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Perception of white in the absence of rods
If the retina would not have any cones, one would be color blind. If white is the presence of all colors (in the matter of color mixture, not addition), then what would white look like without rods?

Short answer
Cones mediate the perception of white in photopic conditions. Rods mediate the perception of white in scotopic conditions. The rod system is not needed for cones to mediate white perception and vice versa.
Background
Cones code for red, green and blue. The remaining colors, as you rightfully state in the question, can be generated by mixing these three colors, as shown in Fig. 1.

Fig. 1. Color mixtures. Source: Davidson College
The millions of different color hues that we can perceive are generated by the retina and the brain by mixing colors and adding the weight that each cone class adds to the color percept (Fig. 2).

Fig. 2. Color Triangle. Source: Wikipedia
As you can see in Fig. 2, when all three basic colors are present in equal amount, perceptually a white color is perceived (the middle point of the color triangle). That is, the combination of co-activation of each cone class yields the perception of white, i.e., without the need for rod activation. Rods are not needed for color vision, including the perception of white or black. In fact, under photopic (well-lit) conditions the rods are adapted to high light levels and are less responsive; their photopigments are said to be bleached and the rods become unresponsive to light. Hence, under photopic conditions the contribution of rod-mediated vision is low (Ambler, 1974).
Rods mediate vision in low-lighting conditions (scotopic vision), as opposed to photopic vision where sufficient amount of light is present to feed the photon-hungry cones. While rod-mediated vision operates at much lower lighting conditions than cone-vision, it only mediates the perception of low-resolution gray-scale images.
References
- Ambler, Perception & Psychophysics (1974); 15(3): 586-90
- Gouras, Color Vision. In: Kolb et al. (eds). Webvision. The Organization of the Retina and Visual System. Utah (2012)

So I person who has trouble seeing at night to drive may have low rod count?

@Jen - May be, for example in retinitis pigmentosa sufferers the outer retina degenerates and with it the rods. Among the first signs is indeed night blindness.  I'll edit my answer to include this when I find the time - good point.

A person with an absents of cones and more rods are more color blind. but may be able to see great at night.

Some animals like dogs may only have rods.

@Jen - Like cats do, yes


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Conversion of ATP to NADH without creating a proton motive force?
Is it possible to convert ATP into NADH and vice versa without first creating a proton motive force? If so by what mechanism is it done?

I am not aware of any enzymes that both oxidize NADH and generate ATP.
However, in the absence of oxygen, many bacteria ferment ethanol and acetate (among other products) to oxidize NADH and produce ATP. ATP is produced by acetate kinase and NADH is consumed by dehydrogenases in the parallel ethanol secretion pathway. Together, these pathways consume (or more accurately, recycle) NADH and generate ATP.

http://mmbr.asm.org/content/69/1/124/F6.expansion.html

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Insect identification, Bangalore India
Can anyone identify this insect? It was sitting on my refrigerator.
Size: approximately 1 cm height, 1 inch across
My location: Bangalore, India

Some sort of Plume Moth, but I can't tell what kind specifically.

https://en.wikipedia.org/wiki/List_of_moths_of_India_(Pterophoridae) ... one of those then, pick your favourite

So i did some more research and found some canon photos of two moth species both found in india and super similar to this

both of them have brown spots around them
both of them are found in india
 So it was hard for me to eliminate one of them
here are both the insects
Sphenarches Anisodactylus

Sphenarches caffer

So now its up to you to decide which one it is???

Can you elaborate on your answer a bit - how you determined this, what rules out other genera, etc? Also, please include a photo/image in the actual answer rather than a link.

Those are actually the photos

To me they just appear as hyperlinks. If the photos are showing when you look at the answer, I'm not sure what's happening.

I mean not exactly photos but it was sure a photo when i copied the link and inserted link for the image insertion option

Done I inserted the photos

My pleasure to help people

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Why is the swelling of bread when placed in water not considered to be caused by osmosis?
Why is bread swelling up when placed in water not considered to be caused by osmosis?
Is there a property of water that should make it leave the bread instead of enter?

I'm not sure what your last sentence means. The bread is absorbing the water.

Osmosis refers specifically to the diffusion of water across a semi-permeable membrane.

The phenomena that you are describing, where bread, which is a porous material, similar to a sponge, absorbs water, is the absorption of water by capillary action.
As @Joel mentioned, osmosis is specifically the flow of a fluid across a semipermeable membrane, such as the plasma membrane of a cell or dialysis tubing, that occurs in such a way as to cause a flow from an area of low concentration to an area of high concentration. This flow eventually leads to a state of equilibrium when the concentration on both sides of the membrane is the same.
The wikipedia article on Osmosis gives this definition:

Osmosis is the spontaneous net movement of solvent molecules through a semi-permeable membrane into a region of higher solute concentration, in the direction that tends to equalize the solute concentrations on the two sides. It may also be used to describe a physical process in which any solvent moves across a semipermeable membrane (permeable to the solvent, but not the solute) separating two solutions of different concentrations. Osmosis can be made to do work.
- Wikipedia: Osmosis

- By OpenStax College [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons
The bread is not selectively permeable, and it will continue to absorb liquid until it is fully saturated. This isn't actually an equilibrium, because additional water would do nothing to change the concentration on one side of the bread or the other. If you added more water to one side of a semipermeable membrane in equilibrium, by Le Chatelier's principle, you are will force the reaction (in this case, you change the concentration) to one side, then the liquid would again flow from the area of low concentration to the area of high concentration.
Capillary action is the result of water flowing into the small spaces, such as the air bubble that form in bread when it bakes, in the absence of a force "pushing" it into those spaces, or against the force of gravity. The liquid accomplishes this through intermolecular forces that cause adhesion of the molecule to the surface of the material that is absorbing it and cohesion of the molecules in the liquid keep them associated to one another, and as the liquid moves into the spaces, it is able to pull the other liquid molecules along into the space.


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Why is the quality range of fastq format so broad?
Referring to fastq format, it is clear that in fastq format, there are 94 quality value for a sequenced Nucleic Acid of a DNA sequence read and they are:
!"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHIJKLMNOPQRSTUVWXYZ[\]^_`abcdefghijklmnopqrstuvwxyz{|}~

So, I have two questions:

Why is the quality value range so broad (94 levels)?
In a particular case of analyzing data, we saw, the frequency of I is so high, which is not a good quality. So, why would we accept such a poor quality in research?

Initially, there were several quality encodings that used to follow different ranges of ASCII characters to denote the quality of read. The range that you mention is a union of all those encoding formats. Nowadays, the most common encoding is Phred+33 (used by Illumina, Sanger, Ion Torrent and other popular sequencers) which uses these characters:
!"#$%&'()*+,-./0123456789:;<=>?@ABCDEFGHI

Character I denotes a phred score of 40. Aligners, when they read fasta files, by default assign a score of 40 (I) to all positions. This might be one why reason you are seeing a lot of I.
Anyways, if your fastq follows the phred+33 format then 40 (I) is a pretty good score which denotes a good quality read. Or you could be aligning fasta files. It would be a bad score if your encoding is phred+64 which I guess, is not the case.
ADDITION
The file that you linked is a fastq file. This sequencing experiment has been done on 454 GS FLX Titanium machine. 454 machines use a different way of calculating quality scores compared to the traditional basecalling phred scores. From the manual:

6.6 Phred-equivalent Base Quality Scores
Quality scores for individual called bases are determined by a method developed in
  collaboration with the Broad Institute (Genome Research,18(5): 763-70,
  2008), whereby the methodology described by Ewing and Green (Genome
  Research, 8: 186-194, 1998) for the creation of quality scores as part
  of the Phred basecalling algorithm is applied to generating quality
  scores for 454 Sequencing reads. The quality scores computed for each
  called base are written to the CWF and SFF files (and optionally to a file paralleling the basecall FASTA file). Briefly, the method
  compares the properties of each base’s flowgram signals against
  properties that have been found to correlate with accurate and/or
  error-prone signal information, using training sets of read data. A
  multivariate analysis of those properties determines the sets of
  property values that best describe “bins” of basecalls, then assigns
  the training set accuracy rates of the basecalls in each bin as a
  quality score using the following scale:
$$Q = -10\ \text{log}_{10}(\text{error rate})$$

Usually, you'll have two files for 454 experiments — one that holds the sequence and the other that holds the quality at each position. These files can be combined to generate a fastq. This file is encoded in the phred+33 (also called Sanger/Illumina 1.9) format which I mentioned above. Phred+33, I guess, is also the standard encoding format adopted by NCBI/ENA/DDBJ and all new sequencing runs are encoded in this format. If you do not know the encoding you can run fastqc on your fastq file and it reports the type of encoding.
In your case, I would denote a score of 40 (ASCII value - 33) which means an error rate of 10-4 i.e. the read is of good quality.
The below graph is obtained by a fastqc run on your file. The bars denote quality statistics at each position. Note that the mean quality drops towards the end of the read.

A fasta file does not indicate quality but when you map them to your target, the aligner (I know of Bowtie based ones) assigns a default score of 40 at each position, during the alignment (and in the output).

I am sure that they are fastq files. This is an example file. However, now, my question is: how could I be a pretty good score? On the other hand, does fasta also give the quality value in this way? I did not find them here. Thanks for trying to help me.

FASTA format does not have this scores. I believe FASTQ is just an extension of FASTA to include the scores (and possibly other information). But I have no evidence this is actually the case.

@WYSIWYG Do aligners actually assign a default score of 40? (I really do not know!). Any reference I could take a look at regarding this? Thanks.

@ddiez Bowtie does it; that I am sure of. You can check the manual or try a dummy run. I think STAR also does it but I am not sure. The aligners also, by default assume a phred+33 encoding.

