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Why are there no known animals with an odd number of legs?
In my 6th grade science book it is said that there are no three legged animals, and that no animal with an odd number of limbs exists. I checked Wikipedia and could confirm this:

There are no known naturally occurring three-legged animals

On yahoo it is said that

When an embryo is developing, it grows by cell division - the first single cell divides into two, then four, then eight etc. It doesnt' divide into odd numbers - each cell divides in half. So, this means that every creature develops the same on each side of it's body - same number of limbs per side.

It seems to be a valid explanation. So is it true that any organ in any living organism is either one in amount or is in even number? And the explanation of yahoo.com is fine?
I am a beginner in Biology. Please explain in simple terms.

related: http://biology.stackexchange.com/questions/19318/list-of-asymmetric-animals

Starfish (sea stars) have radial symmetry and often have five "natural" limbs.

That Yahoo answer thing is rubbish, by the way. Growing by cell division is not sufficient to ensure bilateral symmetry, for example plants grow by cell division. And as others have said, even within animals not all show bilateral symmetry.

Gastropods only have one so-called foot.

What about starfish,which have 5 arms?

Are you really in 6th grade ?! You are asking great questions ! Keep up the good work and don't always believe what the textbooks say :)

@biogirl No I'm not in 6th grade. I am an Engineer who has started to study biology.

@user31782 LOL ! Sorry for the misunderstanding... Have fun studying bio ;)

Sea stars can have odd numbers of arms (such as 5 as mentioned in other comments) but they have many hundreds of legs underneath their arms. There are possibly an odd number of legs but not necessarily the same number of legs per individual from the same species.

@SteveJessop "That Yahoo answer thing is rubbish, by the way." Hence the entire reason for Stack Exchange's existence :-)

related: Why do we have two of some organs, but not all?

Also @SteveJessop was right to say the Yahoo answer is rubbish. Specifically what happens if we have 6 cells, or any other even multiple of an odd number of cells. By that same broken logic we have the potential for odd number of limbs or asymmetric division. That's clearly not why bilateral symmetry occurs.

@GoodGravy I could not understand your comment. "6 cells, or any other even multiple of an odd number of cells" So what 2N will always be even whatever N you choose.

@user31782 Asymmetric expansion can occur due to directional growth from an odd number of nodes (even if the cell count remains even). But here's the kicker of why that argument is broken; it is taking a cellular principle and making a lot of assumptions about it (constant cell cycle period, uniform cell death etc)  and oversimplifying it (for example it ignores inter-cellular communication and genetic control systems), and then applies that watered down concept at a complex multi-tissue organism scale involving not millions, nor billions, but tens of trillions of cells.

Dear all people everywhere: do not believe what you read on Yahoo Answers. Ever. Or anywhere on the internet for that matter, unless there are citations or some form of expert support. Also, Google Scholar is 100% free to the public...

@theforestecologist Although, note the conspicuous lack of primary sources cited in accepted biology.se answers... we could certainly do a better job of this ourselves. I would love to assume any answer on here constitutes "some form of expert support," but that is a precariously specious assumption.

It depends what you mean by 'leg'.
The instinctive way to define a 'leg' is based on its functional use: we use legs to walk on. But if we adopt that definition of 'leg' then there certainly are animals with odd numbers of legs: kangaroos, for instance, have a five-legged gait, functionally using their tail as a fifth leg. There is no developmental process that stops an animal from growing an odd number of appendages, and if one of those appendages happens to be used as a leg, evolution and development will have no problem with that.
However, there is another way to define 'leg', and that is by homology - 'legs' are the appendages derived by evolution from the legs of a common ancestor. Under this definition, (for vertebrates, at least) you're a bit more hard-pressed to find examples of animals with an odd number. This is because those legs are paired appendages, and the developmental pathways for the leg on one side of the body are tied into the developmental pathways for the leg on the other side of the body, so it is hard to evolve an odd number of legs from these appendages.
Hard is not the same as impossible, though. A comparable piece of evolution is the severe reduction in size of fins from one side of the body in flatfishes (flounders, sole, etc). I am struggling to think of terrestrial examples, but it is certainly evolutionarily possible to lose one appendage from a pair but keep the other.

Among terrestrial animals, gastropods have lost one from some paired appendages (although that happened in an aquatic ancestor). And although their "foot" (or perhaps at a stretch for the purposes of this question "leg"?) isn't one of the appendages that became un-paired in this way, they do have an odd number: one.

A kangaroo's front legs only touch the ground when it is eating. When standing it uses its tail like the third leg of a tripod. When it is running only its hind legs touch the ground, both together, using its tail for balance with its front legs dangling high off the ground. So when running it's using an either one or two legged gait, depending whether you consider two legs in unison to be one or two. Even when eating it moves its legs in pairs instead of individually. So although it has four limbs and a tail it uses them as two limbs and a tail, but with extra lateral stability.

@CJDennis: It's not true that kangaroos only use their tail as 'the third leg of a tripod'. In the study I linked to, the authors defined the kangaroo's tail as functionally a leg because the tail provided forward propulsion in the animal's five-legged gait. In fact, while walking on five legs, the tail provided as much forward propulsion as both the front legs and hind (should I say middle?) legs combined.

I did say "when standing" not "when walking".

Consider also the case of Hopsorrhinus Aureus

It might be worth mentioning that Hopsorrhinus aureus is fictional. Entertaining, but fictional.
https://en.wikipedia.org/wiki/Rhinogradentia

By "Leg" I mean a specific type of body part(perhaps organ). Leg is different from tail because in leg there are two straight bone connected with a joint(perhaps socket joint) on the other hand in tail there is no joint nor does the end of tail terminate with a hand like structure. There can be one tail, two tails, four etc and one leg, two leg, and four leg etc, everything in even numbers. Just as we have two kidneys, eyes etc in pairs.

@user31782: It sounds like your definition of 'leg' is by structure. I would argue that it is not a useful definition of 'leg' for evolutionary questions. e.g., the hindlegs of horses are not 'two long bones with a hand-like structure at the end', because there are three long bones (the bones that are homologous with the arch of our feet are fused into a third long bone, IIRC). But they are definitely 'legs' in the way most people understand the term! Biologists avoid semantic problems by defining from homology - in which case, see the second part of my answer re: development and asymmetry.

@user31782: if you're defining legs in terms of "bones", then you're talking about vertebrates, not all animals. Which is a fair enough thing to ask about, but this restriction means that straight away, all terrestrial vertebrates are tetrapods, who all (including kangaroos) have inherited a basic body plan with bilateral symmetry from a common (fish) ancestor. The success of this body plan has yet to be challenged by any odd-limbed species, other than those using their tail as a limb. Depending on your view of "arms" and vestigial limbs, they all have 0, 2 or 4 "legs".

Short answer
The body plan of terrestrial organisms that feature limbs is typically bilaterally symmetric, and hence these organisms have an even number of appendages.
Background
Terrestrial animals featuring appendices for motility (legs, arms) are typically higher organisms. Typically, the body plan of higher animals such as us mammals is typically bilaterally symmetric (Fig. 1). Lower animals may be radially symmetric (e.g. round worms, jelly fish and star fish). Only the simplest of animlad have an asymmetric body plan, such as sponges. With a symmetrical body plan comes an even number of appendages.

Fig. 1. Different body plans. Source: Estrella Mountain Community College.
The symmetrical body plan is already defined in the blastocyst stage during development. The blastocyst in humans forms in the first two weeks after gestation and contains 10 to 20 cells only (Fig. 2).

Fig. 2. Human blastocyst at day 5. Source: University of NSW
While the blastocyst is not more than a globular clump of cells, it has two well-defined poles and a well-defined axis. In fact, it is thought that the single-celled zygote already has a well-defioned axis as it is has been shown that surviving polar bodies during oogenesis (the formation of egg cells in the ovaria) have well-defined highly non-random positions in the zygote (Fig. 3.). These findings show that the single-celled zygote in bilateral symmetrical animals may already be defined at a single-celled stage (Gardner, 1997).

Fig. 3. Blastocyst bilateral symmetry based on a mouse model. Source: (Gardner, 1997)
Reference
- Gardner, Development (1997); 124(2): 289-301

-1 this does not answer the implicit question why are animals symmetrical.

@QuoraFeans - How about now, see my edit showing embryonic development in bilateral symmetrical animalia

Also it does not explain internal asymmetry. Appendix, heart?  As a rider, I'd ask (and I don't know the answer) whether we have odd numbers of internal appendages where n>1.

@chaslyfromUK - that's a different question altogether - feel free to ask a new question, though.

Leaving aside the extra part, my objection was to your statement, "With a symmetrical body plan comes an even number of appendages."  If that were true then surely it would apply to internal appendages.(?)

@chaslyfromUK - This may be another question entirely. I would think that internal (organ) formation has more to do with hormone secretion and division timing (both of which are intended to trigger the differentiation of specific cells) and external (limb) formation would have more to do with symmetry. Would you agree?

@AliceD - +1 for a great answer.

In your "Background" paragraph, you switch between talking about "animals" and "organisms". Plants can be extremely complex, are defined as organisms, and also have varying types of symmetry, depending on the plant and the portion being studied. I think you need to carefully clarify your language.

@MattDMo - thanks for your critical reading. Done.

The other part of the question has already been amply answered, so I will concentrate on the part of the question which asks about "doesn't divide into odd numbers"
The assumption that organisms must have even numbers of cells merely because cells divide into two each time is false. For example, the nematode Caenorhabditis elegans has either 959 or 1031 cells depending on its sex. Cells can be lost due to apoptosis or natural wear and tear.
Even if that was not the case, cells divide at different rates and times, so it is perfectly plausible for an organism to have an odd number of cells. For example, when one of two cells divide, and the other does not, the final result would be 3 total cells, which is an odd number.

