simple biomolecule, Acetyl Coenzyme-A, and its IUPAC name. S-[2-[3-[[(2R)-4-[[[(2R,3S,4R,5R)-5-(6-aminopurin-9-yl)-4-hydroxy-3-phosphonooxyoxolan-2-yl]methoxy-hydroxyphosphoryl]oxy-hydroxyphosphoryl]oxy-2-hydroxy-3,3-dimethylbutanoyl]amino]propanoylamino]ethyl] ethanethioate You can start to see the problems that biologists would face if they tried to adopt chemical nomenclature.

@AMR You're right in saying that the question boils down to something more of information theory rather than biology. I guess I'm just surprised that biologists and information theorists (or people at the intersection of these two) haven't made efforts toward this yet. For your chemical example, I know that names get cumbersome which is why names like acetyl co-A were invented, but at least there is a formal name one could analyze if need be. Gene names don't have "standard" names

@MuhammadKhan people have made effort to systematically name genes.. See an example in my answer below. But they do not make things easier.. It is easy for most people to remember a name rather than a random alphanumeric combination.

Unfortunately there are no rigorous naming conventions for a gene. While some are based on actual molecular function or phenotypic effect, others can be totally bizarre names. Some are actually based on the test-tube and purification fraction labels. Some are named on characters from Mythology, novels etc.
I'll add some examples:
SNARE (proteins involved in vesicle fusion): Soluble NSF Activated protein REceptor (where NSF is N-maleimide sensitive factor).
Nanog: Inspired from an Irish folk tale. There is a magical land called Tír-na-nÓg where if one goes, becomes immortal and forever young. So the discoverers of this gene which responsible for stemness of a stem cell, named it as Nanog.
In fact, a lot of Drosophila genes are named after the visible phenotypic effect of the gene mutation. For e.g. Hairy, Wingless, Sex Combs Reduced etc.
Many genes were actually discovered before the genomes got fully sequenced and since these genes were well studied, the idea of renaming them would not have been very appealing. However, yeast genes have been given formal systematic names.
From SGD

YAL001C   first ORF to the left of the centromere on chromosome I (A is the 1st letter of the English alphabet), on the complement or
  Crick strand
YGR116W   116th ORF right of the centromere on chromosome VII (G is the 7th letter of the English alphabet), on the Watson strand

While I agree that absence of any naming convention would not convey any information about the function of the gene, these wild names do make studying biology interesting. Yeast systematic genes names are so uninteresting and hard to remember (at least for me).
However, there are standard nucleotide repositories such as NCBI, ENA and DDBJ which maintain records about different genes. Moreover, there are standard organism specific databases such as FlyBase for Drosophila, TARE for Arabidopsis etc. In these databases you will find the standard names and description of these genes.

Also have a look at this post: Are there more descriptive ways of naming genes and gene interactions?


text:
How long can you effectively store a glycerol stock at -20 degrees Celsius?
I know that glycerol stocks are typically kept in a -80 °C freezer, however there are some people who do not have access to such equipment. How long would you be able to keep a glycerol stock at around -20 °C (typical household freezer temperature). I would like to create a new stock before anything goes amiss.

-20 is also good enough.. I have revived 1 year old cultures..

I have successfully used own stocks that were about 5 years old and stocks from a colleague which where about 10 years old. So they are pretty stable.

While I believe that it is possible to keep a bacterial culture viable while frozen in glycerol stock at around -20 °C, as attested to by WYSIWYG, it is important to note that your "typical household freezer" may not be suitable for such a purpose.
This is because household freezers usually have an "auto-defrost" function. This makes it temporarily thaw out to remove the frost that condenses from atmospheric moisture. If storing sensitive materials such as bacterial/cell culture frozen stocks, this would lead to repeated freeze-thaw cycles which would damage the viability of the stocks.
For that reason, almost all laboratory freezers do not have that function, and instead need to be manually defrosted routinely.


text:
Is a fat-soluble vitamin a lipid?
I read in a chemistry book that a steroid is a class of lipids, and that the fat-soluble vitamins like vitamin D are part of steroids. So is a fat-soluble vitamin a lipid?
This makes me confused as the lipid nutrients seems to contain vitamins which make another type of nutrients.

Or maybe simply that book was defining and giving examples of steroids and didn't mean that every example is now a lipid!