As mentioned by @WYSIWYG in his answer the quality scores in FASTQ file format are encoded in ASCII characters, and there has been several ways to encode this information. The wikipedia FASTQ page that you link in your question describes some (not sure if all) the different alternatives.
Now, why do we have this wide range of characters for the quality scores comes down to the question of what these characters really mean. What we really care is about the probability that a particular base has been assigned incorrectly. This is the base call error probability (p). We can define a quality score based on the error probability as:
q = -10 x log10(p)

So, if your base call is truly wrong (probability of error p = 1) then q = 0. If your base call is certainly correct (p = 0) then q -> Inf as p -> 0. Imagine your probability of error is p = 0.0001 (that is, most likely the base is correctly assigned). Then q = -10 * log10(0.0001) = 40. Therefore, a score of q = 40 means a probability of error in that base call of 1/10000. Quality scores are considered, as far as I know, between 0 and 40.
Now, another issue is how to include this information for each base in the FASTQ file. It would take too much storage space to include the score as a real value number (i.e. with decimals). A possibility instead is to round it- after all there is no much difference between a score of say 39.7 and 40- we care more about the order of magnitude. But then we will have to still store two digit integer numbers per base. What we can do is map the rounded score to the corresponding ASCII character + some offset. That is, as you can see in the FASTQ page the ASCII value for character I is 73. If you are using phred-33 encoding this actually means that character I = 73 corresponds to quality score q = 73 - 33 = 40, which means p = 0.0001. Voila. Character ! = 33 represents score 33 - 33 = 0 (p = 1). In a phred-64 representation a score q = 40 is encoded with character h = 104. Then q = 104 - 64 = 40.
Of course this is just a rough approximation about how the actual phred score is mapped. Phred is actually the name of a program that was developed to maps the quality scores to ASCII characters. The method in more detail is explained in the original publication (which I admit had only went through):
Ewing B, Green P. Base-calling of automated sequencer traces using phred. II. Error probabilities. Genome Res. 1998 Mar;8(3):186-94.


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Pink growth (aka pink slime) in bathtub or shower
I was wondering if anybody had studied or was knowledgeable about the pink growth that people often find around water fixtures in their homes, especially bath tubs and showers?
My understanding is that this pink growth is actually a bacteria and not a fungus as many assume (source1,source2). Supposedly, the bacteria, Serratia marcescens is airborne and thrives in areas of retained moisture and fatty residue.
My main questions are:

How ubiquitous is this bacteria? What is the bacteria's geographical range of occurrence?

For example, is this species more prevalent in more humid environments?

Are there other species of Serratia that can create similar pink biofilms in tubs? (Are the sources of "pink" separated by geographic location?)

Is S. marcescens even forming a biofilm in these pink stains??

What likely introduces S. marcescens into a bathroom?

I ask, because I've seen this bacteria both present or absent from similarly clean or dirty bathrooms, and thus far have not really seen any consistent patterns in the bacteria's spatial occurrence.
Any other interesting facts or sources on S. marcescens would be great!

I think that it may be well be inorganic calcium-deposits, or other salts. Tap water is often rich in calcium-salts and the reddish color I've seen pretty often down under too. I don't know where you are located, but in Oz there's a lot of iron in the ground, perhaps explaining the reddish hue. All guesses though.

Is the film slimy ? Try checking with a swab

@WYSIWYG Sometimes but not always. I don't have this in my own home, so I don't get to check too often...

Also @Christiaan: the deposits I'm talking about are  more pink and therefore indicative of S. marcescens. Iron deposits would be more dark reddish (or reddish yellow if also associated with heightened aluminum). Calcium deposits would typically be white.

very difficult to say in this-way without help of microscope

I live in St. Louis, MO and get this in my bathtub over time, but not in my other sinks. I actually think @Christiaan is correct here, but with a few additional observations:

I don't think it's bacteria. When dry, it's not slimy, nor does it grow back quickly when wiped away. It feels much more like a mineral deposit.
It was no longer pink when using a different shampoo. Upon returning to an older brand, the color returned to pink.
It's only directly around the drain, it isn't on the walls or anywhere else.

These lead me to think it's a mix of mineral deposits from the hard water and potential reactions with certain soaps/shampoos, at least in my case. These are only based on my own observations though, there very well could be a pink bacteria/fungi that tends to inhabit damp areas.

No it's definitely bacteria. They like to grow wherever water pools with organic matter or certain  soap deposits. You typically have water around your drain long enough for the chlorine or other treatment chemicals to evaporate off to allow the bacteria to live. Coming or going with different soaps just means that one of the soaps had more of the ingredients (fats and /or phosphorous) they prefer

Well, I guess at least you know that geographically it's present in the midwest as well. For what it's worth, I also live in a basement apartment, so it's likely more humid than most.

It could be Haloarchaea

so @theforestecologist not Bacteria but Archaea!

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

Thanks for the post, but this is very unlikely since salt water is not used in plumbing. Your proposed organism is halophilic, meaning it likes to live in salty conditions!

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text:
What determines the length to which hair grows?
Correct me if i am wrong, if we cut 2mm from eyebrow hair, it will grow 2mm and then stop growing, or if we cut 5mm, then it will grow only 5mm. My question is, does hair know how long to grow ?

Probably easier to understand if you look at the answer for a dogs coat. https://en.wikipedia.org/wiki/Coat_(dog)#Genetic_basis_of_length_and_texture Short answer is it is controlled by gene expression.

Individual hairs fall out after they grow for a certain amount of time. If you cut off 2mm of hair, those hairs will grow to what would be their maximum length (had you not cut them), then fall out and are replaced by uncut hairs that grow to maximum length.


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How "exactly" is Rabies transmitted?
Context: I know a person which has developed a sort of "phobia" with respect to touching things that has (even the slighest) chance of being in contact with something that can transmit rabies. For instance, if something (a coin) falls on the floor of our university, said person almost cannot take it, since dogs sometimes pass around the place. This has reached a severe level which hinders this person experience in life. However, there is apparently some hope of rationalization. Specifically, the person told me that if someone can prove, for example, that the virus do not "live" long enough after dropping from the saliva of a dog to the floor in order to be transmitted to a human being, then maybe she will be more relieved. This led me to search for information on the internet, but nothing was conclusive. This takes me to my question, and sorry for the sidetracking.

Can someone be infected by rabies by merely taking something from the ground where a infected dog may have passed by? How long does the virus "live" (or is active, I don't know the  proper term) after being "exposed" to the environment? More generally, how exactly does the process of infection happen, and how can it happen?

This is actually far more complex a question than you probably know. The country you are writing from matters. There are some rabies virus variants that have a relatively low pathogenicity for humans (dog rabies is one of these; a relatively large innoculum is required, i.e. a bite, commonly a deep one with lots of virus-laden saliva.) The likelihood of canine-associated rabies developing from a non-bite exposure is extremely low; in fact, the exact risk is unknown.
In the US, enzootic (dog-to-dog) canine rabies virus has been virtually eliminated through vaccination and stray control programs, making wild animals (including feral cats) the primary concern. Depending on the country your friend lives in, dogs may not even be high on the list of worrisome sources.
Regarding canine-associated rabies,

Rabies control was accomplished [through dog vaccination programs, responsible pet ownership, and serious population control of stray dogs] in Europe, North America, Australia, Japan, Taiwan, Malaysia, and Singapore.

If you don't live in one of these countries/continents, dog-associated rabies is still a major concern. If you do live in the mentioned areas, you can probably dip your hand in dog saliva and not be concerned.
Rabies is usually contracted by a bite; that is most common.

The most dangerous and common route of rabies exposure is from the bite of a rabid mammal. An exposure to rabies also might occur when the virus, from saliva or other potentially infectious material (e.g., neural tissue), is introduced into fresh, open cuts in skin or onto mucous membranes (nonbite exposure). ...Exposures to bats deserve special assessment because bats can pose a greater risk for infecting humans under certain circumstances that might be considered inconsequential from a human perspective.
how exactly does the process of infection happen, and how can it happen?

The exact way it happens is not completely understood, but that answer won't help you convince your friend of anything. The virus is usually deposited in tissue near a cutaneous (peripheral) nerve. If it gains entry to the nerve, it makes its way to the brain with the typical disastrous results.
Having said all this, your friend is not going to stop worrying, because the virus is only the focus of an irrational fear. Though the foci of irrational fears are fairly stable, OCD is most likely the underlying problem, and conventional rational discourse doesn't really suffice in curing the obsession.
During 1990-2007, 34 bat-associated human cases of rabies were reported in the US: 6 cases reported a bat bite; 2 cases reported a probable bite; in 15 cases, physical contact was reported (e.g., the removal of a bat from the home or workplace or the presence of a bat in the room where the person had been sleeping), but no bite was documented; and in 11 cases, no bat encounter was reported, but the rabies virus was bat-specific.
Any encounter with a bat, even a dead one (as stated above), must be evaluated for possible post-exposure prophylaxis.
Unfortunately, in the US, animal rabies is common, and at least 23,000 persons/ year receive rabies postexposure prophylaxis (PEP). (It is probably considerably higher, as no reporting mandate exists.) With the elimination of canine rabies virus variants and enzootic transmission among dogs, human rabies is now rare in the United States, with an average of one or two cases occurring annually since 1960.
In the US in 2013, of the three human cases reported, 2 were involved in organ transplants (raccoon rabies virus variant) and one was a Guatemalan (canine rabies virus variant).
In 2012, one human died from an exposure to a bat. He touched a bat under a bridge. He did not report a bite to a witness. He became ill while traveling, and died in Switzerland. A number of humans exposed to his saliva (including his Swiss caregivers) received PEP.
*Some people in high-rabies areas without the illness have been documented to have developed antibodies to rabies. The mechanism is unknown.
Human Rabies Prevention - United States, 2008
Pathogenesis of Rabies
A Single Amino Acid Change in Rabies Virus Glycoprotein Increases Virus Spread and Enhances Virus Pathogenicity
Human Rabies Prevention (Comment From a Canine‐Rabies‐Endemic Region)
Epidemiology of rabies post-exposure prophylaxis—United States of America, 2006–2008
Rabies surveillance in the United States during 2013
Use of a Reduced (4-Dose) Vaccine Schedule for Postexposure Prophylaxis to Prevent Human Rabies: Recommendations of the Advisory Committee on Immunization Practices

First of all, thanks for the answer. I really, really appreciate it : ). We live in Brazil. Does that change or add anything to your answer?

