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Are there any methods to quantify H2O2 (hydrogen peroxide) which don't rely on horseradish peroxidase?
I can't use HRP since my substrates interfere with it and I need a real-time method because I want to measure kinetic parameters of some oxidases.

Titrate it with Potassium permanganate? http://phs.prs.k12.nj.us/rcorell/LabREDOXAnalH2O2.pdf

I'm sorry, I forgot to mention that I need a real-time method because I need to measure kinetics parameters for oxidases.

Amperometric detection of H2O2 can be performed without HRP, and gives high-resolution real-time readings.
You will find many different type of electrodes that are used in the literature to detect H2O2, including for instance MnO2-coated carbon paste microelectrodes or gold electrodes derivatized with cytochrome c.
Commercial electrodes also exists. For instance these from WPI are based on derivatized carbon fibers (although they do not specify with what, so I would not exclude HRP...)
Another option is that of using the H2O2-sensitive dye H2DCF (dihydro-dichlorofluorescein).

Thanks to your suggestion (H2DCF) I looked more into it and I found several other options: dihydrocalcein AM, dihydrorhodamines, dihydroethidium and Europium-tetracycline. All of them seems to not require another enzyme. Any experience with one of these?

No sorry, I actually found that while looking for amperometric detection and I thought I would add it as another option. The thing that I would start and check is their specificity, I am under the impression that they are ROS detectors rather than H2O2 detectors, but I may be wrong.

For a purely chemical assay, Manganese dioxide (MnO2) will react to produce oxygen from hydrogen peroxide, which can be detected spectroscopically or by means of direct chemical analysis.
I think the enzymatic assay is less environmentally challenging and produces colorometric results directly, which is probably why it is ubiquitous.

To measure the kinetic parameters of oxidases you could also look into measuring the oxygen concentration directly. Oxygen sensors are much more common than H2O2 sensors, and I know small setups (1 ml samples) based on a fluorescent dye based probe are available.

can you please tell me more about this fluorescent dye probe for measuring oxygen?


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Standard letter for 5-methylcytosine
I'm working on a piece of software that computes melting temperatures for nucleic acid duplexes, and I'm about to add support for 5-methylcytosine as a nucleotide base.  At the moment, the bases accepted by the program are adenine, cytosine, guanine, thymine and uracil, with their standard letters A,C,G,T,U.  Is there a standard letter for 5-methylcytosine?  The only example I've found is this paper, which uses an italic C for 5mc, but I want a distinct letter.  The three candidates I've thought of are:

5 - for '5-methylcytosine'
M - for 'methyl'
B - Since methylation of U gives you T, which is one place earlier in the alphabet, so methylation of C gives B.

Well, don't use M or B, those are already taken (C or A, and not A, respectively).  You can see the full list here: http://www.dna.affrc.go.jp/misc/MPsrch/InfoIUPAC.html (The enWiki article on Nucleobases lists a few others but I would ignore those as 1. D is present in both and 2. they are rare and inapplicable)
5-methylcytosine isn't on there.  If you want to be pedantic about it, 5-methylcytosine is an epigenetic marker and as such is by definition not a genetic sequence; that remains simply a C and, genetically, the sequence is the same, despite the fact that it may indeed make a difference.
Most of the time people use m5C, so I'd go with 5 if I were you.  That certainly isn't used for anything else and if you must use a single character most anybody will know what you are talking about.

As Amory suggests the IUPAC "Recommendations on Organic & Biochemical Nomenclature, Symbols & Terminology etc." (http://www.chem.qmul.ac.uk/iupac/) are probably the best place to start. From a quick scan the obviously relevant documents would be:

"Abbreviations and Symbols for Nucleic Acids, Polynucleotides and their Constituents"
"Nomenclature for Incompletely Specified Bases in Nucleic Acid Sequences"

These provide the complete description of the commonly used IUPAC nucleic acid codes, including both the one letter and three letter variants.

Just to fully document the IUPAC advice on this, here is the relevant section from the Nomenclature for  Incompletely Specified Bases in Nucleic Acid Sequences as reproduced here in the link provided by @Hamish McWilliam.

5.2. Modified nucleotides
In a number of organisms DNA and RNA are modified at certain positions. For instance, the DNA of Escherichia coli is usually methylated on N-6 of the adenine residue in the sequence 5'-GATC-3' [23]. The present nomenclature does not allocate any specific symbol to these modified nucleotides for the following reasons. (1) The presence or absence of a given modification depends upon the location of the DNA. Sequences modified in one organism may not be modified in another. (2) Modification is usually statistical, in that only a proportion of possible sites for modification may actually be utilised in vivo. Modification of a nucleotide or base in a given polynucleotide is not a function of the sequence per se. Although it is recognised that stable RNA species (tRNA and rRNA) often carry a constant pattern of post-translational modification. the present nomenclature is not intended to overlap with or supplant existing systems. It would probably be impossible to devise a simple and logical system that avoided all conflict with previous usage. One should therefore recognise that such conflict is possible and take steps to prevent it from generating confusion, for example in relation to the symbols B, D and S, which have been recommended for 5-bromouridine, 5,6-dihydrouridine and thiouridine respectively [1], or W, which is sometimes used for wyosine.

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Which mass spectrometry database search algorithms include the fragment mass accuracy in the calculation of protein scores?
E.g. in a MASCOT search, the accuracy of the fragment ions in a ms/ms spectrum does not have any influence on the scores of identified proteins (unless the fragment ions are out of the set ms/ms tolerance of course).
I want to know other search algorithms that do include the fragment mass accuracy in the protein identification scores.
Also, if the protein scores are not influenced, i would like to know in which way other evaluation values of MASCOT or SEQUEST results are influenced.
Thanks for your time.

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To what extent is eating and nutrition important in recovery from minor illness like viral fever?
I'm guessing it is important,  but just to be a little more precise,

What would be the maximum amount of calories above which it is just a waste (or even harmful)
How much does the metabolism raise during the illness?
More carbs or more proteins? (or less?)

During infection a body has to produce absolute masses of immune cells, raise your temperature via increased metabolism, repair tissue damage, migrate components of the immune system including proteins and cells, produce masses of antibodies and probably lot's more.
A lot of protein components need to be made which require protein synthesis and energy. Metabolism of fats and carbs goes up too. Also, importantly, vitamins are a key part of the immune system serving to migrate the immune system  such as vitamin D aids migration of cells to the skin. Vitamin C is required for collagen synthesis in repair. Minerals are required for the metalloenzymes. However your dependency on each component depends on the type of infection, your immune response, your natural state including your reserves of everything.
How important is it? Very. I've listed what the things are needed for which gives an indication of how important they are. If starved, the body will do the best it can by focussing its resources on the thing it deems most important.


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How do cells figure out the big-picture shape?
I'm wondering what makes cells to divide (and stop) in such a way that they make our hands the shape that our hands are...

with hands, there is cell division initially to give rise to a palm bud (fingers not separate). Subsequently, the cells between the fingers (digits) die by apoptosis to give hand its shape.

That is exactly what is studied in developmental biology, which is a huge field of research.