Yes steroids are a class of lipids which include cholesterol and sex-hormones such as testosterone and estrogen. Only vitamin-D belongs to the class of steroids.
Vitamins A, E and K are isoprenoids. In fact even steroids are synthesized from simple isoprenoids. You can refer to a standard biochemistry book to understand steroid biosynthesis pathway.
There are other classes of lipids too, such as fatty acids, phospholipids, ceramides etc.
Yes all fat-soluble vitamins are lipids. This is the definition of Lipids from the IUPAC goldbook:

A loosely defined term for substances of biological origin that are
  soluble in nonpolar solvents. They consist of saponifiable lipids,
  such as glycerides (fats and oils) and phospholipids, as well as
  nonsaponifiable lipids, principally steroids.

Both fats and fat-soluble vitamins are nutrients but are functionally different. Fats provide energy whereas vitamins perform regulatory activity and are required in little amounts in the diet compared to essential fatty acids.

The book actually said that fat-soluble vitamins (not just D) are steroids, were they not accurate enough do you think?

@YoussefDir the book is wrong in that case.


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Where is sialic group in gangliosides that form ABO blood groups?
A ganglioside is a molecule composed of a glycosphingolipid (ceramide and oligosaccharide) with one or more sialic acids (e.g. n-acetylneuraminic acid, NANA) linked on the sugar chain. (source: https://en.wikipedia.org/wiki/Ganglioside)
Gangliosides form ABO blood groups.
Do gangliosides always contain sialic acid? If true, then where is sialic acid in blood groups?
Structural formula of ganglioside GM1a:

Blood Group Antigens:

I suspect this is a product of differentialy expressed glycosyltransferases. Instead of adding a sialic acid, for example, if you're coding for Enzyme B which is an alpha 1-3-galactosyltransferase, you're going to add a Gal to the glycan chain forming B antigen, and so forth. Sialyltransferases can add sialic acid groups, but to the same structure it looks like there is competition between the glycosyltransferases to add sugar moieties that results in different structures getting produced from backbone structures. Source, pages 5-10

Type-1 units may be modified by glycosyltransferases that transfer sugars to either terminal galactose or subterminal GlcNAc, generating sialylated structures or blood group determinants. The synthesis of type-1 units and expression of the corresponding β1–3 galactosyltransferases are regulated in a tissue-specific manner...

Structures Common to Different Glycans
So that's to say there shouldn't be a sialic acid group on ABO antigens, though sialyltransferases are capable of forming Lewis Antigens (Source). In the anabolic pathway the backbone structure is simply getting attacked by glycosyltransferases and the pathway goes the direction whichever one wins out (level of protein vs level of substrate). Being said, I'm unsure it's proper to say ABO antigens are produced from gangliosides, but if anyone finds some faults in my explanation please let me know!
I'm looking into catabolic pathways that may produce ABO antigens by recycling gangliosides, probably resulting from some cleavages by other glycosyltransferases, I just haven't gotten there yet, I'll try to update if I find anything.


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Where do I find microsatellite instability annotation for TCGA data
I have searched through the TCGA data portal but I was unable to find MSI annotation for TCGA Colon Adenocarcinoma (COAD) and Rectum Adenocarcinoma (READ) datasets.
I am searching for the annotation on samples, i.e. if a specific sample is annotated as MSI (microsatellite unstable) or MSS (microsatellite stable). In particular, I found this page, and followed the path:

Data Matrix & Bulk Download: Select 'Fragment Analysis Results' for Data Type

but with no results.

I'm voting to close this question as off-topic because this is about the computational aspect of Bioinformatics. While questions on interdisciplinary subjects like bioinformatics are welcome, they must focus on the biological part of the subject.

@AMR No we have clearly agreed that any question on analysis or understanding of bioinformatics data is on-topic. Frubudu, can you please provide a link to these databases. Your question, as it is, is unclear.

I tried to provide links and to specify better what I am searching for. I am searching for a link to these databases, but if I can provide more information tell me.

And it really isn't hard to find out why the OP cannot get access to this information. It is controlled-access data and that requires special authorization to access as it has information that is unique to an individual. https://wiki.nci.nih.gov/display/TCGA/Open+Access+and+Controlled+Access+Data

Thanks. So I need authorization to access them. May you put it as an answer?