"More generally, how exactly does the process of infection happen, and how can it happen? How long does the virus "live" (or is active, I don't know the proper term) after being "exposed" to the environment?" Good open-access article going over some of the molecular pathology and epidemiology (1). I'd also mention that enveloped viruses are very sensitive to the environment unlike lots of naked viruses, so they don't generally survive long outside the host or get killed easily by detergents and/or desiccation.

@Kendall Is rabies "enveloped"?

@anongoodnurse Also, the person has (as you correctly suppose) been diagnosed by a psychologist as having OCD. Is there anything I can do?

@AloizioMacedo Yes, Rabies virus is a Baltimore V or (-)ssRNA enveloped virus. This basically means there is something similar to a lipid bilayer encasing the nucleocapsid, and the ssRNA has to be transcribed to (+)ssRNA before it can produce it's encoded proteins. The envelope has some advantages in vivo but an exposed enveloped virus is very susceptible to environmental hazards!

@Kendall Thank you, that is very informative. Sorry to be bothering you, but would you mind telling how long is "survive long"? Matter of seconds, minutes?

It varies greatly by virus but, broadly, you can imagine days for enveloped viruses, weeks for naked viruses. There's an open-access article on the matter here.

Let us continue this discussion in chat.

The routes of transmission for rabies are concisely described on the CDC website. To summarize:

The vast majority of cases of rabies are transmitted through the bite of a rabid animal.
For non-bite exposures, there is potential for transmission if an infectious material (such as saliva) enters the eyes, nose, mouth, or wound of a person. There is also potential for aerosol transmission however this is only a risk to laboratory workers.
Petting a rabid animal or contact with blood, urine, or faeces of a rabid animal does not constitute an exposure. (See the CDC guidelines for detailed information on special case contact with certain wildlife species.)

It is possible that if a person touches a fomite (such as a coin) that had very recently contacted the saliva of a rabid animal, they could be infected if that coin came in contact with an open wound or mucous membranes. Neverthless, this is extremely unlikely. Such a case has never been described. Fomites are not considered a route of transmission for rabies.
Furthermore, the rabies virus cannot survive very long in the environment. The virus will die within hours since it is very sensitive to ultraviolet light and desiccation, therefore once the saliva is dry there is no risk of transmission. This process is not instantaneous (the virus does not die as soon as it leaves the host). I was unable to find a precise length of time that the virus can survive in the environment, but this probably has not been researched because there has been no reported cases of transmission via this route. A 1974 study found that the virus in mouse brain tissue died within days at room temperature, and it is plausible that the survival in fluid exposed to the environment would be much shorter.
Most animal workers such as veterinarians receive a pre-exposure rabies vaccine but this is due to the risk of being bitten by a rabid animal.
In summary, we cannot categorically exclude transmission via a fomite, but I cannot stress enough how extremely unlikely exposure to rabies in this manner would be.

This is a good, but not precisely correct answer. Bats are an exception; there have been cases of rabies in people exposed to but not bitten or even scratched by bats. The mechanism is a "postulated unknown bite", but it is postulated. Petting a rabid bat most certainly constitutes an exposure and such a person would be given post-exposure prophyllaxis per CDC guidelines.

@anongoodnurse PEP is not indicated for category I exposures, such as petting a rabid animal - even a bat. It is somewhat dependent upon the history, however. You are correct in that if a person cannot completely exclude the possibility of being bitten by the bat (e.g. they were sleeping in the same room) then they will likely receive PEP. We do err on the side of caution, so I'm sure category I exposures often get PEP, but this has to be balanced against the cost and inconvenience of getting the injections.

Actually, it has to be balanced against the seriousness of the disease; even if the risk is very small, the disease is 99.999999999% fatal. "Cost and inconvenience" may be a concern in underdeveloped nations, but the CDC doesn't consider it in their recommendations. The guidelines are pretty clear; bat encounters are treated very differently (see above).

@anongoodnurse PEP treatment costs several thousand dollars, so of course cost is a consideration. Of course the severity of the disease is the major factor, which is why I said we err on the side of caution with treating. For category I contact where there is an extremely unlikely risk of transmission (no bite, no scratches, etc) then the CDC would not always recommend treatment as you suggest. In this answer, I am just trying to convey that the risk is never 0, but extremely low.

I don't like to debate in comments. I don't know how decisions are made in your country, but I'm familiar with how they are made in the US. I am fully aware of CDC recommendations (as well as regional and state department of health recommendations) and I disagree with you. Furthermore, you might find the fifth reference interesting; it discusses the very issue.

Let us continue this discussion in chat.


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What would happen if Carbon-14 was in a glucose molecule and decayed into Nitrogen?
This interested me because of Melvin Calvin's experiment with photosynthesis where he used radioactive Carbon-14. If a plant used it as a reactant to make glucose, and that Carbon-14 decayed into nitrogen, what would happen to the molecule?

I don't think this is biochemistry. This is clearly radiochemistry and should be asked here: http://chemistry.stackexchange.com/questions/43616/what-would-happen-if-carbon-14-was-in-a-molecule-and-decayed-into-nitrogen ;-)

I'm voting to close this question as off-topic because it should go to chemistry or physics. It is a very interesting question!! But just offtopic here.

Carbon likes having 4 bonds, nitrogen likes having 3, though 4 is possible when the nitrogen is positively charged. The molecule would most likely break a bond when the C became an N, but going from C to N requires converting a neutron to a proton by beta decay. The energetic electron ejected during beta decay might disrupt other parts of the molecule on its way out, but I don't really know, so this is a comment.

Also, it looks like chemistry won't take this question until it's deleted from here, so pick one.

@user137 I don't really know either, but I posted an educated guess. :D

@user137 I think I found the solution, the decay has far more energy than the chemical bonds can withstand, so the molecule will fall apart.

Carbon 14 has a half life of about 6000 years. the only way to know for sure is to synthesize a bunch of radioactive glucose and leave it a few centuries to see what reaction products are formed. An issue is that regular glucose may decompose on a shorter timescale anyway.

@steveverrill You never heard of atomic force microscopy I assume.

I am not experienced in the topic, and could not find any article related to these kind of reactions, but my guess is the following. During the nuclear transmutation the radiocarbon will lose an electron (beta particle), so the nitrogen product will have positive charge. After that there are 2 possible scenarios.
a.) less plausible scenario
The beta particle carries away the energy of the decay, so the molecule will have low energy and it will be able to rearrange.
The electron shells will collapse a little bit, since the nitrogen has smaller nuclear radius. The part after that depends on which carbon we are talking about in the glucose molecule. I would guess the following rearrangements:

${-CH2OH} \rightarrow {-NHOH} + H^+ $
${=CHOH} \rightarrow {=NH} + H^+ $
${-CHO} \rightarrow {-NO} + H^+ $

It is not easier to break an N-H bond compared to the N-C and N-O bonds according to this table, but I think what really matters here is the stability of the final product, and $H^+$ is way more stable than any $^+O*$, $^+C*$, etc. ion.
b.) what really happens
The beta particle carries away the energy of the decay only partially. So the nitrogen will have a lot of energy, which is more than enough to break all of the bonds. According to wikipedia the decay energy is 0.156476 MeV. Let's compare it with the bond energies:
$ 0.156476 MeV = 2.50702189 \cdot 10^{-17} kJ $
${2.51 \cdot 10^{-17} kJ} \cdot {6 \cdot 10^{23} \cdot 1/mol} = 1.51 \cdot 10^7 kJ/mol$
According to our table the covalent bonds have about a few hundred kJ/mol energy, e.g. a C-N bond has 305 kJ/mol energy. So it is very likely that the chemical bonds will break immediately after the decay and the molecule will fall apart.

My guess is it's hard to study because even the C-14 to N transition is slow on lab scale, so getting enough decay products to do structural analysis is hard.


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Why is stimulation of nerve tissue with a negative pulse called "cathodic" stimulation?
By definition, the cathode is defined as the terminal through which current exits a polarized device. But in the context of neuromodulation, such as spinal cord stimulation, deep brain stimulation, the "cathodic" pulse refers to a negative current pulse that elicits action potentials. A negative current is by definition a current flow that enters the electrode.
Can anyone explain where this terminology comes from and help me resolve this apparent contradiction? It's driven me mad for the past years.

The answer to your (excellent) question is a matter of definition, which has its roots in the 18th century.
A cathode is the electrode where conventional positive current leaves a current source. Conventional current is positive, due to historic reasons. Around 1750, Benjamin Franklin described the flow of current between wool and wax after electrostatically charging the former. He defined the flow of current as being positive, flowing from the surplus side (which he defined as positive) to the current sink (defined as negative). This unfortunate choice is sometimes referred to as the Franklinian approach to electricity, and is still widely used today to describe electronic circuits and referred to as the conventional flow notation (Fig. 1) (Efron, 1960).

Fig. 1. Franklinian approach: the conventional flow of current still in use today for electronic circuits. Source: All about circuits.
The electrical current was only later found to consist of negatively charged particles, namely electrons. The work of Luigi Galvani on electrical stimulation in frog muscles around 1780 and the invention of the electric battery by Alessandro Volta in 1800 eventually led to the discovery of the electron in 1897, attributed to J.J. Thomson and his work on cathode rays shown in Fig. 2. As the figure shows, the true flow of electrical current is the reverse, namely an electron current flowing from from negative to positive. In the meantime, however, the convention of positive current flowing from the positive pole (cathode) to the negative (anode) was already established. Note that this holds for a discharging device. In a charging device, such as the battery, the cathode is negative, and the anode is regarded as positive.

Fig. 2. Cathode ray showing electron flow. Source: TutorVista
Hence, in a stimulating (discharging) device, the cathode is in truth negative, because it is the source of negative current (electrons). Cathodic stimulation therefore means electrical stimulation with a negative current. A cathodic pulse is therefore injection of a negative current pulse.
Reference
- Efron. Chapman & Hall London, Rider Publisher New York (1960)

Thanks for this @Christiaan . You write that the positive pole is the anode, is this a typo (in all my electronics courses, confirmed by Wikipedia, the cathode is the positive terminal)?. I do however understand what you mean. This leaves me to assume that in biology or neuromodulation, the cathode is defined as the terminal through which the "charge" leaves the device? In this case it would indeed be the negative terminal. So basically, in electronics we still use the conventional definition of current flow, whereas in biology we use a more accurate, charge based definition?