Hands are complicated and the genetic machinery behind their shape doubly so.
It's easier to figure out worm segments first, and then work up from there. An egg has head/tail information encoded in it even before fertilization: see here
You can imagine the first or second cell division would give a 'head' cell with higher concentration of head polarity transcription factors. These transcription factors switch on other regulatory genes, and the complexity works upwards from there. For more information about how worms and other segmented animals work out what goes where see Hox genes. The sad truth is that most of how this is done is unknown or not well understood.


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Systematic difference of diversity between sister taxa?
When looking broadly at the tree of life, my feeling is that, after a divergence there is almost systematically one taxon that speciates way more than the other.
(There will have some approximations below it is not really the point of my question to discuss whether the urochordata is a sister group to the vertebrates or not.) Let's look at the kingdom Animalia for example:

Chaonflagellata vs "the others"
Sponges vs "the others"
Cnidaire and cténaire vs "the others"
Protostomia vs Deuterostomia (both are fairly equally diverse diverse! Some might not be happy with this claim!)...let's continue with the Deuterostomata
echinodermata vs chordata
cephalocordata vs vertebrata

etc ...
My questions:

Is there really a systematic difference in diversity between the branches?
Is this difference can be explained by chance?
Is it only a bias due to out ability to recognize more species in animals that look more like us (or a bias due to something else)?
Does it make sense to say: the more diverse is a taxon, the more likely it is that it gets even more diverse (because each species might have an equal chance to speciate or something like this)?

Neat question. I'm tempted to assume that this must be related to where we recognize splits as being? I.e. its an artefact of our typology, rather than a property of the external world. It bears thinking about, though! You might use "key trait" or "key innovation" as a search term (I think I remember Galis gives a good introduction)

Bond and Oppell address your question points one, two and three empirically by looking for what they call "unbalanced bifurcations" as a sign of adaptive radiations in a well-resolved phylogenetic tree (spiders), and find that the number of unbalanced bifurcations does indeed exceed what they would expect to occur by chance.
As you mention and as I suggested in the comment, there are some serious problems that arise in trying to answer your question. Many of these are well presented in Cracraft, including assuming that higher taxa are comparable with one another, making arbitrary choices about what rank of taxa to compare, ignoring counterexamples, and qualifying rather than quantifying diversity. I think that Bond and Oppell effectively address most of these problems through rigorous, apriori definitions.
There's a diversity of opinions and evidence from biological systems on your fourth question point. Bond and Oppell connect these significantly unbalanced bifurcations to key traits (like orb-weaving) that open up new adaptive zones. I suppose therefore they might say that there's a fundamental factor (a key trait, and therefore open adaptive zones) driving diversification, and therefore might not agree with you that diversification would necessarily beget more diversification (at least, not in the absence of open adaptive zones). For instance, in Hawaiian tetragnathid spiders, ecomorph niches on an island are filled either through immigration from another island or through adaptive diversification (Gillespie). No ecomorph is represented by two sympatric species, so a niche filled by immigration will presumably not spur adaptive radiation. However, species radiations in Andean lupines (Hughes and Eastwood) and plethodontid salamanders (Kozak et al) seem not to have been accompanied by any key traits or particular ecological opportunity, and could theoretically be driven by the self-reinforcing mechanism you propose. As a related point, I suppose more diverse lineages could be less likely to go extinct; which could support diverse lineages becoming more diverse.

 Bond JE, Opell BD. 1998. Testing adaptive radiation and key innovation hypotheses in spiders. Evolution 52: 403–415. (Behind paywall, free pdf here).
 Gillespie R. 2004. Community assembly through adaptive radiation in Hawaiian spiders. Science 303: 356–359. (Behind paywall, free pdf here)
Cracraft J. 1990. Origin of evolutionary novelties: pattern and process at different hierarchical levels. p. 21-44 in Evolutionary Innovations, ed. M. Nitecki, U Chicago Press.
Hughes C, Eastwood R. 2006. Island radiation on a continental scale: exceptional rates of plant diversification after uplift of the Andes.
 Kozak KH, Weisrock DW, Larson A. 2006. Rapid lineage accumulation in a non-adaptive radiation: phylogenetic analysis of diversification rates in eastern North American woodland salamanders (Plethodontidae: Plethodon). Proceedings of the Royal Society B: Biological Sciences 273: 539–546.

Thks a lot for this excellent answer!


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Why do parasites sometimes kill their hosts?
It's bothered me for a while now. I understand why a parasitoid would do this, as it only temporarily requires the host, and that not all parasites kill their hosts.
There seems to be no evolutionary advantage in killing a host, because the parasite relies on the host for resources. Yet some organisms, usually microscopic pathogens, seem to fatally damage the host with no immediate benefit to themselves. Why is this? Won't it be better to have a commensalism relationship with the host so both exist healthily?
I know this is asking for a broad soft answer, but I don't want the question to get bogged down by a specific species, although it would be good to have examples.

Great question. I wonder if metapopulation dynamics could have something to bring to this conversation. That is, it can be appropriate to exhaust your resources in one "patch" (eg., glade, island, host organism) if it's relatively easy for you or your offspring to move to another "patch"

I can think of several (non-exclusive and probably non-exhaustive) hypotheses:

Maladaptive. It is maladaptive. Maybe because it is a virus coming from another species (e.g. SIV and HIV) or because it is not adapted to our modern lifespan.
Benefit of the host immune system to the parasite. Some parasites might benefit from host immune defence (e.g. sneezing helps bacteria to spread) and death is a consequence of the selection for increasing disease symptoms to the host.
Pathogen's and host's fate. The pathogen's fate is not linked to the host's fate. This is especially true if the pathogens spread well (easily jump from one host to another) I guess or for parasitoïd because the pathogen leaves its parasitic life after the death of its single host.
intra- and inter-host selection. Among hosts, there might have a selection for reducing resource consumptions and therefore for decreasing the probability for the host to die. But within a host (among individuals of a parasite population or even among parasite species), it is a prisoner's dilemma (tragedy of the commons). The more you invest in foraging, the more competitive you are. This might not be adaptative at the population level but it is at the individual level. We might think of this prisoner's dilemma happening among individuals of a single parasite species or among several parasite species. You may want to have a look at the work of Martin Nowak on the subject incl. Consider for example his book; Evolutionary Dynamics.
Consequence of harming on trade-offs. Harming an individual will cause him not to spend energy into reproduction in order that more energy is available for the pathogen use. Moreover, by causing symptoms, the infected individual will be sexually less attractive and will again have less opportunity to spend energy into reproduction.
The pathogen does not mean much harm. When fighting pathogens, many of the symptoms we experience (such as fever typically) are actually caused by the immune system and not the pathogen itself. A maladaptive overreaction of the immune system can cause our death.

The book Why we get sick by Randolph Nesse and George Williams, will probably interest you.

#3 is a common answer, and linked to #2,4,5.  Lots of viruses for instance simply reproduce and spread to other hosts.  If a host dies it doesn't hurt the pathogen if it's timing is good.

I like #3, but what exactly do you mean by well spread? Are you talking about method of infecting new hosts, or general population?

@GoodGravy I meant "if pathogens have good dispersal abilities (good abilities to jump from one host to another), then it is likely that the survival of the parasite is not linked to the survival of the host". Does it make sense? I don't really understand your question above. But I said "spread well" not "well spread".  Maybe here comes the doubt.

I think you should make the 4th paragraph more clear.

@Mockingbird I'm not sure how to edit it to clarify this point. I made some modification but I am not sure it helps. If you have specific ideas, feel free to suggest them.