Imagine if the tail of a fish did behave like a leg (imagine a one legged frog). One side, either the left side or the right side, of that tail would naturally dominate and the fish would end up swimming naturally in circles.
Now assuming that being able to go in a straight line over longer distances is a small evolutionary advantage. It would make sense that that a fish tail evolved and grew an internal muscle symmetry that allows it to eventually maintain a straight line.
The same goes if you were to grow a third leg tomorrow. In order for that third leg to be useful to you in evolutionary terms, it would have to be placed in such a way that it doesn't interfere with your balance and your maximum propulsion. Also, its muscle structure would need to be symmetrical between the left and the right side, so as not bias one side over the other.
And of course, such a third leg wouldn't behave like the two other legs because of its forced internal symmetry, so we humans wouldn't call it a leg, we'd most likely call it a tail instead (a cat tail, a kangaroo tail, a snake tail, a fish tail, etc.)
Now let's take a star fish with five "leg-like" appendages (although, that number can vary depending on the kind of star fish). Does my reasoning work with that kind of star fish also? The internal muscle structure of those five appendages are internally symmetrical, just like tails would be, not legs. Also, take a look at how a star fish moves. The propulsion doesn't come from its five appendages. Those five appendages help more with its balance and its positioning. And the propulsion actually comes from its many little tube legs at the bottom of those five appendages. So I'd say "no", a star fish is an interesting example, but it doesn't just have only five legs.

What about the Haggis? http://www.maths.ed.ac.uk/~jcollins/Haggis.pdf

Not all animals are symmetrical. Look at the adult flounder, for example.

I didn't say they were. This is what I said:  "It would make sense that a fish tail evolved and grew an internal muscle symmetry that allows it to eventually maintain a straight line. [...] Also, its muscle structure would need to be symmetrical between the left and the right side, so as not bias one side over the other." The flounder is also a perfect example of this. Its tail has a left-to-right symmetry.

The reason 'there are no known animals with an odd number of legs' - if that is indeed the case, given that stating a negative truth of high probability requires a great deal of examination of facts and records! - could be because it was a stage of development of organisms of a pre-Cambrian period stage of development, or at latest Early Cambrian.
What I am thinking of specifically is the 'Ediacaran' organism/fossil named Charnia.  It shows 'glide reflection' in its development and organization, in which successive branches are opposite to the previous branch and a little further along the body axis.
Charnia was, of course, a frond-like animal, resembling nothing relatively modern so much as a fern (which is a plant of course).  Given that it was an animal not a plant, and a very early animal for certain, it did not have opposite symmetry and thus, if it had evolved directly into a perambulating organism with legs, it might have had an odd number of them.
When thinking of the conformation of animal life, it is as well to keep the Burgess Shale fossils in mind:  animal life that long ago, would appear to have been somewhat 'experimental' still (or, in a phase where all the basic problems were being worked out), and many differing types, some nowadays unrepresented, occurred, outre' in appearance, such as Hallucigenia and Opabinia.
So to sum up, though I cannot point out a known and discovered odd-legged animal (in natural form, as opposed to through amputation or loss of limbs), it is quite possible there was such an animal in Cambrian or pre-Cambrian times, whose fossil remains are as yet undiscovered or not-yet-clearly-interpreted.
Citations:
https://en.wikipedia.org/wiki/Charnia
http://paleobiology.si.edu/burgess/


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Why do home-grown fruits tend to taste better than mass-produced consumer fruits?
It is often heard that home-grown fruits and veggies are a lot tastier than the produce found in the supermarket. Although this question may contain a skeptics element in it, it is so often heard there must be at least some biological ground behind it.

Your whole question is built on a supposition that hardly anyone can truly prove.  Even if you narrowed this down to an objective measure of taste under "organic" versus "non-organic" techniques, it's still driven by opinion.

I'm voting to close this question as off-topic because it is based on an unsupported presupposition.

I must say that home grown stuff (fruit, veggies) always taste better (bar the stuff is not overripe and the likes).

Welcome to Biology.SE. Your post might have better to be reformulated to something along the lines of: "it is common knowledge (hope you'll agree) that home grown stuff are better than industrial ones. Why is that? Intuitively, I would think that biotechnology should allow to make fruits that are much more tasty than what a random individual can do in its garden."

"Industrial" fruits and vegetables are not grown as much for flavor as for convenience, pest resistance, appearance, resistance to peel problems, resistance to bruising, etc. etc. Profitability is the main consideration.
There are many varieties of apple grown in orchards that taste wonderful (better than my grandmother's gnarly green apples) but don't hold up to shipping and storage well.
Finally, please don't get your information from fantasy tales. There are so many good sites for attaining information.

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Does antibacterial soap work chemically?
Normal soap requires scrubbing, does anti-bacterial soap require scrubbing too? Since it (I assume) works chemically, can I produce the same cleansing effect without lathering with soap and using anti-bacterial soap instead? It could save me a lot of time showering in the morning.

The point about scrubbing with soap is usually not to get rid of bacteria (which colonize your skin anyway) but to get rid of dirt. I am not sure, if it is really advisable to always use a real antibacterial soap, since the bacteria on our skin are not doing any harm. It will probably irritate the skin.

most antibacterial soaps contain triclosan, which would work just on application. However, the objective of bathing is not just to get rid of microbes but also to clean the dirt, dust, oily sebaceous secretions etc and therefore scrubbing is still important. If you have rashes/cracked skin then you can avoid scrubbing..

How does "waiting a minute or two" as opposed to "scrubbing for a minute or two" change the time it will take you to shower? How long do you scrub for?  Why in the world do you shower using antibacterial soap? Depending on the soap that can be dangerous and is almost certainly unnecessary and very likely counter productive.

What the comments are trying to say might go something like this.
The antibiotic triclosan that's used in almost all 'antibacterial' products works pretty quickly - by interfering with several processes in the bacterial and fungal membrane.  It doesn't need much more than contact to work.
That being said, the longer your exposure to the antibiotic, the more thoroughly it will work.  Triclosan can penetrate the blood stream through the skin.  If you have soap suds scrubbing may or may not get the triclosan into more contact with a greater surface area as it diffuses into the skin, but probably won't affect the substantial effect it has killing surface bacteria and fungi/yeasts.
Its worth noting that the FDA doesn't recommend the use of antibacterial soap or other antibacterial products.  Soap itself is a powerful agent for killing bacteria and other microorganisms and biocides like triclosan probably encourage the emergence of antibiotic resistant strains which present a medical risk to people.

This is a very good question, and a very important topic in the healthcare and biological world.  It is something that everyone should consider, as the answer is not as self-evident as it may appear.  The responses here are excellent.  I would like to add a few things from a healthcare perspective.
This is the WHO recommendation on how to wash your hands.  It is in agreement with the CDC recommendations. This includes use of antibacterial soaps.
The reason for friction in handwashing is as Chris and WYSIWYG said: removal of oils, dirt, bacteria and other things accumulated in the crevasses of your skin and nails (including microbes and biological residues).
Regular soap on its own is a surfactant; it is a molecule with a polar end (and a non-polar end.  It basically dissolves in both oils and waters.  It is perfect for removing oils and rinsing them off in water.  Detergents such as soaps are cell membrane disrupters, and as such, it is capable of rupturing cell membranes of many microbes on its own.
Shigeta is right-on with the FDA recommendations to not use antibacterial soaps.  They are completely unnecessary is most situations and actually do harm by putting selective pressure on bacteria strains to become stronger by killing off all but the most resistant ones, which then breed and overgrow.
In daily use, alcohol foams are a convenient way to sanitize if soap and water are unavailable, but it's often overused.  Soap and water are better in the daily environment, and always better before eating, because alcohol does not kill spores nor denature toxins.
Overuse of antibiotics in general is the reason why MRSA and other multi-drug resistant bacteria have emerged, and these are extremely dangerous because they are so difficult to treat.  We're struggling to catch up with antibiotics to kill the newly emerging strands.  There are cases I have seen where all efforts to treat an infection failed due to resistance.  So I guess I'm saying all this to emphasize that yeah, it's important to not go overboard on antibacterial cleansing :)  /end soapbox.
Well, one more quick thing - I do want to add that healthcare settings are slightly different.  The use of antibacterial soap in hospitals is approved for the purpose of reducing the microbial load on skin between patients, to reduce transmission as much as possible.  Alcohol foams have been found to be comparable, but are insufficient in several cases (such as spores). (See the CDC for more info on alcohol foams: http://www.cdc.gov/oralhealth/infectioncontrol/faq/hand.htm#a3).
In daily use, alcohol foams are a convenient way to sanitize if soap and water are unavailable, but it's often overused.  Soap and water are better in the daily environment, and always better before eating, because alcohol does not kill spores nor denature toxins.
References for following information:  I personally have been involved in patient counseling discussions in clinic with a patient and an attending physician (a supervisory teaching doctor) discussing best practices in hygiene.  This includes two dermatologists, two Emergency physicians, an OB/Gyn physician, and a pediatrician - and all concur:
For general washing in the shower, unless you sweat a great deal or are exposed to dirt and chemicals, the majority of your exposed skin does not require extensive scrubbing to become clean.  In fact, scrubbing can irritate skin, worsen dry skin, or exacerbate conditions such as eczema.   Warm water, normal soap (or even better for sensitive skin / eczema, moisturizing body wash like Dove), and a soft washcloth are completely sufficient. If using a pouf or exfoliator, only apply light pressure, never aggressive. Armpits, groin, and feet do require more attention, but hard scrubbing is unnecessary.
Interestingly (and hopefully not TMI in this post), I learned from the OB/Gyn's patient counseling that it is unnecessary (and actually irritating to the mucous membranes) for women to use more than warm water to clean between the labia majora. I looked this up and found supporting information for this. Other genital surfaces should be washed well, but as mucous membranes, that area has a self-cleaning system of secretions.  This is similar to the strong recommendation for women not to use vaginal douching - it upsets the balance of natural bacteria (flora) in the vaginal canal.
The WHO handwashing instructions:

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How to know if your breathing is normal?
Is it possible for a device to measure how much air we breathe in and out over the entire day and at what rate? I think if we have access to this data we can compare it across people.

it is certainly possible to make. might be clumsy to wear though.