@Moppentapper No worries, and yes, it was a typo - and corrected. And yes, your comments are correct. In Bio the 'real' situation is used, because it is important to know what really happens in a prep; negative current has often opposite effects over anodic stimulation.

Excellent @Christiaan thanks so much. It's incredible how simple things are made confusing when different conventions are used!


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Spider Identification: Is this an Arizona Recluse?
I found this spider in my toilet bowl. It was after dark. We live in Prescott Valley, AZ at around 5100' elevation at the edge of a development fairly close to the mountains in grass land.
I'm concerned its an Arizona Recluse (or Desert Recluse). We saw a few of these around the house during the warmer months; this is the first I've seen in a while since its gotten cold, but my wife just did some extra cleaning.
I don't see a violin shape, but this article points out that desert recluse's don't have a noticeable violin. It also looks like it has 3 sets of eyes, but the 4th may just be hidden due to the angle since it looks like the 3 I see in the pics aren't centered quite right. Anyways, if anyone has some insight I would be happy to know. The leg span was a bit bigger than a penny.

Hmmm. I had one like this on the bathroom counter. It was huge by comparison, 3 inches leg span, and a dark green fuzzy abdomen. I am in the northern Sonoran Desert. I am trying to find my spider. It ran up the mirror to get away from me. Definitely non-aggressive.

I don't think it's an Arizona recluse. Characteristic of all recluse spiders (including the five varieties found in Arizona):

Long thin legs
Oval shaped abdomen
6 eyes in dyads (pairs)
Uniformly colored abdoment with fine hairs
No spines on legs
Legs are uniformly colored
Light tan to dark brown in color
Distinct violin-shaped mark on on the back points to the posterior of the spider (less obvious on Arizona recluses)
Body not more that 3/8" in length

Your spider has spiny legs. That, plus the fact that Arizona recluses are even less likely to live where humans do (as your article states), and are attracted to dry places, makes your spider an unlikely candidate, but I could be wrong.
Loxascelidae, Loxosceles reclusa

That makes me feel a bit better, although it doesn't look like a wolf spider either, because of its more uniform color. So I'd be curious to know if anyone has a positive ID. Maybe Southern House Spider?

@Ian Probably a huntsman, I'd say, based on the eye arrangement.

@augurar - Wouldn't a huntsman have crab shaped front legs? These look vertically jointed.

@Ian Based off of this site and this one a huntsman seems the most likely.  You can see the sideways leg orientation is not always obvious, depending on posture.

@augurar, Yeah I guess the first photo on your second link looks similar, especially the eye pattern (assuming the fourth top eye is hidden in my photos).

The key for this spider is the set of four 'tailpipe' spinnerets.  That's characteristic of the Ground Spiders in the family Gnaphosidae.  Recluses don't have that - the bulbous Recluse abdomen has the spinnerets oriented underneath like most spiders.  The recurved upper row of similar-sized eyes on this spider is also consistent with that group.  Not being familiar with western spiders, I'll just leave it at that.
Ah!  I finally realized that I need to add further details in the answer itself!  So, for sources, I refer you to Kaston, BJ, 1972 How to Know the Spiders; Cushing and Ubick 2009, Spiders of North America; and Bradley 2012, Common Spiders of North America.  An invaluable site is also Bug Guide, from which the following photos come: https://bugguide.net/node/view/1970/bgpage .
Note particularly the 4-pipe spinnerets.  I'm not suggesting any of these as yours; just that yours is most probably also a Gnaphosid of some kind.  Also, I now realize that I can only add 1 photo to this.  Well, this will do.


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Are the genes for transcriptional factors close to their targets in the genome?
Transcriptional factors (activators and repressors) are proteins which regulate transcription. Being proteins, they themselves are also made from expression of certain DNA sequences/genes.
For example, the lac operon repressor is coded for by the lacI gene. Now, in the case of the lac operon, the gene for the transcriptional factor is next to the promoter sequence. It is, in fact, a part of the lac operon. Similarly, the trpR gene is a part of the trp operon.
Is this always the case? Is the gene coding for the transcriptional factor always present next to (or close to) the transcription unit?
The two mentioned operons are only in prokaryotes. Could it be that this fact is valid for prokaryotes only, and not eukaryotes' DNA?

Is the gene coding for the transcriptional factor always present next
  to (or close to) the transcription unit?

Not necessarily. You can find several counter-examples. Even for prokaryotes this is not necessarily true. The genes regulated by a common factor are called regulons and though the target genes need not be proximal to the regulator, it has been observed for E. coli and B. subtilis that operons within a regulon are clustered in the genome (Zhang et al, 2012). In the same study, the authors note that small regulons have the regulator proximal to them (See the figure below).


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How the chaotropic agents help in purification of DNA molecule?
Those plants which are rich in secondary metabolites and polysaccharides DNA isolation can be done using certain chaotropic agents? can any one explain how it works?

Chaotropes would disrupt protein structure. Maybe they help by removing the DNA binding proteins?

Chaotropic agents are cosolutes that can disrupt the hydrogen bonding network between water molecules and reduce the stability of the native state of proteins by weakening the hydrophobic effect. a chaotropic agent reduces the amount of order in the structure of a protein formed by water molecules, both in the bulk and the hydration shells around hydrophobic amino acids, and may cause its denaturation (biochemistry).
A chaotropic agent is often used in DNA isolation. It's purpose is
a. To degrade membrane lipids
b. To destroy the endoplasmic reticulum
c. To degrade mitochondria
d. To limit the amount of magnesium salts in the lysate
e. To destroy the three dimensional structure of proteins
To make it simple, a chaotropic agent destroys the 3D structure of a protein, thereby leading to subsequent protein degradation. It serves as a proteinase enzyme, cleaning the cellular proteins in your DNA isolation and purification process.
http://www.hindawi.com/journals/bmri/2009/574398/
http://www.ncbi.nlm.nih.gov/pubmed/16152629

Thanks a lot for valuable answer..... but does it also any effect on removing secondary product or lipid or polysachharides

Nucleic acids share many structural similarities with polysaccharides, and they will therefore co-purify through most fractionation steps.


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Why is it necessary to have both cone and rod cells in the eye?
Our eyes have both cone and rod cells. Rod cells measure the intensity of light whereas cone cells identify the colour of the image formed in the eyes. So cone cells must also be able to identify white, black and grey and also their shades.

So it wouldn't have been that much trouble to just have cone cells cells as identifying black and white would have been the same as measuring the intensity of light. Wouldn't it?

Duplicate of http://biology.stackexchange.com/q/42216/3340

@WYSIWYG this question is different

The question might sound different but the answer there completely answers your question. There is no point in repeating the same answer, isn't it. If there is something that is missed out in that answer that your question pertains to, then you can add some details to clarify.

Jen asked that what would white look without cone cells. I wish to ask is it necessary to have both cone cells and rod cells.

Please see Christiaan's answer to Jen's question.

It is pretty much similar but i am still having trouble understanding why rod cells are required. As stated  Rods only mediates the perception of low-resolution gray-scale images, so couldn't the same image be provided by cone cells by only using black, white and gray.

It is clearly mentioned in Christiaan's answer that rods are required for vision in low-light conditions.

First off - both the rod and cone system measure light intensity; both sensory cells increase their responses when excited by more photons (Purves et al., 2001). Hence, your introductory sentence that rod detect luminescence and cones color is incorrect. They are both sensitive to luminescence.
You are correct that rods detect gray scales, while cones perform color coding. Both systems can detect gray shades; while rods are limited to that, cones are not. Rods are very sensitive to light and in a dark-adapted state are capable of detecting a single photon. Hence, they operate under conditions of low-lighting at night and as such they mediate night (scotopic) vision. Cones are photon-hungry and need more light to operate (photopic conditions).

Why have cones? Because color vision helps to detect and differentiate stuff.
Why have rods? Because night vision is helpful.
Why have both? To be successfully equipped to thrive in both light and dark environments.
Do we need them both? No - even nocturnal hunters that don't have rods have been shown to be able to hunt at night. Not only that, these geckos have been shown to be able to detect color in starlight (Röll, 2000). Under these lighting conditions, human retinae rely on the rod system and are unable to detect color.

References
- Purves et al., Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates
- Röll, J Neurocytol (2000), 29(7): 471-84

But in night couldn't we have managed off with just using grayscale vision with the help of cone cells to view images. During night the cones don't work?

our cones don't work at night.

So, as cones don't work at night, we need rods to help us with grayscale images.

@Reptile1234 It's more that you need rods to help you see at night. Not having functional rods results in nightblindness. As you can imagine, not being able to see at night will affect one's ability to survive.


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Pedigree Analysis: Problem
I'm struggling to arrive at the answer to the following question, which appeared on a pre-test of mine and which I am now using to study the material we've learned. According to this helpful video, I am assuming the possibilities for my question are also autosomal recessive, autosomal dominant, x-linked recessive, or x-linked dominant. I tried each approach as Mr. Douch did in the linked video, but I struggled to find a definitive answer. No matter which approach I picked, it seemed plausible that either the boy or the girl could have the trait, but it seems there's no guarantee that both the boy and the girl have to have the trait. During the pretest, I picked the first answer choice, both the boy and the girl, and got the answer correct by mere chance. But to say that the boy and girl are expected to have the trait would imply that there is a great deal of certainty that the trait will be passed on, right?

The pedigree below shows how a physical trait caused by a mitochondrial gene is passed from one generation to the next in a family.

Using this diagram, which children highlighted in yellow would you expect to have this trait?
(A) Both the son and the daughter -- correct, per answer key
(B) Neither the son nor the daughter
(C) The daughter only
(D) The son only

Please let me know what I am doing wrong or if I am not understanding the question wording correctly. Does it have to do with the fact that it's a mitochondrial gene? Thanks.

The key here is that it is a question about mitochondrial DNA. mtDNA in humans is inherited maternally (from the mother). Both sons and daughters inherit mtDNA, but only the daughters will pass it on to the next generation.
A child's mtDNA has to come from his or her mother, and all of a person's mitochondria are genetically identical. Therefore, children of an affected female will almost certainly have the abnormal trait, while children of an affected male will not.