Some parasites aren't natural hosts of humans, instead we are an accidental host in which they cannot replicate. Zoonoses such as this can be quite fatal as the parasite is not adapted to us. Although viruses are often separated, they are parasites and you can see just in influenza that the animal derived flus are more fatal than those that are well adapted to humans.
Otherwise because there is no need for the host they can be fatal. If they have finished their round of replication or require death of the host to be able to spread. Still this is less common than simply a badly adapted parasite.
HPV causes cervical cancers. It is adapted to increase replication of its host cell which is obviously beneficial, but this also kills the host in the long term. Thus some viruses are not yet adapted to the new longer lives we live, but may never do so due to less of a survival pressure hence vaccines.
Please feel free to ask questions.

+1 - a number of the parasites that cause human disease aren't supposed to be in us. We're an odd side-note in their lifecycle.

This is related to Remi.b's answer, but a common reason is that sometimes parasites/pathogens actually need to kill the host to spread.  A lot of viruses, in particular phages, are only released from their host by bursting out of the cell.  If the parasite can't leave the host, there's no point in any of it, and death may be a good way to achieve that.  A number of diarrheal diseases in humans cause death because massive diarrhea (aka water loss) is how they spread.

A virus usually destroys its host cell to get released (this cell has been reprogrammed by the virus to produce only viral products anyway) but this does not necessarily mean the death of the host.

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Why isn't a virus "alive"?
The recent news about a new supermassive virus being discovered got me thinking about how we define viruses as non-living organisms whilst they are bigger than bacteria, and much more complex than we first gave them credit for.
What biological differences between viruses and cellular organisms have made viruses be deemed non-living?

You might be interested by this [http://biology.stackexchange.com/questions/1842/how-did-viruses-come-to-be] post as well. It concerns the origin of viruses.

If this is a topic that really interests you, I'd suggest searching for papers/reviews/opinions written by Didier Raoult.  Raoult is one of the original discoverers of the massive Mimivirus and his work will lead you to some truly fascinating discussions that I couldn't hope to reproduce here.
The main argument for why viruses aren't living is basically what has been said already.  Viruses are obligate parasites, and while plenty of parasites are indeed living what sets viruses apart is that they always rely on the host for the machinery with which to replicate.  A parasitic worm may need the host to survive, using the host as a source for energy, but the worm produces and synthesizes its own proteins using its own ribosomes and associated complexes.
That's basically what it boils down to.  No ribosomes?  Not living.   One advantage of this definition, for example, is that it is a positive selection (everyone "alive" has got ribosomes) which eliminates things like mitochondria that are sort of near the boundary of other definitions.  There are examples on either side of something that breaks every other rule but not this one.  Another common rule is metabolism and while that suffices for most cases some living parasites have lost metabolic activity, relying on their host for energy.
However (and this is the really interesting part) even the ribosome definition is a bit shaky, especially as viruses have been found encoding things like their own tRNAs.  Here are a few points to think about:

We have ribosome encoding organisms (REOs), so why can't we define viruses as capsid encoding organisms (CEOs)?
Comparing viruses to a living organism such as a human is absurd, given the massive differences in complexity.  A virus, really, is just a vehicle or genetic material, and would be more rightly compared to a sperm cell.  Is a sperm cell alive, or is it a package for genetic material that is capable of life once it has infected/fertilized another cell?
The really large DNA viruses often create cytoplasmic features called virus factories.  These look an awful lot like a nucleus.  What is a nucleus anyway?  Maybe it's just a very successful DNA virus that never left.
Viruses can get viruses.

I'll wind down here, but suffice to say that while our current definition may have sufficed for a while, and still does, it is no longer quite solid.  In particular, there is a theory alluded to above that eukaryotic life itself actually formed because of viruses.  I can expand on this if you like, but here are some great sources:
Boyer, M., Yutin, N., Pagnier, I., et al.  2009.  Giant Marseillevirus highlights the role of amoebae as a melting pot in emergence of chimeric microorganisms.  PNAS.  106(51):21848-21853 (http://dx.doi.org/10.1073/pnas.0911354106)
Claverie, JM.  Viruses take center stage in cellular evolution.  2006.  Genome Biology.  7:110. (http://dx.doi.org/10.1186/gb-2006-7-6-110)
Ogata, H., Ray, J., Toyoda, K., et al.  2011.  Two new subfamilies of DNA mismatch repair proteins (MutS) specifically abundant in the marine environment.  The ISME Journal.  5:1143-1151 (http://dx.doi.org/10.1038/ismej.2010.210)
Raoult, D. and Forterre, P.  2008.  Redefining viruses: lessons from Mimivirus.  Nature Reviews Microbiology. 6:315-319. (http://dx.doi.org/10.1038/nrmicro1858)
Scola, B., Desnues, C., Pagnier, I., et al.  The virophage as a unique parasite of the giant mimivirus.  2008.  Nature.  455:100-104 (http://dx.doi.org/10.1038/nature07218)

One correction: by the suggested definition, mitochondria are alive since they have ribosomes. (See, e.g., Properties of human mitochondrial ribosomes).

The rRNA in mitochondria is encoded there, but the ribosomal proteins are all nuclear.

I came to reread this and was fascinated all over again! Great answer.

It is only a question of definition. You can set the boundaries between living things and not living things anywhere.
Some philosophers have argued that using a clear boundary between living and non-living things is not such a good solution. In nature, there would rather be a continuum from a stone to a bacteria.
It is true that in thinking of viruses such as Lausannevirus or Marseillevirus we might be willing to integrate them in the category of living things. These viruses are giant, and even can be parasitized by other viruses.
Viruses are made of proteins and contain nucleic acids (RNA or DNA). If you consider that they are alive, what would you say about viroids? A viroid is just a nucleic acid that is able to infect a host and cause the replication of itself. What about a prion? A prion is a protein that, roughly speaking, has the same consequences as that of a viroid.
I think (one should check the literature, I might be mistaken) that there is a species of parasitoid wasp that produces out of its own genomes, viruses that reduce the host immune system in order to make the caterpillar a suitable habitat for the egg. Is this virus alive? Isn't it just a toxin of the wasp?
I guess one reason for considering viruses as non-living is that we do not know how to branch them in the tree of life! Some might argue by the way that viruses would not at all form a monophyletic group.
There are several people tackling the question of "what is alive". Unfortunately, the best book I know on the subject comes from the French literature; it is Comment définir la vie? by Bersini and Reisse. In this field, the most popular authors are Varella and Maturana. Again, if I'm not mistaken, the definitions of life are quite different among philosophers, people having an interest in the origin of life, and people seeking a definition suitable for extra-terrestrial life.

There is a nice discussions along these lines also at the very beginning of the very nice essay by Jacques Monod "Le hasard et la nécessité", where he speaks about distinguishing "natural" (living) objects from human artefacts.

only a question of "definition" ?  not seems so.  Its' a question whose answer we don't know... so we try to guess it in various ways. No guess could be considered as correct.

The indirect question is basically "what is 'life'?". In other words it is a question of the definition of 'life'. Now, sometimes there is a natural category that fits well our intuition and sometimes there is not. I would argue there is not for 'life' but this, I agree is a question open to debate (mainly in philosophy). However, it changes nothing to the fact that the question is about the definition of life. The term 'life' did not exist before humans and is here to be discovered. It is obviously a human choice to offer a sense to a term.