What you are looking for is a spirometer. There are different types of spirometers serving different purposes like the Incentive spirometer and the peak flow meter. I would suggest that you go through the wikipedia page on it to get more info.

thanks, but then the most advanced spirometer seems to measure breathing only temporarily and not on-the-go i.e. complete day analysis when doing routine tasks. so i guess the state-of-the-art has not reached that level.

@user13107 Might be in development if the need arose but I am unaware of it.

Another possibility is K4 device and K4 device. Beyond spirometry it can measure other variables such as:

Pulmonary Gas Exchange (VO2, VCO2)
Breath by Breath Technology
Telemetry Data Transmission up to 1000m
Indirect Calorimetry
Integrated GPS System
Integrated Oxygen Saturation (SpO2)
Integrated 12-lead Stress Testing ECG


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Quantitative Differences : DNA and Gene
After HGP, we are not having many databases which consist of several notepad files of ATCG....
Can we distinguish quantitatively a given A,T,C and G stretch as DNA or Gene?

What exactly do you mean with your first sentence? There are many databases containing nucleotide sequence data. One of the biggest is GenBank, which could be considered a collection of "notepad files of ATCG". Also, except for RNA viruses, all genes are encoded in DNA. So it does not make sense to say "DNA or Gene". It sounds like you are asking how gene prediction works?

I interpret your question as: Given a stretch of DNA sequence, can we determine if it encodes a gene? My summary of the answer would be: "Sometimes".
The problem you ask about is called "Gene prediction" and is described in some detail by Wikipedia:  http://en.wikipedia.org/wiki/Gene_prediction
The most basic indication that a gene may exist is the presence of an "Open Reading Frame" (ORF). An ORF is a stretch of DNA from which a single protein may be produced.  However, an ORF is not strictly required for a gene (as not all genes encode proteins), and not all ORFs are genes. There are many software tools for gene prediction available which use different rules to predict if a given region of DNA is functional (contains a gene or a regulatory element). They may be usable on any kind of DNA sequence, or on sequences from certain organisms only, depending on the program.
Two commmonly used gene prediction tool are GLIMMER (http://www.ncbi.nlm.nih.gov/genomes/MICROBES/glimmer_3.cgi, used for microbial genomes) and GeneMark (http://opal.biology.gatech.edu/gmhmm2_prok.cgi). See also http://en.wikipedia.org/wiki/Gene_prediction
As a quick check, you may also use NCBI BLAST (http://blast.ncbi.nlm.nih.gov/Blast.cgi) to see if your sequence aligns to a known gene.

Thanks a lot for making me understood about the principle. I am anxious really how the genes are ordered as a finite length string of four bases? How random as a finite string of four bases when we consider it as a gene? My conviction is that genes are not randomly arranged as a finite string. There must be a beautiful organization. I would like to know in detail about the organization of them. And definitely that organization would be missing in any arbitrary DNA stretch.

Yes, the statistical properties of coding and non-coding sequences are different, and this is exploited by some gene-prediction programs. Note that some non-coding sequences might be the remains of a gene which is no longer expressed, and so may have similar statistical properties as an expressed coding sequence. Such sequences are called "pseudogenes".  The following links might be a place to start: NCBI Book on computational genomics (http://www.ncbi.nlm.nih.gov/books/NBK20261/) and a review on identifcation of protein-coding genes:  http://genomebiology.com/content/10/1/201

This is possible and is an important topic in bioinformatics. Lots of tools have been written and papers have been published, most important

A random sequence usually "encodes" only very short protein sequences before the "stop" codon (three nucleotide combination marking the end of the protein) is met just by chance. Coding sequence encodes a reasonably long protein.
Same amino acid can usually be encoded by multiple alternative sequences of three nucleotides (codons). In a real coding sequence they are not equally probable, some codons are preferred over others (which ones, is organism-specific).
It is possible to find characteristic nucleotide patterns inside or in some cases near the coding sequence. Dropping the coding sequence alone into genome would only result in a non-functional pseudogene.
Most often, encoded protein sequence is more or less similar to the sequence of some already known protein.

.. and so on. Try GenScan, for instance.

My conviction is that genes are not randomly arranged as a finite
  string. There must be a beautiful organization.

In bacteria, you will have a whole series of genes required for a pathway all next to each other, so that their expression can all be controlled from one point upstream of them.  We call that whole suite of genes and the upstream binding site an operon.
But in eukaryotes, there is no grand organization of genes with regard to their position on the chromosomes, in general.  Regardless of what you think they should look like, we don't observe a wonderful organization.  Evolution results in things looking pretty haphazard.  Go browse ensembl.org if you want to see for yourself.


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Genomic location-coordinate of RdRp of SARS-CoV2
I understand that nsp12 is the RdRp protein in the ORF1 of SARS-CoV2 genome. And nsp12 starts from the starting nucleotide base of orf1ab. Could you please tell me the exact genomic location coordinate of RdRp?
Is there and database from where the FASTA sequence (nucleotide and aa) of RdRp of SARS-CoV2 can be obtained?
Any answer to this question would be highly appreciated.

The following is a standard and quite straightforward way to obtain the information requested that is generally applicable and does not require any programming.

Go to the NCBI website or its Genbank page, select Genome from the pull-down menu and type your search term, ‘SARS-CoV2’ into the search field:

On clicking Search, you will be taken to a page with a brief summary of information about the genome. In the Reference genome summary box click on the RefSeq ID, NC_045512_2:

This takes you to the record for the nucleotide sequence of the virus genome. Scroll down (or do a Find in your web browser) to the gene of interest, nsp12. There you will find an entry with the genomic co-ordinates (13442–13468 and 13468–16236) and a cross-reference to the protein, [YP_009725307.1(https://www.ncbi.nlm.nih.gov/protein/1802476815).

If you click on that ID you will be taken to the Genbank entry for the protein encoded by nsp12, with the sequence in FASTA format.

You can download a file containing the sequence from the Send to pull-down shown. There is also a link to the graphical interface for viewing the protein in the context of the genome (available from the nucleotide sequence page as well).

This is more informative.

Tks I didn't notice the hidden entries 1 and 2

A useful database and exploratory tool is the UCSC Genome Browser wuhCor1 assembly browser instance.
A synonym for nsp12 is Pol. Its position range in the wuhCor1 assembly is NC_045512v2:13,442-16,236.
There are several ways to extract sequence, but one programmatic way is to get the FASTA from UCSC Goldenpath for the assembly, and extract the characters of interest from the position range for the gene of interest using standard Unix tools:
$ wget -qO- ftp://hgdownload.soe.ucsc.edu/goldenPath/wuhCor1/chromosomes/NC_045512v2.fa.gz | gunzip -c | tail -n+2 | tr -d '\n' | cut -c 13442-16236 | awk '{print ">nsp12"; print $0}' > nsp12.fa
$ cat nsp12.fa
>nsp12
TCAGCTGATGCACAATCGTTTTTAAACGGGTTTGCGGTGTAAGTGCAGCCCGTCTTACACCGTGCGGCACAGGCACTAGTACTGATGTCGTATACAGGGCTTTTGACATCTACAATGATAAAGTAGCTGGTTTTGCTAAATTCCTAAAAACTAATTGTTGTCGCTTCCAAGAAAAGGACGAAGATGACAATTTAATTGATTCTTACTTTGTAGTTAAGAGACACACTTTCTCTAACTACCAACATGAAGAAACAATTTATAATTTACTTAAGGATTGTCCAGCTGTTGCTAAACATGACTTCTTTAAGTTTAGAATAGACGGTGACATGGTACCACATATATCACGTCAACGTCTTACTAAATACACAATGGCAGACCTCGTCTATGCTTTAAGGCATTTTGATGAAGGTAATTGTGACACATTAAAAGAAATACTTGTCACATACAATTGTTGTGATGATGATTATTTCAATAAAAAGGACTGGTATGATTTTGTAGAAAACCCAGATATATTACGCGTATACGCCAACTTAGGTGAACGTGTACGCCAAGCTTTGTTAAAAACAGTACAATTCTGTGATGCCATGCGAAATGCTGGTATTGTTGGTGTACTGACATTAGATAATCAAGATCTCAATGGTAACTGGTATGATTTCGGTGATTTCATACAAACCACGCCAGGTAGTGGAGTTCCTGTTGTAGATTCTTATTATTCATTGTTAATGCCTATATTAACCTTGACCAGGGCTTTAACTGCAGAGTCACATGTTGACACTGACTTAACAAAGCCTTACATTAAGTGGGATTTGTTAAAATATGACTTCACGGAAGAGAGGTTAAAACTCTTTGACCGTTATTTTAAATATTGGGATCAGACATACCACCCAAATTGTGTTAACTGTTTGGATGACAGATGCATTCTGCATTGTGCAAACTTTAATGTTTTATTCTCTACAGTGTTCCCACCTACAAGTTTTGGACCACTAGTGAGAAAAATATTTGTTGATGGTGTTCCATTTGTAGTTTCAACTGGATACCACTTCAGAGAGCTAGGTGTTGTACATAATCAGGATGTAAACTTACATAGCTCTAGACTTAGTTTTAAGGAATTACTTGTGTATGCTGCTGACCCTGCTATGCACGCTGCTTCTGGTAATCTATTACTAGATAAACGCACTACGTGCTTTTCAGTAGCTGCACTTACTAACAATGTTGCTTTTCAAACTGTCAAACCCGGTAATTTTAACAAAGACTTCTATGACTTTGCTGTGTCTAAGGGTTTCTTTAAGGAAGGAAGTTCTGTTGAATTAAAACACTTCTTCTTTGCTCAGGATGGTAATGCTGCTATCAGCGATTATGACTACTATCGTTATAATCTACCAACAATGTGTGATATCAGACAACTACTATTTGTAGTTGAAGTTGTTGATAAGTACTTTGATTGTTACGATGGTGGCTGTATTAATGCTAACCAAGTCATCGTCAACAACCTAGACAAATCAGCTGGTTTTCCATTTAATAAATGGGGTAAGGCTAGACTTTATTATGATTCAATGAGTTATGAGGATCAAGATGCACTTTTCGCATATACAAAACGTAATGTCATCCCTACTATAACTCAAATGAATCTTAAGTATGCCATTAGTGCAAAGAATAGAGCTCGCACCGTAGCTGGTGTCTCTATCTGTAGTACTATGACCAATAGACAGTTTCATCAAAAATTATTGAAATCAATAGCCGCCACTAGAGGAGCTACTGTAGTAATTGGAACAAGCAAATTCTATGGTGGTTGGCACAACATGTTAAAAACTGTTTATAGTGATGTAGAAAACCCTCACCTTATGGGTTGGGATTATCCTAAATGTGATAGAGCCATGCCTAACATGCTTAGAATTATGGCCTCACTTGTTCTTGCTCGCAAACATACAACGTGTTGTAGCTTGTCACACCGTTTCTATAGATTAGCTAATGAGTGTGCTCAAGTATTGAGTGAAATGGTCATGTGTGGCGGTTCACTATATGTTAAACCAGGTGGAACCTCATCAGGAGATGCCACAACTGCTTATGCTAATAGTGTTTTTAACATTTGTCAAGCTGTCACGGCCAATGTTAATGCACTTTTATCTACTGATGGTAACAAAATTGCCGATAAGTATGTCCGCAATTTACAACACAGACTTTATGAGTGTCTCTATAGAAATAGAGATGTTGACACAGACTTTGTGAATGAGTTTTACGCATATTTGCGTAAACATTTCTCAATGATGATACTCTCTGACGATGCTGTTGTGTGTTTCAATAGCACTTATGCATCTCAAGGTCTAGTGGCTAGCATAAAGAACTTTAAGTCAGTTCTTTATTATCAAAACAATGTTTTTATGTCTGAAGCAAAATGTTGGACTGAGACTGACCTTACTAAAGGACCTCATGAATTTTGCTCTCAACATACAATGCTAGTTAAACAGGGTGATGATTATGTGTACCTTCCTTACCCAGATCCATCAAGAATCCTAGGGGCCGGCTGTTTTGTAGATGATATCGTAAAAACAGATGGTACACTTATGATTGAACGGTTCGTGTCTTTAGCTATAGATGCTTACCCACTTACTAAACATCCTAATCAGGAGTATGCTGATGTCTTTCATTTGTACTTACAATACATAAGAAAGCTACATGATGAGTTAACAGGACACATGTTAGACATGTATTCTGTTATGCTTACTAATGATAACACTTCAAGGTATTGGGAACCTGAGTTTTATGAGGCTATGTACACACCGCATACAGTCTTACAG