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Ions in different cell compartments
I would like to understand the distribution of metal ion concentrations (such as Mg2+) in the different cell compartments. I tried very hard but still couldn't find such information. Could anyone help?  Also, could you recommend a good reference on this problem? Thank you!


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DNA extraction for LAMP assay
I am trying to set up a LAMP assay (Loop-mediated isothermal amplification) for the detection of E.coli.
I was told that EDTA can chelate the Mg in my reaction and thus prevent the assay from working (similarly to PCR). Therefore, I hesitate to use TE buffer. Can I prepare my primer mix and extract DNA (using the boiling method) in DNAase free water?
will that affect the quality of my DNA and primers during storage?
Thanks a lot!
Alex

Although this is theoretical a problem, in fact it isn't one. Lets do the calculation around it. EDTA complexes equimolar amounts of bivalent cations (e.g. Magnesium), so 1mM EDTA will complex 1mM Magnesium ions. Lets assume that the PCR reaction contains 2mM Magnesium.
A typical PCR reaction I do has a total volume of 25ul and contains 1ul DNA template in TE buffer (10mM Tris, 1mM EDTA). The final reaction contains 1/25th mM (or 0,04mM or 40nM) EDTA which can complex 0,04mM Magnesium. So instead of running the reaction with 2mM Magnesium, you do it with 1,96mM, which will not be noticable.
Additionally other errors in setting up (pipettes not accurately calibrated, not setting small amounts into the liquid etc.) easily add up to 5-10% error in total, which has a much higher impact in the Magnesium concentration of the reaction than the EDTA. If you use much higher template concentrations (which is usually not necessary), then you can correct for this, but normally this is not necessary.

The conventional Eiken LAMP formulation has an excess of Mg2+.  5 µl of TE with EDTA at 1 mM going into a 25 µl reaction will have minimal impact.  In any case the LAMP formulation can be up adjusted in Mg2+ to compensate, but I doubt this is even necessary.  Besides, bugs will lyse better in the boiling method with EDTA present and it will hinder nucleases.


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Xylem Properties
 In a biology lecture, I was told that the xylem vessels were 'narrow so that the water column does not break easily and capillary action can be effective'.
My question is why is this? Is the reasoning similar to an artery in the human body, whereby the narrow property can increase the pressure of the blood and force it out faster? Or is the reasoning different?
Thanks.

While this is a slightly different question http://biology.stackexchange.com/questions/42223/why-is-the-swelling-of-bread-when-placed-in-water-not-considered-to-be-caused-by/42233#42233 , the answer will help to explain how adhesion and cohesion work to maintain the water column in the xylem. This is different from the human circulatory system,

I'd suggest reading about capillary action. The article is a bit technical in places, but what part of it boils down to is the narrower the capillary (up to a certain point), the stronger the effect and so the water column can go higher.

Related answer to How do trees lift water higher than 10 meters?

What are you referring to with "...can increase the pressure of the blood and force it out faster" (specifically the "force it out faster" part)

Xylem's main job is to transport water, and therefore the inorganic nutrients in the water. Now, to answer your question, we need to know how water is transported.
Water is transported due to both cohesion, adhesion, and surface tension. Water is known for forming hydrogen bonds, and this is known as cohesion. When it forms hydrogen bonds with other molecules, this is called adhesion. In the xylem, some of the water molecules are evaporating, but pulls the water molecules below back up. The adhesive forces also do a similar job of pushing the water up.
Now, if the xylem was smaller in diameter, then the surface the water is exposed to increases. This means the adhesive forces are stronger. Therefore, the water is transported a higher distance. This is important for really tall plants.
Now to answer your second part, the arteries analogy is so wrong. This has nothing to do with how fast the waters goes up, but the height at which is reaches. Also, the human blood vessels depend on pressure and pumping (the heart's job).

Surface tension is the result of the differential between cohesion and adhesion, it isn't a property per se. "At liquid-air interfaces, surface tension results from the greater attraction of liquid molecules to each other (due to cohesion) than to the molecules in the air (due to adhesion)."

Also, read the OPs question again, they are asking about a comparison between xylem and the circulatory system of the human body. Your answer really doesn't address that.

@AMR ok. I will edit ASAP


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Polar bodies in females
What is the fate of first and second polar bodies formed during the menstrual cycle in human females?
Do they degenerate?
Does any other mammal also produce polar bodies?

According to this article polar bodies sometimes apoptose but sometimes are "capable of developing into complex, highly organized structures, or even enabling parthenogenesis". Despite their fate being far less than the oocyte.
It also states they're present not only in other animals, but also some plants.
"In other animals and some plants, polar bodies give rise to vital tissues that protect and nourish the embryo. These apparent “oddities” reveal the diverse mechanisms used during reproductive development and may even allude to the origins of meiotic strategies."
It looks like polar bodies are very important in humans, but not other organisms:
"Polar bodies may, however, give rise to human embryoids if fertilized and twins may even result when one spermatozoa fertilizes the ovum and a second sperm fertilizes its sister polar body (Bieber et al., 1981). No twin pairs resulting from fertilization of the second (haploid) polar body have been reported (Machin, 2009), but clearly polar bodies have cellular and developmental potentials beyond apoptosis, even in humans."
"But in many other organisms, polar bodies are not dispensable. They are not simply waste bins for three-quarters of the genetic material produced during oogenesis, and they do not disappear following meiosis."

So the second sperm fertilises the first polar body? But wouldn't that require two sperms entering the ovum? Is it practically possible?

The first polar body is separate from the ovum, so the second sperm would fertilize the first polar body as if it were an egg. Two sperm can enter one ovum though, but the majority don't survive. When they do, the egg needs to split. If it doesn't, it results in something called a mole pregnancy; the offspring will eventually miscarriage unless aborted.


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What is allelic effect sizes and direction?
In a paper, Berkley, C. A., and C. Lexer. 2008. Admixture as the basis for genetic mapping. Trends in Ecology & Evolution 23:686–694, the definition of Genetic architecture is given. It says:

Genetic architecture: the number and genomic location of loci that
  contribute to variation in a trait, as well as the allelic effect
  sizes and direction, the genotypic effects (additivity and dominance)
  and the extent of epistatic interactions among loci.

What is the allelic effect sizes and direction?
I found that allelic effect sizes is the same thing as penetrance. But the direction?

These two concepts are different from penetrance.
Allelic effect size
An allelic effect size is the magnitude of the effect of an allele on a phenotype.
The detailed definition seems a little bit trickier than it sounds I think (and I would love confirmation by other users on what follows and or a reference). For example, a phenotypic trait might be influenced by 20 QTL. At one such QTL (say QTL8), you may observe two alleles in the population: QTL8_A and QTL8_B. The effect size is the absolute phenotypic difference between two individuals differing exclusively at QTL8. I suppose it is also possible to define an allelic effect size as the average difference between the phenotype of QTL8_A and QTL8_B over all possible genetic background (eventually weighted by the average frequency of each background in the population at a given instant). In the case of a QTL that contains more than two alleles, then the allelic effect size can be defined either between each pair of alleles or between one allele and the average effects of all the others. Strong epistasis make the whole thing more complicated if one wants to average over all possible genetic backgrounds.
Direction of an allelic effect
The direction of an allelic effect is the direction (add or subtract) that an allele has on a phenotype.
Talking about direction makes sense only in the absence of sign epistasis.

Do you have a reference that talks about this?

Nope! The term is often encountered but I am not I ever saw a nice and complete definition of it (although it probably exists). This is the reason why I am asking for confirmation from other users. Sorry, cannot do better!


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Where can I find FDist2 executable?
I am trying to download the program FDist2 (Beaumont and Nichols 1996) for Mac but for some reason it appears that all the links I find are broken.
It appears that the program Lositan is an faster implementation of FDist2 but in my understanding Lositan works only through a GUI and not via the command line (and given the number of analyses I want to perform I need to be able to run this algorithm from the command line).

I found this link in Mark Beaumont's web site. The links seem to work. I am not completely sure whether this is a question for this forum though.

Lotterhos and Whitlock 2014 recoded fdist2 in R and it can be found here on Dryad.

The link that ddiez has mentioned, has a download link for a zip file (fidist2). The zip file contains windows executables and C-codes. Just compile the C-codes in your terminal.
This is from the readme:

The .exe files are pc binaries, which is only what most people want. I
  include the source file in case anyone wants to play with them. In
  this case compilation is e.g.:
gcc -o fdist2 -O fdist2.c -lm
gcc -o cplot -O cplot.c as100.c as99.c -lm
gcc -o datacal -O datacal.c -lm

Actually in the readme, the first compile command says fdist.c (no such file) instead of fdist2.c. I corrected that here.
Your system should have gcc. I tried compiling in my system (linux) and it works. It should work in Mac too.

OS X doesn't come with a compiler by default, but if you install XCode and the command-line tools, you'll get clang, which works (in this case) very much in the same manner.

@MattDMo ohh okay.. I didn't know that... That's bad .. This page says that XCode comes with gcc (don't know what version but once you have a compiler you can always compile the other versions).

Well, I'm avoiding a lot of "nerd" details. I think the command gcc will work from the command line once the proper tools are installed (@Remi.b, make sure you run XCode first!). The problem I'm running into currently is that the files aren't compiling. Remi will need to find a C expert, I think....

Yes, the compilation fails on Mac. I'll try to figure this out (eventually with some help from the StackOverflow community) and suggest an edit. Thank you!

@Remi.b Have a look at this page.. Once you compile gcc on your system, you won't have much trouble. Having gcc in your system would be useful for other purposes in future as well.


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Why is a heritability coefficient not an index of how "genetic" something is?
On his blog, Eric Turkheimer writes:

[T]aken as a number, a unit of analysis, heritability coefficients are
  funny things to aggregate on such a massive level.  What exactly are
  we supposed to make of the fact that twins studies in the
  ophthalmology domain produced the highest heritabilities?  Should eye
  doctors, as opposed to say dermatologists, be rushing to the genetics
  lab because their trait turns out to be more heritable?  No.  Whatever
  else a heritability may be, it is not an index of how "genetic"
  something is.  It is not, for example, a useful indicator of how
  successful gene-finding efforts are likely to be.  If nothing else,
  differences in reliability of measurement are confounded every
  heritability tallied here.  My point is this-- although it's nice to
  know that on average everything is 50% heritable, it's hard to attach
  much meaning to the number itself, or especially to deviations from
  that number, to the fact that eye conditions have heritabilities
  around .7 and attitudes around .3.  Having two arms has a heritability
  of 0.