I agree with the answers already given, these are the reasons that viruses are not considered alive. I want to point out though that this isn't an area you find 100% agreement on; there is a decent subset of biologists who do consider viruses alive. I would say - completely on the basis of personal observation - that virologists themselves are the group most likely to claim that viruses are alive.
This paper and this article from the Scientific American have some coverage of the debate if you want to read more.

Do you know of any specific literature pushing towards the definition of a virus as a living being? I would be curious to read that.

@nico: I've updated my answer with a couple of links.

There are quite some different definitions of being "alive", but a common one includes the need to have responsiveness, growth, metabolism, energy transformation, and reproduction (found from the Encyclopedia Britannica). Viruses depend on host cells to do all this, so seen alone as a virus outside a host cell, they are not alive.
There's another short, but to the point blog entry about this.

A neat answer, but I'm not satisfied. There are lots of parasites (and symbiotes) that rely on the host for biological processes, so I'm not sure if this covers such a niche point of taxonomy. I also disagree with that blog post about "passive" chemical reactions. In that case we are all none living as all our cells just passively carry out reactions with one another.

But the parasites, symbionts and multicellular organisms do reproduce and act (not only re-act). As I said, there are different definitions of life. But most of them agree, that to be called alive an organism has to at least fit one of the criteria (some definitions also include more criteria to choose from, for example when I was at school, movement was in the books.). Viruses fit none, but parasites do, as far as I am aware. And as far as science is aware. "Life" is a critical point, it is hard to define both scientifically and philosophically.

@GoodGravy, most reactions in living organisms are active, in that they are specifically regulated by enzymes. Reactions related to virus replication are not, or they take advantage of the enzymes of the host cell.

@BrandonInvergo, that's not really true.  Many viruses encode proteins that regulate viral replication.  In fact that is a major part of the replication cycle for many viruses, determining the early/late or lytic/lysogenic activity during infection.  Many other viral proteins are enzymes that specifically cleave or modify both viral and host proteins.  Viruses often play a very active role in their own replication.

Interesting. I stand corrected!

Despite great answers from Amory and Remi.b, I want to emphasize this: there is continual debate about the definition of life because "life" is not something that exists in the real world.
People seek a definition of life that satisfies an intuitive notion of what alive should mean.  They feel that, say, intracellular parasites should be considered alive, but (say) only if they have an enclosing membrane, like Rickettsia, and not if they are just a virus, or just an RNA molecule like a viroid.
While people have a built-in intuition that, for example, reliably categorizes a tiger as alive and a rock as not alive, that intuition can't be precisely bounded by a definition such that everyone is satisfied by the boundary.  There are arrangements of matter in the physical world that fall outside the clear region of the intuitive concept of life, and this leads to continual, unresolvable, argument on what a precise definition of life should be, and what it should include.

Concept of life is difficult, but not "unreal" or "false".

@AlwaysConfused, my point is that the definitional controversy about "life" is only a controversy about how to define a word, and not a controversy about the characteristics of the actual arrangements of physical entities and how they interact.  There is no controversy that both viruses and Rickettsia are "replicators" (that is, things that replicate themselves in suitable environments), nor that viruses do not have a lipid membrane but Rickettsia do.  The "life" controversy is just one of definition: "Include viruses."  "No, don't."  "Yes, do!"  "No, don't!" ...

I didn't commented about defining virus as living or nonliving. I commented on your statement ""life" is not something that exists in the real world."   Life, and its main-characteristic, consciousness not at all so simple. If someone enters a sword in your body, it is true you shout due to chemical reactions in form of neurological computation, it is also true you shout of "pain". Science can fairly explain that computation, but not pain, yet. But that doesn't make that pain unreal or false. it is quite unclear like numbers, shapes, sets etc. but it is never unreal.

In strict logic, someone canNot prove (yet) a given-other organism whether contains life (and consciousness) or not. We can just "guess" from the similarities (which you've called "intuitive notion"). If you are telling a piece of brick has no life (and no consciousness), and a deer have life (and consciousness), you're making a "guess" by watching the  similarities like cell-membrane, cytoplasm, DNA, respiration etc.

@AlwaysConfused You might want to further your understanding of the question in play on Philosophy.SE as you seem to have issue in philosophy of logic and philosophy of knowledge.

In addition to the good answers given here, I would like to propose a more intuitive argument against viruses being alive.
Viruses are, at one point of their "life", simply a piece of DNA (or RNA). Would you consider a piece of DNA to be alive? If so, then are transposons alive? Are chromosomes alive? How about synthesizing a piece of DNA - is that creating life? The answer will probably be "no" for most people.

One could argue that that is true for any cell...

@nico sorry I didn't understand - how is a cell a piece of DNA/RNA?

at some point a cell was just a piece of DNA, before its mother cell split in two... Really the important point is that the virus is not able to replicate itself without the "help" of some other cell

@nico: I disagree: a cell is never simply a piece of DNA, it always has membranes, organelles, proteins, etc. The division of mother->daughter is not the creation of a novel cell de novo from DNA but rather a process of growth followed by division. Even DNA replication is semiconservative - both copies are one part original, one part newly synthesized so neither can really claim to be more original than the other.

@JackAidley: dsRNA viruses also have semiconservative replication so that doesn't really apply... I am just saying that your answer does not give an explication because you need to define what "life" is. You cannot just say "A virus is not alive because DNA is not alive", as that just begs the question "why is DNA not alive?".

@nico that is why I wrote "the answer will be no for most people", i.e. under most definitions of life. I do not know of any robust definition of life that considers a piece of DNA to be alive. Also I completely agree with Jack - a cell is never a piece of DNA, under any possible definition.

@nico: You said that a cell is a some point just DNA. This is false; it is never just DNA.

@JackAidley: and why would that be? It really depends on definitions, which are not given here. When the DNA replicates is the newly formed DNA already part of the new cell? Or it is part of the mother cell? Is the new cell "coming to life" only after division? You cannot just skip through those (and many other) points when defining whether a virus is alive. Otherwise you are just saying that a virus is not alive because it is not alive. Not very useful definition...

@nico a cell has a relatively clear definition and it must have its own membrane. A cell with double the DNA is not 2 cells, it is one cell with double the DNA. There is a point at which the cell divides and the membranes are separated - that is when it becomes a separate entity.

Perfect, then the point of the virus being a DNA at some point is just non existent. A virus without capside is not a virus. A virus starts existing as a separate entity the moment it assembles its DNA/RNA into a capside, before it is not a virus. And that does not give us any clue on whether it is alive or not.

@nico actually you are mistaken. It is not true that the virus exists only when it is assembled into a capsid. The correct name is virus at all stages (you can check the definition). When it is in a capsid it is called a virion.