Another option is to visit the Pol link again and look for the "View DNA for this feature (wuhCor1/SARS-CoV-2)" link, click on it, and click on "get DNA" to get a similar FASTA file. But if you're going to do bioinformatics, knowing how to string together Unix tools is a valuable skill.
To get the amino acid sequence, visit the Pol link, look for the Swiss-Prot record information, and do a search through UniProt for the record P0DTD1.
Via the "RNA-directed RNA polymerase" entry for P0DTD1, you can click on the "RNA-directed RNA polymerase" post-translation product to get to a record with the amino acid sequence: https://www.uniprot.org/blast/?about=P0DTD1[4393-5324]&key=Chain&id=PRO_0000449629

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


text:
Truncated ORF3a protein of SARS-CoV2! Why? How does it formed?
Across the world so far, we have three truncated ORF3a proteins in SARS-CoV2 in India only.
Can you illuminate me how does a protein (here accessory protein of SARS-COV2) generally get such nonsense mutations and what happens to such proteins in protein-protein interactions?

Your question couldn't be answered using just suggestions: we need proofs. In this study (from which I've quoted the sentence below) authors suggest an implication for inflammation response in patient.

Among the mutations, the ORF3a-Type-3 and ORF3a-Type-4 mutations are restricted to only the Indian patients based in Ahmedabad so far it is identified. These mutations (Q to H, D to Y, S to L) are located near TRAF, ion channel, and caveolin binding domains respectively, suggesting that Type-3 and Type-4 might have effect on NLRP3 inflammasome activation. This unique non-synonymous mutations might affect the virulence of the virus and this needs a special attention from pathogenesis perspective by the medical scientists

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


text:
Why is green fur not a thing?
In most biomes on earth, and certainly in the most densely-populated, the best camouflage color or pattern for an animal would be a variant of green, so as to blend in with the leaves and grasses of the surrounding environment.  Whether predator or prey, the art of not being seen is hugely important in the natural world, and yet to the best of my knowledge there isn't a single mammal on the planet with fur that is even partially green.
Is there a reason for that?  It seems like animals have evolved some pretty crazy color patterns to break up their silhouette or blend into the background, but why haven't any mammals taken the obvious route of "look like leaves"?
Is it really THAT not-easy being green?

I don't know if this is related, but I've done enough computer graphics programming to know that brown is hard color to reproduce on a computer. It's a mixture of red and green. If animals don't have good color vision, they might not be able to tell the difference between red and green, and it all looks brown anyway, kind of like colorblind men. However, I don't know how many animals have this issue, I think lack of blue vision is more common than lack or red or green.

i wonder if its because small mammals started out as terrestrial - bound to the ground where green is not as much a color.  certainly birds can be green when they need to be.

But we clearly need it for the Green-beard effect

The technical answer is: Because the coloration of skin and hair is done by the two forms of melanin: Eumelanin, which is dark brown to black and Pheomelanin which is yellow to red. This enables colors from white (not pigmentation) to black (dense eumelanin pigmentation) and also colors in between by different ratios of the two pigments.
The evolutionary answer is that it obviously made no evolutionary advantage to have other colors. If you look closer at this, you will see that most habitats are not green or only for a part of the year. If you think about african plains, these are mostly brown, something like artic landscapes are only green for a very short timeframe in the summer, for the rest of the year these are white to brown. And even tropical rainforests are mostly dark to brown on the ground. They would clearly stick out of the environment with green colored hair.
For all these different habitats the animals living there have adapted their hair color. It is not uncommon for artic animals to change their hair color with the course of the year, dark to brown in the summer and white in the winter (artic foxes and snow hare) for example. Animals which live in deserts will have a paler color than those which live in dark colored mountain areas.
See this article for more information: "The Adaptive Significance of Coloration in Mammals"
Also interesting in this context is this article which looks at the reason for zebra stripes: "The function of zebra stripes"

Whoever downvoted me, can you please explain why? If there is criticism on my answer, it will be helpful to know about it, so I can improve the answer.

+1, I am not a biologist, but I would also expect a kind of an evolutionary baggage argument. Reptiles tend to be in similar habitats and grow to the same sizes in comparison to plants as many mammals, yet they developed chromatophores and mammals just melanocytes. It would also be interesting to understand bio/chemically why melanogenesis produces such a limited variety of colors.

I am not much into chromatophores, I know this only for zebrafish. There three different pigments are available, dark melanophores, blue xantophores and silvery iridophores. It doesn't happen there, but it is imaginable to combine blue and yellow (pheomelanin) to get green. Still it didn't happen evolutionary.

Just to add a different dimension to the answer from @Chris. Not all animal colouration is produced by melanin. A whole range of bright colours in insects, birds and reptiles comes under the heading of structural colouration, which basically involves having a repeating structure at the microscopic level to interact with light. This is the basis for macaw colours, peacock feathers, and some butterfly wing colours.
It also occurs in mammals - see for example the mandrill. In this case the coloured patches are bare skin containing ordered collagen fibres to create the effect, (science here). I have no idea if collagen could be structured to produce a green colour.
Finally, an anecdote: a number of years ago a polar bear in the San Diego zoo was seen to develop green patches. Upon investigation this was found to be due to damaged hair shafts in areas where the animal rubbed against surfaces in its enclosure. In the polar bear the hair shafts are hollow, for insulation, and the damaged hairs were being colonised by algae. So you could imagine a green mammal could evolve by using this effect.

That algae colonize the sloth happens quite regulary. But I would see this under the pigmentory aspect. See here for details.

I would be surprised if collagen structures could make red and blue but not green, as green is between the two in wavelength. I had no idea mammals did structural colouration.

Polar bears have hollow hair shafts? Forget alpaca and mink, I want to knit polar bear yarn!

Tropical tree-dwelling sloths often have green fur, the pigments due to possibly symbiotic algae; see this.

A dimension not explored by the other (excellent) answers has to do with color perception under trees. Leaves are green while on the tree, which tends to make mostly green light available to the understory.
Viewed under green light, a green-furred animal would appear bright green, roughly the same as a white creature viewed under green light. A red or brown creature would appear grey-brown or black, and reflect much less light.
Orangutans apparently do this for camouflage, according to this book I haven't read:

Russon, Anne E.  2000.  Orangutans:  wizards of the rain forest.  Firefly Books, Buffalo, New York, USA.

which I was told about by these guys. It's not the first place I've heard this factoid, but it does make first-pass sense.
There is a difference between looking the same as a background of green leaves under sunlight and looking the same as a background of tree trunks or leaf litter under a greenish light.

Very good point.


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Evolution in fruits
So, I saw a video on YouTube that says the banana we eat today is not what a banana looked like years ago. Since the banana has been genetically modified over the years, does that qualify as evolution?

Yes. Modern domesticated bananas have evolved from ancestral wild species under the influence of humans. Quoting D'Hont et al.: (1)

The [banana] domestication process started some 7,000 years ago in
  Southeast Asia. It involved hybridizations between diverse species and
  subspecies, fostered by human migrations, and selection of diploid and
  triploid seedless, parthenocarpic hybrids thereafter widely dispersed
  by vegetative propagation.

Modern bananas have undergone extensive evolution from the original wild species. The selection pressure has in part been provided by humans, who have selected the most nutritious/tasty/desirable examplars and facilitated their reproduction. This can be considered "artificial selection" as opposed to "natural selection", but does not change the fact that an evolutionary process has taken place. The UC Berkeley website "Understanding Evolution" gives the following definition of "artificial selection".(2)

A process in which humans consciously select for or against particular
  features in organisms. For example, the human may allow only organisms
  with the desired feature to reproduce or may provide more resources to
  the organisms with the desired feature. This process causes
  evolutionary change in the organism and is analogous to natural
  selection, only with humans, not nature, doing the selecting.