As I understand this, one reason Turkheimer believes heritability coefficients are not an index of how genetic a trait is is that they are confounded by varying levels of measurement error. So, for example, maybe the relatively low heritabilities in skin conditions compared to eye conditions are because there is more measurement error in relation to skin conditions.
Turkheimer implies that there are other reasons why it's not appropriate to say a heritability coefficient is an index of "how genetic" something is. What are those other reasons?

Heritability is indeed an index of how genetic something is; it is just that there are useful caveats (mentioned in the answers). That "something" is "a phenotype within a specific population in a specific environment at a specific point in time," not just "a phenotype."

Rather than discussing what heritability is not through wordy sentences, let's just talk about what heritability is. There are two "types of heritability":

Heritability in the broad sense
Heritability in the narrow sense.

I will discuss a few concepts and slowly introduce the concept of heritability in both senses.
Phenotypic trait
The phenotype is the consequence of the genotype on the world. In brief, a phenotypic trait is any trait that an individual is made of!
Quantitative trait
A quantitative trait is any trait that you can measure and ordinate, that is any trait that you can measure with numbers. For example, height is a quantitative trait as you can say that individual A is taller than individual B which is itself taller that individual C.
Variance of a quantitative trait
In a population, different individuals can have different values for a given phenotypic trait $x$. Because we are talking about quantitative traits we can calculate the variance of the trait in the population. Let's call this variance $V_P$ such as
$$V_P=\frac{1}{N}\sum_i (x_i - \bar x)^2$$
In the above equation, $x_i$ is the value of the phenotypic trait $x$ of individual $i$. $N$ is the population size (there are $N$ individuals in the population) and $\bar x$ is the average phenotypic trait $x$ in the population.
$$\bar x = \frac{1}{N}\sum_i x_i$$
What is causing phenotypic variance
Why would a population display any phenotypic variance? Why wouldn't we just look exactly the same? What explains these differences?
For some traits, we see very little variance. To consider the example the OP gave in the post, the number of arms in the human population shows very little variance. However, there is quite a bit of variance in terms of the number of IQ, in terms of height or of weight.
There are two (main) sources of variance that are underlying this phenotypic variance. The first one is the genetic variance and the second one is the environmental variance. We will call the genetic variance $V_G$ and the environment variance $V_E$.
If in a population, people vary a lot in terms of how many hamburgers they eat, then there is a non-negligible $V_E$ underlying the phenotypic variance $V_P$ for weight. If in a population, there is a lot of variation of genes affecting weight, then there is a non-negligible $V_G$ underlying the phenotypic variance $V_P$ for weight.
By the way, a gene (or another non-coding sequence) that is polymorphic (i.e. has more than 1 allele in the population) and which explains some of the variance in the phenotypic quantitative trait is called a Quantitative Trait Locus (QTL). A locus is a sequence (of any length) on the genome.
Math reminder
Variances of uncorrelated variables can simply be added! For simplicity, we will assume for the moment that we are considering uncorrelated variables. As a consequence, we can express the phenotypic variance $V_P$ as a sum of the phenotypic variance that is due to environmental variance $V_E$ and the phenotypic variance that is due to genetic variance $V_G$
$$V_P=V_E+V_G$$
This equation is slightly simplified and this will affect the below calculations. See the section Other sources of phenotypic variance for more info.
We can now talk about heritability!
Heritability in the broad sense
Heritability in the broad sense $h_B$ is defined as the fraction of phenotypic variance $V_P$ that is explained by genetic variance $V_G$. In the equation, it gives:
$$h_B=\frac{V_G}{V_P} = \frac{V_G}{V_E+V_G}$$
Heritability in the narrow sense
Heritability in the narrow sense $h_N$ makes one further trick. We have to consider that the genetic variance $V_G$ that is underlying the phenotypic variance can itself be decomposed into a sum of variances. The variances that we like to consider the additive genetic variance $V_{G,A}$ and the dominance genetic variance $V_{G,D}$.
The additive genetic variance is the genetic variance that is due to additive interaction between alleles. The dominance of genetic variance is due to non-additive interactions between allele.
We can now define the heritability in the narrow sense $h_N$ as the is defined as the fraction of phenotypic variance $V_P$ that is explained by the additive genetic variance $V_{G,A}$. In the equation, it gives:
$$h_N=\frac{V_{G,A}}{V_P} = \frac{V_{G,A}}{V_E+V_G} = \frac{V_{G,A}}{V_E+V_{G,A}+V_{G,D}}$$
In the special case, when all the genetic variance $V_G$ is exclusively done through additive interactions, then $V_{G,D} = 0$ and $V_{G,A}=V_G$ and therefore $h_N=h_B$
Interpretation of the heritability
If all of the phenotypic variance is due to genetic causes (and regardless of whether there is a lot or a little variance), then $h_B=1$. If all of the phenotypic variance is due to environmental variance, then $h_B=0$.
So what does a $h_B=0.3$ means?
It means that 30% of the phenotypic variance is explained by genetic variance and that 70% of the phenotypic variance is due to environmental variance.
So, what if there is no phenotypic variance in the population? if $V_P=0$, then the heritability is undefined (as dividing by zero is undefined). However, in general, we tend to think that there is always a tiny bit of environmental variance and most people would just go on saying that heritability is 0 when $V_P=0$.
What will affect the heritability?
A measure of heritability is true for one population, in one environment.
If you change the population, add a few mutations for example, you might well create a polymorphic locus that is causing some phenotypic variance. If you put the same population in another environment, you could suddenly have more or less phenotypic variation due to environmental variance. Typically, if you measure heritability in the lab in a controlled and constant environment, then you will likely overestimate the heritability (as you underestimate $V_e$) compared to the same population that is living in a very heterogeneous environment.
What heritability is not!
If a trait has low heritability, it does NOT mean that it is (or is not) an adaptation. It only means that there is no genetic variance that explains the phenotypic variance.
Why do we care about heritability?
If there is no genetic variance for a trait, it means that the only way this trait can change through time is by changing the environment (or by creating a non-zero genetic variance through mutations). If there is a non-zero genetic variance and if there is a difference in fitness between individuals having different trait value then, the trait is under natural selection.
The most commonly used index of heritability in the heritability in the narrow sense $h_N. $Why do we care about $h_N$?
Let $\bar x_t$ be the mean phenotypic value of the trait $x$ at time $t$. One generation later, that is at time $t+1$, the mean phenotypic value is $\bar x_{t+1}$. Let's define the response of selection $R$ as the expected difference between these two quantities, that $R=E[\bar x_{t+1} - \bar x_t]$. Let's define the strength of selection $S$ and the heritability in the narrow sense $h_N$, then
$$R=h_N \cdot S$$
As a consequence knowing $h_N$ allows us to predict the effect of selection on a given trait.
This equation is called the breeder's equation (see this post about its interpretation).
Other sources of phenotypic variance
Saying $V_P=V_G+V_E$ is a little too simplistic. In reality, there are other sources of phenotypic variation such as variance due to epigenetic changes $V_I$ and variance due to developmental noise $V_{DN}$ for example. It is also sometimes very important to consider the covariance between any pair of such variance. So, the equation would more correct if stated as
$$V_P = V_G + V_E + V_I + V_{DN} + COV(V_G, V_E) + COV(V_G, V_I) + COV(V_G, V_{DN}) + COV(V_E, V_I) + COV(V_E, V_{DN}) + COV(V_I, V_{DN})$$
Note that everyone is free to further decompose any of the above variance into a sum of variances as we did above for the genetic variance. For example, the environmental variance $V_E$ could be decomposed into the sum of the phenotypic variance due to variance in temperature $V_T$ and the phenotypic variance due to variance in precipitation $V_{\text{precipitation}}$ assuming the other types of environmental variances are negligible.

It is an wonderfully thorough answer! Is it fair to say that if $h_B=0$ there is definitely no point looking for a gene that causes the variation in the trait, because the variation has nothing to do with genetics?

@user1205901 Yes a comment has been deleted. We can now delete all the extra comments. Thanks

@user1205901 Exactly. As you said if $h_B=0$, then none of the phenotypic variance is due to genetic variance. In other words, there exists no gene which is currently polymorphic and which polymorphism affect phenotypic variance in the population in this environment. I added two small paragraphs to try to troubleshoot potential misconceptions about heritability.

So, if $h_B=0$ then there is no point looking for polymorphic genes that affect the trait. Turkheimer says that heritability coefficients are "not...a useful indicator of how successful gene-finding efforts are likely to be". However, isn't it the case that the heritability statistic is somewhat useful in telling us whether to devote efforts to gene-finding? If $h_B=0$ we are definitely wasting our time on gene-finding efforts, if $h_B=0.00001$ we are most likely wasting our time, whereas if $h_B=0.9999$ gene-finding efforts are more likely to be successful?

If $h_B=0$, then you are definitely wasting your time in trying to find genes which variance in the population affect the phenotypic variance in the population because there are none. But if $h_B≠0$, then there are such genes (or other non-coding sequence). All else being equal (typically the number of genes that affect the trait (which are called QTL btw)), the higher the heritability the smaller the sample size you will need to find the QTL.

Note again that when $h_B=0$, you might still be interesting in the genes that are involved into the building of the trait even if these genes are not polymorphic.

@remi.b sorry I removed my comment, I think it generated confusion, I have added another answer, and use the aforementioned Y chromosome work at the end to illustrate

ps @Remi.b I'm curious - why do you use the notation $h_B$, $h_N$, $V_{G,A}$, $V_{G,D}$... ? It's very unusual for me (I'm used to using $H^2$, $h^2$, $V_A$, $V_D$... respectively) - (that's not to say I think you are wrong to use them of course, it's just variants I've not seen [much] before)

I never saw $V_{G,A}$ and $V_{G,D}$ either but I just thought it would highlight the fact they are components of $V_G$. However, I am used to $h_B$ and $h_N$ at least in discussions and conferences. I am not used to $H^2$ and $h^2$.