@Bitwise: I know (I may have passed my virology class a while ago but I still remember this :P), but a virion is not a virus. It is a virion. And whatever the name you call it if you do not exactly define what life is you cannot state something is alive or not. Look at Amory's answer for a great deal of good refs

Good question; science yet don't know anything about "What is Life".
Yes. Everything about life we discuss (whatever by a Newton, Descartes or Schrodinger), it is in a level of Sci-fi, or hardly alchemy. Anyone of us don't know actually what is it.
The best characteristic of life is, "we, the living-creatures, can sense . We have consciousness" .
But alas, anyone can judge its own consciousness. We can-not judge someone else or any-other object contains any consciousness or not. We can just guess other's consciousness from facial expressions (say cry) , behavior, polygraphs, physiological reactions (respiration, growth, ageing etc... ), complication, informational-content, reproduction, genetic-code and such.
(https://www.youtube.com/watch?v=evQsOFQju08 , Is Your Red The Same as My Red? by Vsauce)
(however a living object can lose consciousness for a while such as when we're chloroformed).
In the same-way, we just guess presence of life in other objects from the complication, chemical structure (carbohydrate, proteins, lipid, DNA etc), metabolic reaction etc. and same evolutionary origin . same to us. In strict-logic we can't tell a lovely flying bird  contains life and is conscious that an alien-robot is nonliving, lacking consciousness. We can guess, not prove, yet.

In the same logic, all virus, viroids and prions (the organisms of "border zone") (including biggest viruses) could be (and often is) compared with living-organisms (like we're), due to their similar chemical structure, genetic codes, information content, reaction etc. with us, as-well plausibly same origin with us.

There exist too, causes to consider all virus, viroids and prions (including biggest ones).  I can call you alive. I can call your one organ (say hand) alive, could call a cell alive. But what we could call 1 protein-molecule? Just like a concrete-mixing machine (known to be nonliving), the protein-molecule is similarly made up of atoms... and nothing else. There is no evidence for "vital-forces" also... the protein molecule operates its works just with electromagnetic forces, thermal-collisions etc. There is no "sign" of life . In the same-way, a virus, viroid or a prion is just a lump of molecule. And for a big virus? a small hut (nonliving) : big house :: small virus : big virus. A big virus would be similar to a big bottle of nucleic acid.

Any more-discussion would be completely opinion-based, but in my-opinion it is better to consider these borderline-organisms as alive, due to more valid-logic such as

They're similar with us in chemical structure, genetic code bla bla bla ...
They are plausibly same in origin with us.
Inert structures, like plant-seeds if contain life, then in same logic we can imagine life in virions etc.
We found different level of parasitism in living organisms, such as  ATP-parasites (I forgot example and can't find right now), and consider them as alive. So why we'll not consider a "protoplasm-parasite" a living-organism?

Is there anything unclear or wrong?

Pretty much nobody limit the concept of life to the one of consciousness. While the term consciousness as no single definition everyone agrees on, using most people's definition of consciousness would exclude 99.9999% of the creatures that we generally consider being alive. The use of bla bla bla is in between inaccurate and childish ("etc..." would be equally inaccurate but at least sounds appropriate). You include two citations without indicating the source.

99.9999% of alive creatures not considered conscious? such as an amoeba or a tree ? That would be again a guess that could be true or false. However, all life forms respond to different stresses and stimuli quite like human-being, though in different manners. that could be guessed as an external sign of consciousness?

@Remi.b 'Nobody limit the concept of life to the one of consciousness'? In some places I've read Rene Descartes did that.

If I understand the answer, you're trying to say that living things should have sensation. If that is the case, then why do we consider viruses non-living, and bacteria living? Both have essentially the same limitations on sensation in that they interact biochemically with their environment and respond. I think you misunderstood my vague question. I was looking for a clear-cut answer as to why biologists don't generally include viruses among the various trees of life. I'm not convinced there is a philosophical answer.

@James "I think you misunderstood my vague question". I understood the question as "What could be the causes for considering viruses as nonliving (even after when bigger size and complex forms found)?".  "Both have essentially the same limitations on sensation".. again i remind i did not told about nerve-networks, i told about the entity 'sense' like 'red' or 'green' or 'sour' etc. We may describe every details of change in molecular orbital, but we don't know what are these "red" or "green" etc senses; and we can't tell from observation that an object in front of us have sense or not.

To answer about whether something do have life or not, we must have have   to know "what life is".  but yet we don't know it proper way except some observable signs like metabolism, self-sustenance. Understanding about life will remain incomplete until and unless we would be able to decipher the 'nature' of consciousness (I did not meant it could never be known or it could not be analyzed in scientific way). I just meant since we don't have yet that understanding; trial to 'confirming' an object's category as living or non-living; would be an illogical effort. That is all I tried to say.

Bacteria do have consciousness or not? Logically it is impossible to tell since anyone can observe only own's consciousness so we cannot tell does a bacteria feels anything. But maybe they feels something, we could 'guess' because of these similarities- they  respond to their environmental changes (Some even show motions (flagellary/jerky) on environmental stimuli);  probable-same origin with us; and ocurrence of complex metabolism.

I think you might be going too far down the existential line! See this video to get an overview of why "life" is a tricky thing to define from that point of view, and why viruses complicate that. It basically just generates more questions! If you enjoy the more practical side of the philosophical end of the topic of defining life, then you must read this 2002 essay by Koshland in Science.

@James  both links good articles, but bypasses consciousness.

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


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How far do 2 ant colonies of same heritage have to be in space (and generation) in order to fight?
(Kinda follow-up to this.…)
I've heard before that if you put 2 ant colonies side by side they're going to attack each other.
But then from the previous question, there could be "sister" ant colonies which (assumingly) don't harm one another.
I can probably see that generation-by-generation colonies would just naturally be either too far apart in space, (or too close in "generation"), to have any fights.
But what actually makes ants decide whether to fight or to not?
And whatever it is, is it a spectrum or a limit..? (i.e would there be a case in which some ants of a colony will fight and some wont?)

Space and generation don't directly affect whether ants fight, that's all regulated with pheromones. Some ant species are more tolerant of different smells than others (see the argentine supercolonies mentioned above) while some species of ant have 'rival' nests that they are particularly aggressive to.
So I guess the answer is 'it depends'. On pheromones produced by the queen, and species. And probably diet/weather/local food availability/ some other things I haven't thought of.
I don't think it's possible for some ants of a colony to fight and others not to, but I don't have any evidence to back that up specifically.


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DNA preparation for sequencing

In shotgun sequencing method or some related method that DNA is break up into random fragment. The fragment that have about 3kb in size is inserted into plasmid by enzyme ligase and then plasmid transform to E.coli using electroporator. As i understand, the goal is amplify the fragment to be sequencing.
At this time, i have a question :

After the e.coli growth up, we have too many different type of miscellaneous DNA strand with same size in a colony. How to purify a type of fragment to be sequencing ?

For example, i have 20.000 different DNA strand with the same 3kb in size after break up into random fragment :
-- AAAAAAAAAAAAAAAAAAAA...AAAAAAAAAAAAAAAAATTTTTTT -- (3kb fragment of chromosome 1)
-- GGGGXXXXXAAAAAAAAAAA...AAAAAAAAAAAAAAAAAAAAAAAA -- (3kb fragment of chromosome 2)
-- 19998 DNA fragment left ............................. -- (3kb fragment of random chromosome)
So after amplify them i have :
1000000x of -- AAAAAAAAAAAAAAAAAAAA...AAAAAAAAAAAAAAAAATTTTTTT --
1000000x of -- GGGGXXXXXAAAAAAAAAAA...AAAAAAAAAAAAAAAAAAAAAAAA --
1000000x of -- 19998 DNA fragment left........................ --
These DNA strand is mixed together in a colony. We cannot run sequencing them together as mixed, so how to have the only one for sequencing :
1000000x of -- AAAAAAAAAAAAAAAAAAAA...AAAAAAAAAAAAAAAAATTTTTTT --

I hope I understood your question correctly.
I think what you are missing is that after you break up the DNA, you dilute the concentration so that each bacteria will incorporate ~1 DNA molecule. Then, you dilute the bacteria on a plate and spread it so that they each single bacteria is far from other bacteria. Finally, after they grow you get one genetically identical colony per DNA fragment.