Thus, whether the selection is considered "natural" or "artificial", the end result is evolution.

"Modern" should be understood as "domesticated". The wild relatives and even ancestors are still there:

Yes. Good point.

It's just selective breeding, not evolution. Far from it.

I actually got an answer from watching Cosmos. It's called Artificial Selection - the reason why we have different breeds of dogs today.

You could say it clasiffies as evolution only if you accept that the artificial things humans have done to bananas are actually natural occurences. I personally don't think they are, because intent is at play here, and evolution is a natural process without intent.
Evolution is not when something gets better. That's the misconception behind your question.
If humans would just happen to eat the tasty bananas first, what would happen is negative selection and all the remaining bananas (which lived long enough to reproduce) wouldn't be tasty. Bananas would get less tasty in order to survive.
What actually happened goes against the natural process of selection, and is something completely different to the concepts of evolution which led to us evolving intelligence, for example. This is just selective breeding. Nothing as grand as evolution.
Evolution is a natural process which led to intelligent species from single-cell organisms, and is a continuous process of random mutations being selected for or against by natural causes. Evolution has no intent and is a natural random process. A grand one, as all biology depends on it, and we depend on it.
Genetic engineering, on the other hand, has intent to improve things, and happens on a much smaller scale than the natural process of evolution. Genetic engineering of any kind, whether it be tinkering with the genes or just inbreeding to create a new breed, is artificial and is being done by an intelligent creature as opposed to nature. Calling genetic engineering a tool for evolution is the same mistake that eugenics proponents made.

I must disagree with this answer - I have updated my own in response.

I still disagree with you, as I believe evolution is a grand process that can only be tied to natural selection, not artificial selection. But then again, whenever you reach humans in evolutionary biology you're bound to be up against something that is completely different from the several billions of years prior to development of human intelligence.

I agree somewhat with the "humans are different" idea, but I still think declaring humans and human influence as "unnatural" is rather arbitrary. Species affect each other's evolution all the time, and I see no reason why the level of cognitive abilities of humans should change the name we use for that process. I see your point though.

Evolutionary biologists consider artificial selection to be a valid input into the process of evolution.  Evolution is the gradual change itself, over time, and the varieties it produces are selected against by various criteria.

By this argument human are almost incapable of evolution, since it is humans who decide who they mate with.


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Other than Acetylcarnitine what other orally-bioavailable Acetyl donors exist to assist in the conversion of CoA to acetyl-CoA?
I asked a question on bio stackexchange a few days from which I was hoping to be able to arrive at an answer for this question myself but I have had no such luck so now I am going to just ask outright: other than acetyl-L-carnitine are there any orally-bioavailable compounds (in particular orally-bioavailable to humans)  that exists that can serve as an acetyl group donor for CoA?
My main motivation for asking this question is that I know that acetyl-L-carnitine indirectly promotes the acetylation of histones by serving as an acetyl donor for CoA by serving as a substrate for carnitine O-acetyltransferase and then this resulting acetyl-CoA then donates an acetyl group to histones by means of the enzyme histone acetyltransferase.

You have a good point but it would be just exquisite if you could find some evidence to support the idea that a significant amount of these acetyl-CoA's are used by histone acetyltransferase and thus influence gene expression.

Is there any evidence that acetylcarnitine acts as an "acetyl donor"? I understood that its use as a supplement was to supply carnitine. Could you give a reference for the statements in the second paragraph of the question?

I would assume that acetylcarnitine is not an acetyl donor for CoA. According to this paper, a "typical" ester hydrolysis reaction is less energetically favorable than a "typical" thioester hydrolysis reaction. So hydrolysis of the ester bond in acetyl-L-carnitine will not provide enough free energy for the formation of a thioester bond with CoA. I'm pretty sure @TomD is right about the source of acetyl-CoA. Also, I highly doubt that the acetyl groups used for histone acetylation come from a different source than those used in metabolism.

This is only a guess, maybe acetic acid, ie vinegar?
Acids are effectively hydrogen salts, but the acetyl ion might be alkaline like the hydroxyl ion, making acetic acid less acidic than most? As in water, pH neutral, is a combination of hydrogen and hydroxyl, H and OH, ions?

Hi ! Welcome to Bio Stack Exchange ! I do not know whether your answer is correct or not but I would suggest that if you are unsure of an answer it is better to leave a comment then to write an answer. Also, your answer will be easily accepted if you provide a good source/reference for your answer. Have a great time here !!

Thanks biogirl, I wasn't sure how to just leave a comment.  I found TomD's answer that fatty acids donate acetyl ions interesting.

No worries ! Have fun !

Free acetate is apparently used to acetylate CoA, in an ATP dependent manner, at least according to wikipedia. But I think the question is looking for acetyl donors for which the reaction is favorable on its own (doesn't need to be coupled to ATP hydrolysis to proceed).


text:
Why Do Healing Wounds Feel Warmer To The Touch?
I fell over on my bicycle trying to avoid running over a rattlesnake, and ended up badly skinning my knee. It immediately began to bleed, but soon clotted.
It has been 2 days now and it has formed a thin scab and is healing well as far as I can tell. I was chilly from the air conditioning, and I noticed the wounded knee was much warmer than the healthy knee. It was very warm, while the other was rather cold to the touch.
I read here about skin healing, and thought, maybe it is because the blood rushed there to clot the wound. But, the wound is already clotted and sealed and the worst is over. So my question is:

Why is my wound and the area around it so much warmer days after the injury?

This is personal medical question territory.  Your knee is not yet fulled healed so it is reasonable to expect the ongoing healing process would produce heat.  Heat can also be a sign of infection.

The wound is warm because of increased blood flow to the area.  This may be part of the natural inflammatory process, or you may have infection.  Wait and see what happens.

@Amory: Cryptic didn't ask what to do about it or if it is unhealthy. I think it is perfectly fine to ask about the biological reason for this, even if a personal example is used.

@Amory: I'm not asking for medical advice. I want to know why wounds are warmer than normal, please don't misread the question.

This is a normal part of the inflammatory process. Inflammation is your body's localised defensive response to tissue injury of any kind, and it is characterised by four cardinal signs- redness, swelling, heat and pain (severe inflammation involves a fifth, loss of function).
Your body is performing three main processes here:

Mobilisation of the body's defences.
Involves release of vasoactive chemicals, which cause the blood vessels to dilate and increase blood flow to the area. This causes the pain and heat, The blood vessels also produce cell-adhesion molecules which make immune cells (leukocytes) stick to the walls of the your blood vessels.
Containment and destruction of pathogens.
The immune system then goes to work clearing up any bacteria which have got into the wound. The leukocytes release chemicals called cytokines to attract more immune cells, to contain and destroy bacteria.
Tissue cleanup and repair.
Dead cells, cell fluid and other debris (pus) is then absorbed by the lymphatic system. Platelets and endothelial cells then secrete growth factors which stimulate cells called fibroblasts to multiply and produce collagen. The heat also increases metabolic rate and increases the rate of tissue repair.

Do you think you could provide times to your answer as well (e.g. after 3 hours this happens).  I'm curious as to the timeline of normal inflammation compared to the questioner's timeline of heat after 2 days.

there is increased blood flow during healing as well. also there is some secretion (perhaps histamine) which makes wounds itchy.. the reason for which i dont know myself.. and some involuntary rubbing can again trigger blood flow..

The increase in temperature is due to dilatation of the capillaries in an area of inflammation, here brought about by trauma and is one of the five cardinal signs of inflammation'. This is a natural process which helps to bring in more blood supply for repair and removal of damaged tissue components.

Skin wound healing is a dynamic and regulated process of cellular and molecular mechanisms and starts directly after skin injury.

The first stage of physiological or acute wound healing
is about the hemostasis and the formation of a provisional wound matrix. It occurs immediately after injury. When skin injury breaks up the epidermal layer, blood and lymphatic vessels are traumatized, flushing the wound to remove microorganisms and antigens. The different clotting cascades are then initiated by clotting factors from the injured skin (extrinsic system), and thrombocytes get activated for aggregation by exposed collagen (intrinsic system).
At the same time the injured vessels follow a 5- to 10-min vasoconstriction, triggered by the platelets, to reduce blood loss and fill the tissue gap with a blood clot comprised of cytokines and growth factors.
This blood clot contains fibrin molecules, fibronectin, vitronectin and thrombospondins, forming the provisional matrix as a scaffold structure for the migration of leukocytes, keratinocytes, fibroblasts and endothelial cells and as a reservoir of growth factors.
The vasoconstriction is then followed by vasodilation in which thrombocytes invade the provisional wound matrix as discussed in this article. In addition, platelets influence the infiltration of leukocytes by the release of chemotactic factors. Both platelets and leukocytes release cytokines and growth factors to activate the inflammatory process which results in local warmth (hyperemia) and edema (swelling) of the wound.


text:
The fundamental importance of R.E.M. Sleep. (Rapid Eye Movement)
Question:
I know that experiments have been conducted to determine the importance of R.E.M. sleep in our sleep cycle. It is particularly important for learning, information synthesis, and recovery from distress. Why else is R.E.M. sleep important? What experiments have been done/observations been made to determine the neurological mechanisms underlying R.E.M. sleep? I know that we exhibit high frequency $\alpha$ waves, similar to the waves we experience during wakefulness.
Wiki:
During REM sleep, high levels of acetylcholine in the hippocampus suppress feedback from hippocampus to the neocortex, and lower levels of acetylcholine and norepinephrine in the neocortex encourage the spread of associational activity within neocortical areas without control from the hippocampus. This is in contrast to waking consciousness, where higher levels of norepinephrine and acetylcholine inhibit recurrent connections in the neocortex. REM sleep through this process adds creativity by allowing "neocortical structures to reorganise associative hierarchies, in which information from the hippocampus would be reinterpreted in relation to previous semantic representations or nodes.
Do these reorganized neocortical hierarchies remain this way?
Just HOW integral is R.E.M. sleep to our brain development?