I'm not a Biology person, but variances are not additive. From what I read on Wiki, these variances are or can be additive. In general, variances are not additive.

@BCLC Given 3 variables A,B, and C. If C = A + B, then var(A) + var(B) = var(C) if A and B are independent. Am I right? I said that the equation was a simplification (in the sense that it assumes independence). I now added some more info to avoid the confusion.

@Remi.b If independent. Too strong though you can just say uncorrelated. I think I read on wiki that uncorrelated is good enough here

Briefly, because remi.b gives a lot of good detail about this in his answer, (narrow sense) heritability is essentially a measure of how much of the phenotypic variance is explained by (additive) genetic variance. Phenotype (P) in an individual is the result of genetic (G) and environmental effects (E).
$P = G + E$
Thus the within-population variance in phenotype is
$V_P = V_G + V_E$
Genetic variance further decomposes in to additive (A), dominance (D), and interaction/epistatic variance (I).
$V_G = V_A + V_D + V_I$
Narrow sense heritability ($h^2$) is then
$h^2 = \frac{V_A}{V_P}$
Additive genetic variance and, as a result, the narrow sense heritability can be zero for two reasons.
Firstly, if no genes have an effect on your trait, then additive genetic variance will be zero.
Secondly, if the alleles at the loci affecting the trait are fixed within the population, additive genetic variance will be zero.
Therefore, Eric Turkheimer is correct to say that heritability is not a measure of how genetic something is. However, a heritability of zero does not mean that something is not genetically controlled, just that there is no variance in the effects of genes.
To follow from the example of having two arms, clearly having arms is genetically controlled, its a heritable trait, but the number of arms has very little/no genetic variance. Very few people have >2 or <2 arms, thus any allele for that seems to be exceptionally rare (the alleles determining that two arms are produced are more or less fixed, $p \approx 1$, where p is the frequency of the allele coding for two arms).
The following graph shows the effect of allele frequency on additive genetic variance, additive genetic variance is zero when the locus has a fixed allele, and maximised when the frequency of both alleles (a two allele model) 0.5. In practical terms, when p = 0.5, half of the population are heterozygotes, one quarter are homozygotes for allele 1, and one quarter are homozygotes for allele 2.

For example, in this study, we showed that genetic variance on the Y chromosome explained only ~0.4% of the variation in lifespan, which could be because very few of the genes affecting lifespan are on the Y (likely, because the Y contains very few genes, while lifespan is highly polygenic) and/or the genes on the Y affecting lifespan have low polymorphism (likely, because the Y is subject to various processes that greatly reduce within population molecular variation, compared to other chromosomes).
Heritability and additive genetic variance are important to understand because they determine the rate at which adaptation (evolution as a response to selection) can occur. Following Fisher's fundamental theorem, and as shown in the breeders equation ($r = h^2s$ where r is the response and s is selection), when $V_A = 0$ the $r = 0$.

Heritability is not a measure of how genetic a trait is. It's a measure of how much of the variation in the trait is due to variation in genetics.
I'll try to make this clear with a story, to supplement the answers that rely more heavily on mathematics.

For reference: technically it's the fraction of phenotypic variance
  which is due to variance in genetic effects: $H^2=\frac{V_G}{V_P}$ (if
  you're talking about heritability in the broad sense); or, it's the
  fraction of phenotypic variance which is due to variance in
  breeding values: $h^2 = \frac{V_A}{V_P}$ (if you're talking about heritability in the narrow sense). $V_A$ is also often called
  additive genetic variance.

Suppose we have two islands, side by side. On both of the islands, some people are taller than others.
It so happens that we know (God told us) that there is a particular gene which can make a difference to your height: all else being equal, As are a foot taller than as. It also so happens that we know (God told us) that coffee stunts your growth; all else being equal, people who drink tea are a foot taller than people who drink coffee.
(We also happen to know that, at this moment, there aren't any other factors contributing to variation in height. Convenient!)
Now to our islands.
On the Blue island, we see that some people are taller than others. We do some testing, and we find out that on this island some people are A and others are a. In contrast, we also find that everybody on this island drinks tea and nobody drinks coffee.
There is variation in height: all of it is due to variation in genes, and none of it is due to variation in choice of beverage. Heritability = 1.
But that doesn't mean that the environment isn't relevant to height in this case. On the contrary, we happen to know (God told us) that if they'd all drunk coffee instead, they'd all be a foot shorter.
On the Red island, we see that some people are taller than others. We do some testing and find out that all of them are a's; none of them are As. In contrast, some of them drink coffee and some of them drink tea.
There is variation in height: none of it is due to variation in genes, and all of it is due to variation in choice of beverage. Heritability = 0.
But that doesn't mean that genetics is irrelevant to height in this case. On the contrary, we know (God told us) that if they'd all been As instead, then they'd all be a foot taller.

The most convincing way to remind yourself why heritability isn't about "how genetic a trait is", I find, is to remember that if everyone has the gene, then the gene doesn't vary, and won't contribute to variation; but that doesn't mean the gene isn't relevant!
For example, as far as I know, there is no genetic variation for "having a heart". Everyone is born with a heart. People without hearts are missing hearts because of environmental factors such as this:

So having a heart has a low heritability, but that doesn't mean genes aren't involved in building hearts!
Likewise, a high heritability doesn't mean that environmental effects aren't important to the trait; it just means that differences in the environment aren't currently contributing to differences in the trait.
It also doesn't mean that future environmental factors might not become important. For example, the heritability of eyesight was presumably somewhat high. But that didn't stop whoever did it from inventing glasses!
So that's another lesson. Heritability is not a constant. Natural selection actually tends to push heritabilities down (since it gets rid of the worse genes); and if the environment changes, then the heritability can go up down or all over the place.

Very good reviews of the overall concept have been posted, but I would like to focus in on the soft question of in what ways heritability does not reflect "how genetic" something is.  Of course, that's not really a technically defined statement and in some ways it does, but let's stick to the question:

Environmental contributions vary.  Consider pulmonary fibrosis.  A certain low rate of familial pulmonary fibrosis will always be present due to genetics.  But in a town built around a coal mine, you expect to see a much higher level of idiopathic pulmonary fibrosis.  You could argue the semantics, but probably traits related to this condition are not "more genetic" in the towns without coal mines.
Genetic contributions depend on environment.  The correlation of cognitive deficits with phenylketonuria alleles is quite high under some conditions, but with appropriate diet and supplements these genes have much less influence - "reduced penetrance", you might say.  Is PKU "less genetic" depending on nutrition?  Perhaps eye-tracking software will lead to a new sort of gaming next year, and as "eyethletes" suffer misfortunes the heritability of some ophthalmic traits will plummet, but does that mean the genes are weaker?
Not all genetic contributions are known.  Before the HIV pandemic, delta32 CCR5 would not have been recognized to have an effect on immunosuppression (at least, not by that means).  So we may not truly understand the genetic component that potentially exists even after thorough study of the trait under present conditions.

"If all of the phenotypic variance is due to genetic causes (and regardless of whether there is a lot or a little variance), then hB=1hB=1. If all of the phenotypic variance if due to environment variance, then hB=0hB=0.
So what does a hB=0.3hB=0.3 means?
It means that 30% of the phenotypic variance is explained by genetic variance and that 70% of the phenotypic variance is due to environmental variance.
So, what if there is no phenotypic variance in the population? if VP=0VP=0, then the heritability is undefined (as dividing by zero is undefined). However, in general, we tend to think that there is always a tiny bit of environmental variance and most people would just go on saying that heritability is 0 when VP=0VP=0."
So, the environmental factors being listed in conjunction with the genetic factors is an attempt to explain heritable factors that do not result from modifications in the DNA sequence, or epigenetic factors. I think that this is why heritability coefficients used in the sense of only being the only useful variable to demonstrate heredity is a problem. The current statistical models that are used to try to delineate environmental variance do not take into account (such as the ones shown above) and although these are the best models we have right now, they do not incorporate variables that could potentially affect epigenetic factors such as DNA repair, cell cycles or DNA methylation.

authors: user1205901 - Слава Україні


text:
Why is marginal reconstruction "more correct" than joint reconstruction in some cases?
When reconstructing the ancestral states on a phylogenetic tree given the states at the tips, there are a number of methods for performing the reconstruction. This question is about marginal and joint maximum likelihood reconstruction.
To quote the wiki, marginal reconstrucion "is akin to a greedy algorithm that makes the locally optimal choice at each stage of the optimization problem", while joint reconstruction "find(s) the joint combination of ancestral character states throughout the tree which jointly maximizes the likelihood of the data"
Pupko et al. (2000) describe an algorithm for performing joint reconstruction.
I have a question about a paragraph in the discussion of this paper, where they discuss the differences in the results between the joint and marginal reconstructions.

Deciding which is ‘‘ more  correct ’’ depends  on  the  question
  asked.  For instance, if one wishes to count the number of threonine-
  to-methionine replacements over the entire tree, then the joint
  reconstruction should be used to obtain this number (2,  in  our
  case,  on  the  branch  connecting  node  24  to node 3 and the branch
  connecting node 32 to node 33). However,  if  one  wishes  to
  synthesize  the  hypothetical cytochrome b sequence  of  the  ancestor
  of  Cetartiodactyla,  then  one  should  use  the  marginal
  reconstruction approach. We emphasize that both methods compute op-
  timal reconstructions by using all of the available data.
  Discrepancies originate not from misuse of information, but from the
  difference in the nature of the probabilistic questions asked

I don't understand why you would use marginal reconstruction for estimating the ancestral state at one node, or how the question you ask affects which method you should use. There is only one true ancestral state, I would think that the correct method for any question is the one that most accurately estimates the true ancestral state. Can someone shed some light on why the marginal reconstruction method is preferable in this situation?