You understood my question exactly and have a quick response, thank you so much !


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Stopping the effect of hormone
Many hormones released by endocrine organs travel down in the blood and bind to specific receptors on the target cells. What then breaks that binding of the molecule with the receptor ? ( thus inactivating further stimulation of the target cell )

The binding is reversible typically; part of the potency of a drug is ow well and for how long it binds to its target. There's a natural equilibrium of binding and dissociation. Many drugs, once bound to their cognate receptor, cause a down regulation of their cognate receptor on the target cell. The bound/activated downstream signalling pathways may be inhibited by ubiquitination of the downstream signals themselves or upregulation of antagonists etc. The hormone itself has a half life, which is very important, thus levels naturally decrease and for some hormones this is incredibly rapid. Levels may decrease due to breakdown or excretion. Increase of binding hormones may decrease free hormone thus it's effect also.

Nice answer ! What is down regulation ?

The number of receptors on cells are regulated by sometimes thousands of things. Often the hormone that activates a receptor in addition to its normal effects, also causes the numbers of its own receptors to go down. This is down regulation which prevents against too much of a hormone over a long period of time.

Another point: even if a receptor is not downregulated or inactivated, certain signaling and gene regulatory circuits can prevent prolonged response.


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What in the world is this critter?
We spotted this thing crawling around a (thankfully empty) bowl in our apartment in Barcelona, Spain. I have never seen anything like it. It appears to be some kind of caterpillar-like insect, but it is inside a flat, leaf-like shell. It can only move by sticking its head out a hole in the tip of the shell and it has to pull itself by its front legs (no legs under the shell). But it can actually pop out of either end of the shell! When it's threatened, it just hides inside the shell completely.
I'm completely flummoxed as to what this thing is. Does anyone have any clue?
(click the images for full-size)

related: http://biology.stackexchange.com/questions/15845/what-insect-is-this/15856#15856

Does this answer your question? What insect is this? (India)

Found it. It's a case-bearing moth larva.


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Why do toenails grow much slower than fingernails?
As the title suggests, I've noticed that my fingernail grow much faster than my toenails. For instance, I usually trim my fingernails every two week or so, but for toenails the number would be about 6 to 8 weeks.
A bit of research revealed this wikipedia article:

In mammals, the length and growth rate of nails is related to the length of the terminal phalanges (outermost finger bones). Thus, in humans, the nail of the index finger grows faster than that of the little finger; and fingernails grow up to four times faster than toenails. [12]
In humans, nails grow at an average rate of 3 mm (0.12 in) a month.[13] Fingernails require three to six months to regrow completely, and toenails require 12 to 18 months. Actual growth rate is dependent upon age, sex, season, exercise level, diet, and hereditary factors. Nails grow faster in the summer than in any other season.[14]

But correlation does not imply causation, so why should the growth rate of nails depend on the  length of the terminal phalanges? Then why do babies grow nail much faster? I wasn't satisfied by its answer, so I looked a bit more where I found this other article. They had two possible candidates:

because hands are physically closer to the heart than are feet, fingers get better blood circulation and consequently better access to oxygen and nutrients.

Fingernails experience almost constant trauma through tapping, typing, bumping, and other seemingly insignificant actions. These persistent minor traumas stimulate fingernail growth. Toes, on the other hand, are not exposed to nearly as much trauma as they are usually bundled up safely inside socks and shoes. Similarly, fingernails on a person's right hand grow faster in right-handed people than on their left hand and vice-versa.

However they don't give actual experimental results. So my question is which of the above is the real cause of this difference in the growth rate of nails; or simply why toenails grow much slower than fingernails?

P.S. The season dependence and the lefthand-righthand asymmetry were news to me; it would be really nice if the answer explains them as well.

Interesting! We could test "These persistent minor traumas stimulate fingernail growth. " by doing a study of people who primarily walk barefoot (beaches, temperate climate, etc).  Mark the toenail, measure actual growth (since they will wear faster, being exposed), and compare it.

One factor that occurs to me but I don't see mentioned in your research, and this is just from my personal experience but it seems to me toenails are significantly thicker than fingernails. I might be mistaken of course. But if that is the case, could this not account for at least some slower growth ? (as in, even if they have equal growth on a mass basis it would translate to faster length growth if the nail is thinner).

Going on the abstract of a study by J.P. Pessan, et al., fluoride intake, as well as "the fact that toenails are less prone to environmental contamination," constitutes a lesser need for growth in toenails than that in fingernails. Also, fluorine being a crucial component in maintaining the solidity of bones, the body may redirect more fluorine that is ingested by various means, to the hands than to the feet, due to the arguably more necessary functions of the hands (in that they are used them for agile and precise motions that tend to influence our survival), meaning less growth in toenails as evidenced in the first citation.

are toenails are less prone to environmental contamination?

Well they are kept in shoes most of the time, whereas we stick our hands in everything.


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What use a pair of lips?
Pardon my ignorance ... A lip is apparently a very sensitive tactile device - as it at-least serves to warn it's owner they may just be about to consume something that could cause injury. Primates (including humans), dogs, cats, sheep, buffalo, elephants, some fish, octopodes - to name a few, have a lip.
How have lips evolved to be nearly ubiquitous across animals? Why have they evolved into a beak/bill in some birds & fish? What niche/purpose do they fulfill?

"Why have they evolved into a beak". Is this true? I would guess that lips and beaks evolved to perform occasionally similar functions, but from very different structures, and so lips have not evolved into beaks.

Maybe lips are (nearly) ubiquitous in extant mammals because they all inherited lips from a common ancestor.

I think what you are looking for can be found https://en.wikipedia.org/wiki/Lips#Functions_of_the_lips and https://en.wikipedia.org/wiki/Beak#Functions pretty easily.
To summarize, lips:

Mainly useful in mammals
Food intake
Articulation
Tactile organ
Erogenous zone
Facial expressions

Beaks:

Found in birds
Feeding
Defense
Manipulation of objects
Communication
Heat exchange

What is a lip(s)? A set of muscles around an orifice that can close said orifice.
How about a way to close a hole so that not everything can get in but what we want - to eat, breathe, drink?
The fact that they are also sensitive is just needed so that you can more precisely operate them for whatever need you have.


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What is a zygote?
During fertilization, the nuclear membrane of the pro-nucleus of the ovum and sperm degenerate. Is the cell is stage called a zygote?
After the dissolution, mitosis occurs and two cells are formed.Or is the cell is stage called a zygote?
I'm confused as i knew a zygote was single-celled.

A soon as fertilization occur, the "thing" is called a zygote. It means that a zygote can be a single cell. I don't know where are your difficulties but you might appreciate checking the definitions of: Morula, Blastual, gamete, gametophyte, spermatophyte, plasmogamy, karyogamy. You will easily find all these informations on wikipedia. Did I answer your question ? Where you thinking about a specific species that have an unusual reproctive system like some fungi ?