REM sleep stimulates the brain regions used in learning. This may be
  important for normal brain development during infancy, which would
  explain why infants spend much more time in REM sleep than adults (see
  Sleep: A Dynamic Activity ). Like deep sleep, REM sleep is associated
  with increased production of proteins. One study found that REM sleep
  affects learning of certain mental skills. People taught a skill and
  then deprived of non-REM sleep could recall what they had learned
  after sleeping, while people deprived of REM sleep could not.
Some scientists believe dreams are the cortex's attempt to find
  meaning in the random signals that it receives during REM sleep. The
  cortex is the part of the brain that interprets and organizes
  information from the environment during consciousness. It may be that,
  given random signals from the pons during REM sleep, the cortex tries
  to interpret these signals as well, creating a "story" out of
  fragmented brain activity.

Source: link

Relevant quotes should support your answer rather than form it in it's entirety

@RoryM While I do agree, I think this quote was helpful and answered my question well. By the way, it's: its.


text:
What exactly is neuroplasticity, and can it be demonstrated with a simple experiment?
As far as I know, neuroplasticity is about restoring brain functions by moving some functions to other still functional. Neuroplasticity is more prominent in children than in adults.
What are other examples of neuroplasticity that are unrelated to pathologies? Can it be demonstrated by a simple experiment outside the laboratory? Are learning, or simply the getting used to new things examples of neuroplasticity?
For example, after wearing red-cyan goggles, I see a color mismatch for some time after I take off the goggles. Is it related to neuroplasticity or some other thing?

Can you please include a link for your definition of neuroplasticity? This is not how I understand the term at all.

@anongoodnurse, I just remember reading about it somewhere before. Wikipedia gives this intro: Neuroplasticity, ..., is an umbrella term ... — it refers to changes in neural pathways and synapses due to changes in behavior, environment, neural processes, thinking, emotions, as well as changes resulting from bodily injury.

This is not something you want to be testing in any kind of "home experiment".  I agree with @anongoodnurse, your last example is a bit muddled in terms of its reliance on long-term plasticity.  Your first sentence has some ring of truth to it, as this phenomenon has been observed in the congenitally blind, for example (see http://en.wikipedia.org/wiki/Cross_modal_plasticity), but there is no "movement" per se.

I have voted to close this as a medical advice question due to the "experimentation" aspect, but if you rework it a bit, there are some interesting questions here.  Take a look at some of the work done on lateral connections/silent synapses in the motor and sensory cortexes particularly after cerebral infarct or TBI and you should have plenty of fodder for an outstanding and well-researched question.

@jonsca et al., I have edited the question and removed self-help referencing. I vote to re-open as it is a valid question.

Your question is basically a matter of defining brain plasticity or more broader, neuroplasticity. According to a well-cited paper in Brain (Cramer et al., 2011) neuroplasticity is defined as:

[...] the ability of the nervous system to respond to intrinsic or extrinsic stimuli by reorganizing its structure, function and connections.

Hence, the term can be, and indeed is used very broadly. A more elaborate definition in the same article should answer you question as to whether learning and habituation can be considered to be associated with neuroplasticity:

Neuroplasticity can be broadly defined as the ability of the nervous system to respond to intrinsic and extrinsic stimuli by reorganizing its structure, function and connections; can be described at many levels, from molecular to cellular to systems to behaviour; and can occur during development, in response to the environment, in support of learning, in response to disease, or in relation to therapy. Such plasticity can be viewed as adaptive when associated
  with a gain in function [...] or as maladaptive when associated with negative consequences [...]

Your vision example, however, is more appropriately referred to as adaptation. Although it strictly spoken falls under the above definition of plasticity (...reorganizing its... function,  color adaptation is (at least in my opinion) too short-lived (minutes) to be associated with plasticity.
Lastly, as to experiments - Although learning a chunk of material from a textbook as a homework assignment is definitely related to plasticity, it cannot be seen as proof; it is the result of neuroplasticity. Experiments showing plasticity can and have been done with imaging (most notably fMRI) or with electrophysiological approaches (patch clamp studies showing long-term potentiation reflecting learning). These techniques cannot be applied outside the laboratory, as they require advanced and pricey equipment, careful experimental design, and not least importantly ethical clearance.
Reference
 - Cramer et al., Brain 2011;134:1591–609
Further reading
 - Color adaptation: What is the science behind the   inaccurate perception of colors?


text:
Plant identification
What plant species is this?
Its stalk looks like a grapevine, but the leaves & flowers not. It bloomed this week (Mid-June). I have found it in Turkey, Amasya.

If you want, I can add more shots of plant.

Welcome to Biology.SE and thanks for your question. I edited the question wording a bit to improve clarity. I substituted "body" for "stalk" (the part you are holding), I hope that fits your description. I also rotated the picture. Feel free to roll back my edits, they are just suggestions.

That is a kind of honeysuckle. The picture below is for Japanese honeysuckle (Lonicera japonica), but your specimen is different in the way the flowers are arranged and that the distal-most paired leaves are clasping the stem.

It might be Lionicera periclymenum, or Lonicera etrusca (there are about 150 species of honeysuckle); L. etrusca is pictured below (the color is irrelevant) which is native to Europe.


text:
Plant identification in Turkey
What species is this ? It is a stinky, hairy plant. I have found it nearby a river. It had reached a height of 1 meter. Bloomed three weeks ago. Found in Turkey.

I included the correct picture. @Oğuz İsmayil uysal - links to a webpage will not work. You should post the factual images.

Looks like a Hyoscyamus niger also called stinking nightshade.

I knew I knew it! I thought Chelidonium https://en.wikipedia.org/wiki/Chelidonium but that wasn't it! Thanks! +1


text:
The information carried by nerve signals
Action potentials carry nerve signals in individual neurons and somehow encode information. My question is if it is possible to read that information carried by the nerve signal and feed it into a computer to understand what information it contains?

Neural info is contained in spike trains, mainly in terms of spike frequency and related parameters. These spike trains in individual neurons can be measured by techniques like patch clamp and Ca2+ imaging. These techniques are all pretty sophisticated and computer assisted for sure.
However, by recording of action potentials in e.g. the optic nerve, we cannot  possibly know what the person is seeing. Nonetheless, by cleverly mapping responses of conglomerates of neurons we can make estimates of what the information carried in the nerve fibers mean. For example:

Mapping the responses of an ensemble of place neurons in the hippocampus has been successfully used to predict where a mouse is exactly located in a maze (Guger et al., 2011);
Gross potentials measures with EEG can be used to move artificial limbs, as shown in physically handicapped people. In essence, by mapping out the responses of motor areas in the brain, it can be predicted where a person is thinking their limb is moving.

Reference
- Guger et al., Front Neurosci (2011); 5 85


text:
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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Is Sanger sequencing still used in labs, and therefore worth learning?
If iI were to have access to funds for research, would learning this technique be a boon for me? Or are next-gen sequencing methods all the range now? My knowledge of both are limited.

Sanger sequencing is still used in the labs today - and not only on the side. Next-generation sequencing has its strength when it comes to sequencing very large amounts of DNA (basically whole genomes or exomes).
Sanger sequencing is used when you want to sequence smaller regions or portions of a genome/plasmid. Typical read length is (depeding on the machine and the skills of the operator) 600-900bp. This is enough to verify site directed mutagenesis, the presence of inserts you cloned as well that they are correct (if the insert is longer you will typically nest the single sequence reactions to cover the whole sequence) or look for a polymorphism. There are endless possibilities.
Additionally it is relatively cheap to sequence single samples (which is not really working on the next-gen machines), one sample comes between 8 and 10$ (at least the last time I sent this out). And you don't even have to do it yourself as there are a lot of service providers available. The technique itself is not hard to learn either.

i have additional question, not related to OP's. Do people perform sanger in-house nowadays, or either send samples to company or centralized facility (as in big research centers or universities)?

It depends on a number of things: First, you need a sequencer or at least access to one. If this is the case, people often sequence themselves, as this is more flexible (and you can use much less chemistry than ABI recommends :-) ). Additionally, if you want to sequence yourself, you need at least a minimum number of samples per month, otherwise the sequencing kits (minimum 100 reactions) are too expensive to simply rot in the freezer. Big units often have centralized facilities, but this also depends on their scope.

Moreover the error rate in Sanger sequencing is less than many NGS. I know of a recent genome sequencing paper where they used Sanger sequencing.

No its not Depends on the scale you are workin on

The dideoxy termination method of DNA sequencing (often called Sanger
sequencing after the technique’s inventor, Fred Sanger) has been the
workhorse of pretty much every molecular biology lab for the last 30
years. However, over the last few years the method has been
increasingly supplanted by so-called next-generation sequencing
technologies, which allow incredibly rapid generation of large amounts
of sequence data.
Sanger sequencing is still widely used for
small-scale experiments and for “finishing” regions that can’t be
easily sequenced by next-gen platforms (e.g. highly repetitive DNA),
but most people see next-gen as the future of genomics.

The article also addresses issues on read length and cost between NGS and Sanger.

For Sanger sequencing these reads are routinely 800-1000 base pairs long; next-gen methods produce much larger quantities of sequence, but in the form of much smaller reads (the two best-performing platforms generate 35-75 base pair reads, while a third, lower-throughput platform can manage 400 base pairs).
Read length is absolutely crucial when it comes to assembling accurate sequence, especially for genomes as complex and repetitive as the human genome. If a repetitive region is much longer than a platform’s read length, it can’t really be accurately assembled – so human genomes sequenced with current next-gen platforms actually consist of hundreds of thousands of accurately sequenced fragments interspersed by gaps....