I know this is too late, but since this is something I'm struggling with too I thought I'd post here in case others also find there way here. I don't have an answer but, here are some quotes that might help (I found them at least partially helpful).
Yang (2004): "Marginal reconstruction is more suitable when one wants the sequence at a particular node, as in the molecular restoration studies. Joint reconstruction is more suitable when one counts changes at each site."
http://aracnologia.macn.gov.ar/st/biblio/Yang%202006%20Computational%20Molecular%20Evolution.pdf
Revell (2014):
"Joint reconstruction is finding the set of character states at all
nodes that (jointly) maximizes the likelihood."
"Marginal reconstruction is finding the state at the current
node that maximizes the likelihood integrating over all other
states at all nodes, in proportion to their probability"
http://www.phytools.org/eqg/Lecture_5.1/Revell.ancestral-state-reconstruction.pdf
Joint reconstruction is "not (necessarily) equivalent to picking the state at each node with the highest probability" (Revell 2014), but is the method of picking the tree with the overall highest MLE.

This is just a comment to warn people about the options in the R-package ape for the function ace. Contrary to expectation, "marginal = F" for discrete traits DOES marginal reconstruction (and vice versa). So, keep that in mind.
More here:
http://blog.phytools.org/2015/05/about-how-acemarginaltrue-does-not.html


text:
What distinguishes Mendelian Inheritance from Non-Mendelian Inheritance?
I'm having some trouble determining what exactly is the difference between Mendelian inheritance and non-Mendelian inheritance. For instance, I understand that chromosomal abnormalities such as Down's Syndrome fall under non-Mendelian inheritance because they concern chromosomes, not single genes. And I also understand that Mendelian inheritance concerns single genes, as in Sickle-cell anemia (which is an autosomal recessive disorder).
What confuses me is the fact that our textbook discusses dihybrid and trihybrid (concerning 2 genes and 3 genes, respectively) crosses under the Mendelian inheritance chapter, when to me it seems like these crosses are non-Mendelian because they deal with multiple genes. However, Gregor Mendel did in fact use the dihybrid cross to deduce the law of independent assortment, so I'm completely confused. Could someone please clarify this for me? I'm afraid that I'm maybe misinterpreting something.

You can discuss multiple genes within the framework of Mendelian inheritance; what you're probably thinking of, though, is the fact that Mendelian inheritance doesn't recognize the idea of multiple genes that contribute to a single trait.
For example, if there is a gene that controls petal color (blue vs. white, with blue = dominant) and a gene that controls height (short vs. tall, with tall = dominant), then Mendelian inheritance predicts that two short plants with white flowers will only produce short plants with white flowers.
But if there are multiple genes that interact to determine height in a complex way, that's outside the scope of Mendelian inheritance.

Let me know if I understand this correctly: so dihybrid crosses in which the genes contribute to different traits are still within the scope of Mendelian inheritance, correct? And so things like epistasis fall outside of the scope?

@AleksandrH: Correct.

Okay, and so what about things like Incomplete Dominance and Codominance--are those still a part of Mendelian Inheritance or are they within the separate branch of non-Mendelian inheritance? That was also one of the things that was confusing me

@AleksandrH: Those are non-Mendelian. ("Mendelian inheritance" specifically describes traits that are controlled by a single autosomal gene with exactly two alleles, one of which is dominant and one of which is recessive.)

Thanks again for responding. So if I understand this correctly, then non-Mendelian genetics is everything else, like polygenic inheritance, epistasis, incomplete and co-dominance, poly allelic traits, sex-linked traits, mitochondrial inheritance, linked genes, etc?

@AleksandrH: Yes, exactly. :-)


text:
What are some useful (starter) metrics to use on phylogenetic trees?
I'm doing a computational biology project in which I simulate evolution under different inheritance rulesets and I am generating phylogenetic trees (beautifully visualised in Python with ete3).
My question is: where can I find and test out some simple metrics that can describe these trees in terms of 'branchy-ness' (you can tell I'm not a bioinformatician or phylogeneticist!). I'm looking for kind of mean-field descriptors of the trees. Kind of like degree distribution for networks.
My specific goal is, like in network science, trying to see if I can differentiate between different rulesets that created the tree by examining the [statistical] properties of the tree itself.

Is there any specific goal you want to achieve by comparing these metrics between different trees? You could count the number of branches, time to the common ancestor of all represented lineages, the total quantity of "evolutionary time" as the total length of all branches, the mean speciation time, ...

The specific goal is, like in network science, trying to see if I can differentiate between different rulesets that created the tree by examining the [statistical] properties of the tree itself.

Here are a few metrics you can calculate to get you started. You can use R to perform these calculations.
Net Diversification Rate (r)
Net diversification rate is (rate of speciation - rate of extinction). You can calculate it using the bd.ms or bd.km functions in the geiger package for R.
r = 1:

r = 2:

Tree Imbalance: Colless index (I)
Colless's index measures how imbalanced the tree is. It sums the differences in the number of clades in each pair of taxa. You can calculate it using the colless function in the apTreeshape package for R.
I = 0

I = 21

Branching Times (gamma)
The gamma statistic measures how much later or earlier branching times happen than what you would expect from a normal birth-death process. A negative value means branching times occur earlier, positive means branching times occur later. You can measure gamma (and generate a lineage through time (ltt) plot, as shown below) using the ltt function in the R package phytools
(From this Nature article)

These are just a few of many parameters you could calculate for a phylogenetic tree. It should be enough to get you started.

awesome!  thanks a bunch. i'm using python, so hoping I can find similar packages to measure these things there (maybe in ete3 ? )

Call R from Python: http://rpy.sourceforge.net/rpy2/doc-dev/html/introduction.html

cheers for that. i'll check it out.


text:
Why do we sleep?
While we do know that the human body is regulated by a circadian clock that keeps humans on a sleep/wake cycle, we don’t really know why. Sleep is the time when our bodies repair tissues and perform other maintenance activities, and we spend nearly a third of our lives snoozing. Some other organisms don’t need to sleep at all, so why do we?

It seems that the notion that some animals don't sleep is the core of your question. Could you share which animals don't sleep? The definition of sleep may in fact be crucial to answer your question. An explicit definition in the question is recommended to prevent unnecessary discussions.

https://askabiologist.asu.edu/plosable/who-needs-sleep-anyway  I am not sure if this is correct or not

Possible duplicate of Why did the process of sleep evolve in many animals? What is its evolutionary advantage?

We don't actually know. But these two theories are strong candidates:

Sleep 'cleans' the brain of toxins. Metabolic waste products of neural activity are cleared out of the sleeping brain at a faster rate than during the awake state. This finding suggests a mechanistic explanation for how sleep serves a restorative function, in addition to its well-described effects on memory consolidation.
Source: Xie et al. 2013. "Sleep Drives Metabolite Clearance from the Adult Brain", Science.

Sleep helps the organism alternate between day and night. Circadian rhythms enable an organism to anticipate, rather than passively adjust to, the changes imposed by alternation between day and night. These changes relate to positive functions such as vision and negative effects such as ultraviolet light damage. They also include indirectly generated alternations such as temperature, availability of food and prevalence of predators.
Source: von Schantz & Archer. 2003. "Clocks, genes and sleep", J R Soc Med.

In regards to animals that don't sleep, the affirmation is half valid. Arthropods don't sleep, but enter a metabolic slowdown state. Dolphins put half their brains to sleep while the other half stays active. Basically, anything with a brain needs to sleep, in some way or the other.
Homeostatic regulation is an interesting clue, because it suggests that there are some conserved functions of sleep. The need to make up lost sleep must be there for a reason.
If sleeping didn't have a necessary function, it wouldn't be universal. And it most definitely has to do with the brain, because it is the organ affected the most by lack of it.

There is no actual evidence for a need to "make up" sleep. you need sleep but there is no evidence you need extra sleep after missing sleep.

There are several theories for the function of sleep (with a focus on the brain) with varying amounts of evidence (mostly through sleep deprivation's interference of these processes)...

Energy savings.
A time to open up spaces between brain cells
to flush out metabolites and toxins including beta amyloid.
Memory consolidation - move labile new memories into longer term
storage.
Create more brain space - reduce "synaptic load" gained
during the previous day's experience, so you are better able to make
new memories the next day.
Creativity - make abstract links and
problem solving.
Emotional/mood recalibration.

Why it's thought these occur in the sleep state is that it provides the right neurochemical milieu to perform these necessary tasks, which would be inefficient or even dangerous if it occurred during your conscious experience.


text:
Are there worms/snake traveling by rolling? (see youtube video)
Someone obtained this from a nature simulator :  https://youtu.be/l-qOBi2tAnI
Is there any animals travelling like this?

There is a spider that rolls but I am not sure if that counts.

yes I have already seen those sand spider, but it's far less impressive...


text:
What makes animal to continually reproduce?
I was reading about Trypophobia and reached to Surinam Toad's reproduction methods. Then I had this doubt-
Why would animals want to reproduce so much?
In case of humans we mostly have the offsprings nearby for entire life, so some of them may take care of us. But in case of many other animals after birth they have no connection with their parents.
So why do they always try to reproduce in large quantities in entire life time?
What they achieve in this?

Life begets life. If organisms didn't reproduce, their species would die out. Simple as that.

I think the introduction on trypophobia is not necessary.

I don't get why people are voting to close this Q as "opinion-based". This is clearly answerable from the perspective of evolution of life histories.

@fileunderwater I agree that this question is not opinion-based, but it is rather unclear, and in any case it is rather broad. Organisms would be selected for optimal levels of reproduction, those that reproduce too little or too much would be selected against.

Why organisms reproduce
If they didn't reproduce, they would die out.
More concretely, suppose an animal is born with a mutation that removes the desire to reproduce.  That animal will not have any offspring, so its genes will not be passed on to the next generation.  When that animal dies, that mutation will die with it.
Why some organisms reproduce a lot
Different animals or other organisms have differing strategies for reproduction, based on their ecology.  Some animals, like the Surinam toad, try to have a lot of offspring with relatively little "investment" (of energy, time, effort, etc.) in each one.  Many of the offspring will die, but enough will survive that the organism's genes can persist.  Other animals, like elephants, only have a few offspring but spend a lot of effort in making sure those few offspring survive.
You can read more about this in the Wikipedia article on life history theory.