Oups.... did I write can be a single cell. I'm sorry. It is a single cell. After division, it is no more a zygote.

Conventionally, a zygote is considered to be formed the moment that a spermatozoum, penetrates the cell membrane of the ovum and yields its genetic material into the ovum. Effectually, however, there is a lag between the instant of fertilization and the fusion of the male and female pronuclei. In mammals, the duration of this lag period is ~12 hours. There are also additional actions that must be completed before the first mitosis as in most mammals, including humans, the ovum is actually in the second metaphase of meiosis at the time of fertilization.


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Why are animal births not taken as seriously as human births?
When humans give birth, more than often medical assistance is needed. Others gather around and frantically look for any way to help. But when an animal gives birth, it is usually seen as a moment where you give the female its space and let the birth occur naturally and without any assistance. The animal is of course in serious pain just as a female human but this is more than often not taken into account. Why is it that animal births are not taken as seriously?

When you say "seen", do you mean "seen by humans" or "seen by animals of the same species"? That is, is your question one of human psychology, or of animal behavior?

I don't thing you can generalize this broadly.  There are human societies where the women generally give birth alone.  But more importantly, "animals" is a big group.  Some animals that bear live young labor extensively, but others don't (e.g., kangaroo).  And some others have external fertilization so there is no labor at all.

Our heads are bigger.
There's some debate on the issue, but in essence, human brains, and therefore heads, are very large relative to our body size.  This is handy for all the intelligent things we like to do, but can be rather painful during birth.  Because we walk upright, the size of a newborn's head is actually a non-trivial fact during the birthing process.  There are two major implications.
The first is that human birth hurts.  You can watch the birth of other animals and they seem to brush it off, but for humans, forcing that huge head through a relatively small birth canal is difficult.  Evolution has (supposedly) limited the size of the hips because, while that would allow an easier birthing process, it would negatively impact our ability to walk.  As such, it has to hurt.
Secondly, in order to make the process easier, humans rotate during birth.  The end result is that, unlike even other closely related primates, humans come out backward in a way that is very difficult for a birthing female to attend to.  This almost requires having another person or two on hand to help out.  This would, of course, be a huge reinforcement for social connections.
A few books I know of touch on this.  Up From Dragons deals with the brain size/hip size issue and The Invisible Sex talks about rotation during the birthing process and the social implications.

And, if your question pertains to "seen by animals of the same species", there are at least anecdotal accounts of animal-assisted births, as in this case of a "monkey midwife".
The linked article also mentions another feature of "social" births, which is that it can might help juvenile females learn.


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How are blood vessels affected by UV and infrared radiation?
The lining of the blood vessel as an interface and boundary layer is of existential necessity to the life-support of mammals.
My question is:
How are major blood vessels and the blood vessel lining affected by sun-irradiation in humans, when exposed through equal or less than a millimeter of skin in total (including subcutaneous fatty tissue)?
Information regarding infrared exposure is welcome too.

Source: http://www.dermatology.ucsf.edu/skincancer/General/prevention/UV_Radiation.aspx
Thanks.

UV rays cause damage is by thinning the walls of surface blood vessels, leading to bruising, bleeding, and the appearance of blood vessels through the skin. Longwave UV radiation (UV-A) accounts for up to 95% of the UV radiation that reaches the earth's surface. Although UV-A is less intense than UV-B, it is more prevalent and can penetrate deeper into the skin layers, affecting the connective tissue and blood vessels, which results in premature aging - Photoaging.
At the same time UVB – is even more dangerous than UVA radiation and also causes skin damage and skin cancer. It affects the surface skin layer. The skin responds by releasing chemicals that dilate blood vessels. This causes fluid leakage and inflammation – better known as sunburn.
I am not quite sure what chemicals are generated by UV radiations beneath the skin surface. I guess it might be excess free radicals which accumulate and cause damage to blood vessels since they are delicate. There is one theory which talks about damages to skin due to Free Radical theory of aging
To give an example how UV radiation affects the blood vessel here:

In actinic purpura, UV radiation damages the structural collagen that supports the walls of the skin's tiny blood vessels. Particularly in older people, this collagen damage makes blood vessels more fragile and more likely to rupture following a slight impact.

Below figure to give an idea of how strong UV radiations are:


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Self pairing in DNA
I know that ssRNA molecule can fold over itself (e.g. in t-RNA). Can DNA do the same? Is there any example of this in nature?
Why is this phenomenon more common in RNA than in DNA?

Are you talking about single stranded DNA?

You may also be interested in DNA supercoiling.

Does this answer your question? Can DNA produce ribozyme-like structures?

DNA can adopt secondary structures like RNA, the main difference is that DNA is usually present as double-stranded DNA while RNA is in most cases present as single-stranded RNA. Double-stranded DNA won't easily adopt any other conformation than the well-known double helix as this one is more stable than possible structures each single strand could adopt on its own.
One example that occurs in nature are G-Quadruplexes which for example occur in telomeres.
There are also artificially created DNA enzymes (also called DNAzymes or deoxyribozymes) that adopt tertiary structures like ribozymes do. But there are no known DNA enzymes that occur in nature as far as I know.

Could you add a link for the DNA (deoxy)-ribozymes? Sounds cooks and I had not heard of them.

@terdon I've added a Wikipedia link. The first one was created by Ron Breaker (who's more famous for having found most of the riboswitches we know so far), if you're looking for some newer papers on this I'd look for Scott Silverman, he has written a few reviews on the topic.

Good answer; might benefit from mentioning ssDNA viruses as the most common natural occurrence of ssDNA, as well as other dsDNA conformations (A, B, Z)


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Why are my faeces black in color after eating Oreos
Why are my faeces black in colour the morning after I eat some Oreos?
Day 1 : Eat a handful of Oreos & the next morning your stool is black.
Day 3 : Eat a handful of cocoa flavored biscuits & the next morning your stool is normal.
Day 5 : Eat a handful of Chocolates & the next morning your stool is normal.
I'm aware of the beetroot digestion story, and how it doesn't happen to everyone. What is surprising in the case of Oreos is that it just takes a
handful of Oreos to turn the stool black. But with any other biscuits or chocolates, my faeces are normal.
I don't have anything other than anecdotal evidence but a lot (NOT ALL) of my friends have had similar experience. Just Googling "Black stool after eating Oreos" & I see a lot of people (not all) having similar experience. Do note that to my knowledge it doesn't affect my body in any way.
Why is that the case? Why doesn't it happen to everybody?
What ingredient in Oreos makes it happen? What is the physiological underpinning?
Asking this question with curiosity than caution. Looking for biological/biochemical perspective.

Hi KharoBangdo! I appreciate your enthusiasm on this site. While this question surely probes deep into the recesses of medical science, it seems as though your data are not well-formed. Perhaps you could carry out a more robust study and then report on the results for the community to respond to.

@jreut sorry, i didnt understand what you are trying to suggest. Are u offended by my little not-so-funny joke at the end. Should i rephrase the question. Was my question unclear?