Taken from: http://www.wired.com/2009/01/sanger-sequencing-is-not-dead/


text:
Explanation of protocol in DNA extraction experiment
In the Materials and Methods section of this paper on DNA extraction and analysis from hair I do not understand some parts of their protocol methods. In particular:

"The digested hair solution was then extracted twice with two volumes of phenol saturated by Tris-EDTA (TE) buffer (Sigma), and once with two volumes of chloroform. "

How do the volumes of phenol and chloroform come into play? I know they are used for an organic-solvent extraction, but what was the actual procedure used, i.e., the steps for adding each chemical?
Another question I had was on the buffer they used:

"0.01 M Tris-HCL(ph8), 0.005 M EDTA, 0.1 M NaC1, 0.039 M DTT, 2% SDS"

That whole combination would be the "Tris buffer" then yes? And the proteinase K would then be added to some of this buffer to digest the hair?

http://www.bionut.ki.se/groups/mer/doku.php?id=mouse_tail_dna_extraction You might want to check this protocol for phenol/chloroform extraction. It is tricky to say which is Tris buffer, but to digest hair, proteinase K would be added into buffer containing Tris, EDTA, NaCl, SDS and DTT. However, I feel 2% SDS is a bit too high. Check the protocol again.

The DNA solution has a fixed volume (e.g., 0.1 mL). To a suitable test tube is added 0.2 mL of buffer-saturated phenol. After closing the test tube the mixture is mixed well, typically using a vortex mixer, but possibly by careful, repeated inversion. The aqueous phase and the organic phase are barely miscible. The tube is centrifuged to speed up the equilibration, and concentrate the denatured protein at the interface. After centrifugation the aqueous layer is carefully removed to a fresh test tube.
That is one organic extraction. This is repeated with a fresh aliquot of buffer-saturated phenol (another 0.2 mL). Then the aqueous phase is decanted again and extracted with 0.2 mL of CHCl3.
According to the recipe you provided, the buffer-saturated phenol was purchased from a vendor (Sigma-Aldrich Chemicals, of St. Louis, Missouri, USA), so you can look up the ingredients and composition on their online catalogue (no doubt).
The buffer recipe you provided is the proteinase K digestion buffer. It is typically performed at an elevated temperature.
This protocol is designed to isolate DNA from the nuclei of hair cells. Fully half of the contents of a eukaryotic nucleus are chromosomal proteins, by mass, so the proteinase K digestion step not only breaks open the hair cells, but also helps to remove all of the unwanted, contaminating cellular and nuclear proteins.

How does the cholorform come into play though?

Chloroform is also an organic reagent. It forms a dense immiscible layer and helps to remove any residual phenol from the aqueous phase, and also should clean up the last traces of denatured protein.  You should consider obtaining a biochemistry laboratory manual that explains these basic techniques.

Would you have any suggestions for a biochem lab manual?

@RoSiv Sambrook & Maniatis Molecular Cloning is a good start.


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How sterile is sterile when working with nucleic acids to prevent contamination?
I am reading up on preparatory work on working with nucleic acids and a lot of the instructions speak on excessive procedures on cleaning environments with high %ethanol and making sure the equipment is nuclease free, and autoclaved.
Are these sterilization steps really necessary when doing research /running gels? Buying all of this equipment seems very excessive, and given that just one nuclease could compromise my results why bother?

If in doubt, add controls.

Short answer: Yes
Long answer: Depends what you are working with.
DNA: If you are working with DNA, its pretty stable and you can usually get away with a 70% ethanol wash/autoclave (mainly to prevent contamination and obtain consistent results). EDIT: Read Chris's answer also below
RNA: If you are working with RNA well.. whatever you did for DNA doesnt apply anymore. You have to take it to the next level.  You will need to replace everything, you'll need nuclease free water, tubes, reagents and whatnots. Throw out ethanol and bring in RNAZap, DEPC water or something like that.

An RNase free environment is essential when working with RNA samples. There are two main reasons for RNA degradation during RNA analysis.
First, RNA by its very structure is inherently weaker than DNA. RNA is made up of ribose units, which have a highly reactive hydroxyl group on C2 that takes part in RNA-mediated enzymatic events. This makes RNA more chemically labile than DNA. RNA is also more prone to heat degradation than DNA.
Secondly, enzymes that degrade RNA, ribonucleases (RNases) are so ubiquitous and hardy; removing them often proves to be nearly impossible. For example, autoclaving a solution containing bacteria will destroy the bacterial cells but not the RNases released from the cells. Furthermore, even trace amounts of RNases are able to degrade RNA. Note that RNAses are present everywhere (skin, reagents, normal plastic etc).
Therefore, it is essential to avoid inadvertently introducing RNases into the RNA sample during or after the isolation procedure.

Remember that following microbiological aseptical techniques is usually good practice (and a requirement) when working in a molecular biology lab.
There are excellent guides available online for working with RNA:
I took the above paragraph from here:
http://www.bioline.com/us/rna-hints-and-tips
Life tech has a few more tips for you: https://www.lifetechnologies.com/uk/en/home/references/ambion-tech-support/nuclease-enzymes/general-articles/working-with-rna.html
Here is a good pdf to have in your labbook as a reference sheet:http://genomics.no/oslo/uploads/PDFs/workingwithrna.pdf
If this scares you , that's good because when working with RNA there are a million things that can go wrong the first few times you try it. You have to be very careful, and adapting a cavalier attitude such as not bothering is going to come back and haunt you at night...

I tend to disagree. What use will 70% ethanol have on most contaminations? Mostly none, and I even doubt that it will inhibit bacteria (as people only spray it on or do a short wipe).

@Chris What I meant was for surface cleansing. We tend to spray the ethanol and wait a few minutes and then wipe it out ? I was always told that ethanol denatured proteins ?

I keep the surface of my bench clean, so I don't need any extra cleaning before I start working. And yes, ethanol can denaturate proteins, but I wouldn't rely on this. Besides that: Your reaction will take place inside plastic tubes which are clean.

@Chris true that, but I always assume the worst. I was trained in cell biology before mol biology, and yeah... suffice to say I my just have a 70% ethanol spray somewhere in my pocket :)

I do a lot of cell culture, too. And many people spray everything (even the outside of single-packaged plastic pipettes, which will never get into contact with everything.

@Chris Alcohol is a solvent and a solution ;)

First of all, sterility is not necessary. It takes much more effort to reach this than just to wipe down everything with ethanol. What you need is a clean and controlled work environment (but this is something you need anyway to get reproducible results) and good and clean equipment. You will need more precautions for RNA work as RNA is more sensitive and RNAses are ubiquituous, but the general rules are the same. Some remarks from me about it:

There is no need to wipe down everything in your environment before working. Will you DNA touch the desk or the outside of you pipette? Simply wear gloves, use fresh plasticware, do not touch the plasticware with your bare finger and you will be fine.
There is no general need to autoclave everything what you use (unless you explicitly need it sterile). Do not touch the stuff with your bare fingers. Autoclaves can also be a souce for contamination when they are badly maintained or used to also autoclave trash. Plasticware is generally nuclease free, thanks to the production process (melted plastic is not a good place to live on).
If you work with RNA try to set up a separated working space to avoid contaminations by your normal work. If you use glassware, wash it with DEPC treated water and autoclave it to get it RNAse free. Use gloves! Also use a different set of chemicals for this work to avoid cross-contamination. Filter-tips can be a good idea here. Besides being careful, RNA work is no magic but solid handcraft.
If you do PCR try to set up a different work place seperated from your normal work. PCR is very sensitive to contaminations sitting in you pipettes from your normal work. I have seen a number of cases of false positive amplifications from normal work.

Re #1: Many people work with DNA without wearing gloves (including touching the plastic ware), and it rarely causes problems if your tips and the insides of your tubes are clean. Re #4: In many cases (cloning or synthetic biology), it is extremely unlikely that the contaminant would have the right primer annealing sequences to compete with your intended reaction. See for instance Colony PCR, a very "dirty" PCR full of "contaminants".

@Superbest True. But I have also seen people working with sequences (which they cloned) and then used the same set of pipettes to search for the same sequence. It took a while for them to find out that they managed to contaminate their pipettes through inproper pipetting. But otherwise I agree.


text:
Is lysergic acid diethylamide (LSD) metabolized in the body?
Is LSD broken down into other compounds by enzymes or hormones? If so, at what point and where in the body does this happen? I researched several papers appearing in a google search, but unfortunately I did not understand most of it.

Short answer
LSD appears to be enzymatically broken down in the liver.
Background
First off, hormones do not break down anything; enzymes are the work horses that mediate metabolism.
According to a review paper (Passie et al., 2008), humans metabolize LSD into structurally similar metabolites (Fig. 1) by NADH-dependent microsomal liver enzymes to the inactive 2-oxy-LSD and 2-oxo-3-hydroxy LSD. LAE is formed through enzymatic N-dealkylation of the diethylamide
radical at side chain position 8. Di-hydroxy-LSD and nor-LSD are also metabolites, as well as 2-oxo-LSD, 13- and 14-hydroxy-LSD as glucoronides, lysergic acid ethyl-2-hydroxyethylamide (LEO), and trioxylated LSD.
Note that the monoamine oxidase (MAO) system is unlikely to break down LSD. MAO are enzymes that catalyze the oxidation of monoamines. Monoamine neurotransmitters contain one amino group that is connected to an aromatic ring by a two-carbon chain (such as -CH2-CH2-). This structure is not present in LSD (fig. 1). A cursory Google Scholar search did not yield any relevant hits ('LSD' + 'monoamine oxidase'), loosely indicating that MAO is unlikely to be involved in LSD metabolism. However, as I suspect some self-help here - I am unsure about MAOI and LSD interactions, and I highly discourage any toying around with MAO inhibitors and any drug in general. For example, 5-HT is a typical example of an MAO substrate and LSD impinges on 5-HT2A receptors. Hence, interactions in pharmacodynamics with combined LSD and MAOI intake are likely to occur.

Fig. 1. LSD metabolites. source: Passie et al. (2008)
Reference
- Passie et al., CNS Neuroscience & Therapeutics (2008); 14: 295–314

LSD is metabolized in the liver in humans by enzymes of the Cytochrome P450 hemoprotein. The specific enzymes are CYP3A4 and CYP2D6.
CYP2D6 is generally regarded as non-inducible (meaning there appears to be no way to boost its production in humans), and can only be inhibited by other drugs that would cost more than LSD and be dangerous to take anyway.
CYP3A4 carries the answer you are looking for. It is strongly inhibited by... grapefruit! Pomegranate also has the same effect. So ingesting a lot of these fruits will make the LSD take longer to metabolize.

What is in such fruits that causes this inhibition?

@Max https://en.wikipedia.org/wiki/Grapefruit%E2%80%93drug_interactions. The effects are caused by furanocoumarins (and, to a lesser extent, flavonoids).


text:
Case study and speculations on the brain of Edward Mordake
I am very interested in the case of the man named Edward Mordake who lived in the 19th century. In particular, he had two faces. If you have not heard of this man, please, search this up as there are a very few amount of photos, but it is something very, very strange.
However, all the information on him seems to be speculation, so I am looking for a scientific look at this. I am unsure if it will even be possible seeing as how the years have passed and records may not have been accurate.
To be specific, has this condition been noted before? There seems to possibly be differing opinions onto wether the face was indeed its own individual inside, or a low functioning other half of the same man.
Indeed I am looking for any info on the biology of his brain, possibly the neuroscience and or physiology, and of course any comments and discussion.
Thank you

A similar modern case: Chang Tzu Peng. Short video: https://www.youtube.com/watch?v=ZgB0-2vb9HU

@Corvus - is that case 'true'? The wiki page has been deleted and it seems obscure fiction.

I suppose I could have been duped. I guess the lesson is the old "Don't believe everything you read in the wikipedia...."

Mordake was a conjoined twin fused at the head (Fig. 1). Twins conjoined at the heads are rare, occurring only once in every 2.5 million live births. Moreover, in Mordake's case it was a parasitic twin head with an undeveloped body that was fused with his own head. This condition is referred to as craniopagus parasiticus, or épicome / epicomus. Craniopagus parasiticus is an extremely rare teratology, of which only six cases have been recorded in the medical literature (Bondeson et al, 1989).

Fig. 1. Wax reproduction from Edward Mordakes face. Source: Bosmia et al., (2014).
The story of Edward Mordake is, however, obscure and met with skepticism. Moreover, no medical details are known as far as I know. However, he was reported to be intelligent and healthy, just depressed by the second parasitic head (Bosmia et al, 2014). To me it appears a story of a person with a normal brain and a parasitic face attached to his head. However, there are rumors that the parasitic head could talk independently, leaving open the possibility that the parasitic head may have contained a separate brain, or shared Mordake's own brain.
More is known about the double-headed Bengal of Everard Home (Fig. 2).

Fig. 2. Skull of the double-headed Bengal (museum exhibit, left) and an artist's impression of the case (right). Source: Bondeson et al, (1989)
The natural head and body were perfectly normally developed, but a number of anomalies were noted on an examination of the parasitic head, such as excessive tearing and the absence of pupil reflexes. Upon dissection the parasitic head was shown to show various anomalies, such as missing anatomical elements (e.g. auditory canal) or underdeveloped structures (e.g., small lower jaw bones).  Importantly, the brains were separate from each other and covered in individual and proper coverings. The dura mater of each brain adhered firmly and contained
many large vessels. Bondeson et al. (1989) describe the remainder of the six cases as well, which were still-borns or lived just very shortly. They had completely separated brains too.
References
- Bondeson et al, Surg Neurol (1989); 31:426-34
- Bosmia et al, Childs Nerv Syst (2014)


text:
What is the relationship between radiation and evolution?
There is always a certain amount of background radiation present, for example due to ionizing radiation from the sun and other stars. Also certain materials like granite may emit relatively large amounts of radiation.
Ionizing radiation may cause mutations in the DNA (Gevertz et al, PNAS 1985). Mutations, in turn, may lead to altered phenotypes. Altered phenotypes and survival of the fittest are key to evolution and formation of new species.
What is the (relative) contribution of background radiation on the formation of new species?. In other words, is background radiation a critical component in evolution and would the course of evolution have changed substantially when there would be no such background radiation?

Welcome to bio.SE! Sorry for the skepticism, but... this question may be too broad. Spontaneous mutations (due to e.g. radiation) may indeed lead to beneficial traits and hence formation of new successful species. However, evolutionary biology is a big discipline and radiation contains many potential candidate particles. Are you talking background radiation, cell phones, UV light, nukes...

Sorry so unclear.  I'm curious about natural radiation  ie elements, stars, etc., and if it is essential to biology in the broadest sense?  Would the lack of radiation have a negative/positive impact on evolution?

Thanks for explaining. I took a bash at re-wording your question and voted to re-open it. Feel free to roll back or change when it does not reflect your initial question. However, it its previous form the question is not suitable for Biology.SE as it needed editing.

Welcome. I suppose one could come up with estimates of how much "background radiation" influence the mutation rate. The link between mutation rate and speciation is not an easy subject though. I vote to re-open but I think it is good to accept answers to "how much different would the mutation rate be if there were to have no "background radiation"?".

This might be an interesting start to an answer.

I realize that this is broad, but I think it is important for people to understand, and I would like to officially answer this as I find that I often get questions that seem to come from the largely incorrect understanding that evolutionary change is driven by external insults like radiation rather than damage caused by replication errors.

This is more on the historical side, but concerns about the effects of radiation were major drivers in the development of evolutionary genetics in the mid-twentieth century, particularly via the work of H. J. Muller. Muller and Theodosius Dobzhansky had very different views of the role of standing genetic variation because they studied very different types of variation: radiation-induced mutation in the former case and chromosomal inversions in the latter.

Thank you for the edit.  Your edit is exactly the question I wanted answered.  Do I change the question now?

Is background radiation a critical component of evolution? No, it most certainly is not.
The DNA replication and DNA repair mechanisms aren't perfect and errors happen without any external cause or catalyst. You could say mutations happen on their own. There are mutagens that also cause DNA damage or mutations, but they're merely affecting the DNA replication in a negative way, causing it to err more often.
So, the effect of background radiation isn't the key here, the key is that the biological processes of DNA replication and repair are not infallible, although radiation does increase the error rate (the rate of mutation) just like many other mutagens do.

A few points for looking deeper into this question:

Radiation is not the only extrinsic source of mutations. One that has to be necessarily mentioned alongside the radiation is the exposure to chemicals - via smoking, drinking and food consumed. These are not necessarily industrial chemicals - e.g., many things found in soil will find their way to water and to the organisms.
For multicellular organisms one has to distinguish somatic and germline mutations. The former are relevant for the evolution of cancer tumors (which can be viewed as generations of cells), but this is not what we usually mean by the evolution, since this does not affect the offspring of the organism as a whole. In other words, to affect the evolution the mutations must happen in the egg/sperm cells.
Now we are down to the question raised by @DanHorvat: whether the rates of errors during replication are higher than those due to radiation. The former vary wildely among the organisms (e.g., $10^{-4}$ per nucleotide per generation in HIV, but $10^{-8}$ or less for human). The effects of radiation and chemicals may vary depending on the surrounding environment, time period in question, etc.

Thus, I would say that there is no a general answer to this question, although one may certainly compare numbers for a specific organism.


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Can a woman possessing 1 mutated allele show attenuated color-vision deficiency?
Women possess two X chromosomes. However, during development, when the embryo has about 32 - 64 cells, one of these chromosomes is randomly inactivated (in each cell) by an lncRNA named Xist. As a consequence, females are mosaics.
I was interested if this might affect phenotypes of X-linked genetic diseases, for example...
1) Is it possible for a woman who is heterozygote to color vision deficiency be "partially" color blind, considering that some of her cones will only possess the mutated allele?
2) Is it possible that a heterozygote female who carries a dominant allele for a X-linked disease be asymptomatic?
Any references on these issues are welcome.

Short answer
Skewed X-inactivation may lead to phenotypic manifestation of X-linked color blindness.
Background
What an interesting question!
In a study by Jorgensen et al. (1992) two female identical twins that were heterozygotes for X-linked deuteranomaly were investigated. Phenotypically, deuteranomaly refers to anomalous trichromacy, i.e., reduced perception of a color. Note that deuteranopes are totally color blind. Deuteronomaly in the twins was associated with a defective gene derived from their father. Interestingly, while monozygotic twins are genetically identical, one of the twins was phenotypically deuteranomalous, while the other had normal color vision.
Analysis of skin cells of the color vision-defective twin revealed that almost all skin cells had the paternal abnormal X chromosome active, explaining her color-vision defect. In contrast, skin cells from her sister with normal color vision had predominantly the maternal X chromosome active. Hence, deuteranomaly in one of the twins could be explained by an extremely skewed X inactivation.
As pointed out by @mdperry, extreme skewed X-inactivation is rare, and most heterzygous females for color blindness (carriers) are indeed asymptomatic (Jordan & Mollon, 1993). Regarding your second question, all gene mutations leading to color blindness are recessive (NIH).
References
- Jordan & Mollon, Vis Res (1993); 33(1): 1495-1508
- Jorgensen et al. Am J Hum Genet (1992); 51: 291-8

Your theoretical understanding of the ramifications of X-chromosome inactivation is excellent (e.g., the two situations you described).  However, it is important to consider the size of the resulting clones. At that early stage of embryogenesis only ~ half (or less) of those cells will go on to contribute to the fetus, the rest will form the placenta. Also at this stage each cell is likely totipotent, and capable of contributing to all of the different tissues, but eventually the daughters of these cells will become committed, or determined in their developmental lineage. Depending on how much mixing of cells occurs prior to determination, I think it unlikely that within one retina the cone cells would originate from more than a single clone--so I would think that either they all are + or the all are mutant. Since there is L-R symmetry between the two optic cups that will give rise to the developing eyes, I think it is more likely that one female could have one eye that is mutant and one eye that is +.  Given that the prevalence of red-green color-blindness in males approaches 7 % of the population, we can infer that heterozygous females are very common, yet to the best of my knowledge there are not millions of females with partial color-blindness--they either have it (m/m), or they don't (+/+ & m/+). So I think a mosaic female with one eye color-blind and one eye normal must be exceedingly rare.
Re: autosomal dominant diseases, it all depends on the tissue(s) and the affected developmental stage. The OMIM, Mendelian inheritance in Man database may have some discussion of this interesting point(?).

Although a nicely approached answer, it seems to be build from assumptions rather than facts. -1 With some references it would be an excellent answer