Before you put any more effort into rephrasing your question, just know that's not what I'm asking you to do. I'm saying that your assertion that 'a handful of Oreos' vs. 'excessive beet root' causes similar magnitudes of color change in your excrement is not well-formed or founded in evidence. You simply need to be more specific in the amounts of either food you've eaten and describe more concretely the effects.

its based on the food coloring so
the food coloring is black so then it caused by that and the choclate just don`t to much oreos

This is a perfectly reasonable question based on a self-adminstered (human) trial. Morever, the proposer bases their observations not on one subject but several reports. The impromptu survey of friends etc. is also acceptable. By the way, self-reported intakes/output records are an accepted method in nutrition research.
My 2-year-old child exhibited the symptoms described above, after consuming two Oreo biscuits in the afternoon. That evenings soiled nappy (diaper) revealed a dark but otherwise well-textured stool. When my concerned partner brought this to my attention, it immediately reminded me of the use of carmine red and related food dyes for the measurement of gastrointestinal transit times. The principle here is that the dyes are not absorbed in the gut, so the time from consumption to excretion gives a measure of bowel function. Short transit time means no constipation and is considered a sign of great bowel function.
Based on the observations reported for Oreos, my educated guess would be that Oreo products contain miniscule amounts of non-absorbed colorants - something that is generally regarded as safe. Self-reported symptoms are generally considered valid by health professionals. I am still intrigued by the Oreo colouring puzzle, as this colourant must be natural.

Transgenics are also "generally regarded as safe", "because they contain DNA and our species has always eaten DNA". Just a comment.

I agree the question is reasonable, but I don't think you've answered it in any meaningful way. You've provided more anecdotal evidence which OP already has, brought in the example of beetroot (also raised by OP). The answer essentially here is "non-absorbed colorants" which isn't specific enough for me!

According to this site there is something called black cocoa powder, a particularly dark product referred to as an ultra-Dutch processed cocoa powder. The site recommends this for anyone trying to reproduce the colour of Oreos, claiming that it acts more as a colouring agent than a flavouring agent.
The site also recommends two commercially-available products so now you should be able to do a real experiment by baking two batches of cookies that differ only in whether they contain this. Then you can report back here, but maybe this time with photographic evidence.


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In theory, would it be possible to create an injection of Vitamins, Minerals, sugars etc so that eating was no longer necessary?
I am wondering, out of pure curiosity, whether with current medical & biological science, (or indeed with accepted probable future developments in those areas), in theory, would it be possible to create an injection of vitamins, minerals, sugars etc so that eating was no longer necessary, and in fact, an average life with average energy usage could be continued?
I am not a biological professional nor academic, so apologies if this is on the wrong Stack Exchange site, however I thought this was closest to the mark. If there is somewhere more appropriate please direct me, and I shall delete the question and post it there.
Also, if no, would there be certain parts that you couldn't replicate in an injection or something of the like?
NB: This doesn't have to be an injection, any simple method of ingesting or attaining everything the body needs. This could be a pill, or anything. I simply used an injection as an example.
Thank-you very much.
Edit:
Having found this question,
Has there ever been an attempt to create nutritionally tailored food for adult human consumption?
I would like clarify. This has given me a lot of information, however, I am looking for any method APART from food. Thanks.

The quantity of nutrients the body requires takes much more physical space than can be included in a simple pill or injection (used only a few times a day).  But nutrition can be provided by IV (intravenous administration), and it is used today for some medical conditions.  When the IV completely substitutes for normal digestion, it is called total parenteral nutrition (or TPN).  The procedure is simple and reliable enough that it can sometimes be used outside of a hospital setting and be self-administered by users at home.

I'd like to point out that TPN isn't considered simple in hospitals and requires a huge amount of extra patient monitoring and observation in addition to causing a number of additional complications - meaning that its usage is always a last resort.

@mgkrebbs Brilliant. Thanks, very useful. The highlighting of specific terms for future research was the largest benefit of this answer. Thanks again.


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Why do you need you room dark for melatonin release?
There is a light pollution movement that says lighting at night obstructs melatonin production. They say:

What makes you fall asleep are changes in the level of the hormone
  melatonin circulating in your body. During the day, light stimulates a
  part of the brain. This brain part (known as the suprachiasmatic
  nucleus) tells the pineal gland to decrease the melatonin level when
  it is light out and to increase it when it is dark. The brighter the
  light, the bigger the decrease and the darker the dark, the bigger the
  increase of melatonin. By making your days lighter and your nights
  darker, you can improve both the quality of your sleep and the amount
  of time it takes you to fall asleep.

and recommend all kind of protection against the light,

Dark Nights: Make your nights as dark as possible. Draw the curtains,
  close the shades and keep the lights off. Try a sleep mask if you
  can’t get eliminate enough light. The darker your night, the quicker
  you will fall asleep.

Do I sense the light by the whole skin surface or only open eyes? If you sense by eyes, which are closed during the sleep, then what is the problem?
In other words, the question is: is the sleep mask sufficient for melatonin secretion or you need to cover the skin?
update What if I close only one eye? I tend to do this when the blinding sun shines. Does such light eject melatonin?

Close your eyes and look at a bright light. Close your eyes in a dark room. See the difference?

Do they give any reference whatsoever about that (I mean improving sleep quality etc)?

So, the question is: is the sleep mask sufficient for melatonin secretion or you need to cover the skin?

The release of the hormone melatonin is responsible for the feeling of sleepiness. It is released by the pineal gland and production starts when the light fades, as it's production is inhibited by light stimulation of the retina, the onset of the production is called dim-light melatonin onset.
Read more about this at this previous answer.
This study on blind people will show you that the light entering the eyes is the (main at least) regulator of melatonin rhythms. They took blind people, 19 of whom could perceive light and 30 who could not, and showed that 14 of 19 light perceivers had normal melatonin rhythms while 23 of the light-blind people had abnormal or unclassifiable rhythms.

Do you mean that the skin surface is not responsible? Then, why do they recommend the face mask only as the last resort? Why do they want the lights off in the first place?

@Val The quotes you put don't recommend "an eye mask as the last resort," but I assume the more you do the more light you can prevent the better - living here in Sweden I can tell you that blinds and curtains being closed and lights being switched off does not mean you will get darkness during the summer nights - an eye mask is a very effective measure.

@Val I've also added a little about an interesting study on blindness and melatonin production


text:
Why might food spoil faster in Ireland than the US?
An American is staying in my house for the summer and claims that food (specifically, bread and milk) spoils a lot faster here than at home in California. Is there a significant difference in chemical content (preservatives etc.), or other factors, that might explain this?

There are way too many factors that we can never consider for this kind of question.  Does California represent all of the US? What part of California?  What part of Ireland?  What's the humidity and average temperature of each region?  What are the agricultural and chemical preservative regulations?  Is it a matter of how you store the food in your homes?  The quality of your cooling method?  The way people in the household handle the food?  Too many variables.

@KeeganKeplinger, this seems like a good answer, to me – these are are "factors that might explain", which is what he asked for. Why not post it as an answer?

I would think added preservatives are the most likely candidate, for example, Azodicarbonamide is frequently added to bread in the US, but banned in Ireland and most of the rest of the EU. Since it has a preservative effect it is a reasonable candidate for a specific causal factor.
But as Keegan points out there are an awful lot of possible factors so it's impossible for us to say with any certainty.

Going to accept this answer because it tells me one potential reason that I didn't know before. I realise this question was a bit too open-ended and vague, but my knowledge of this stuff is rather limited.

There are more factors than we can ever consider.
As far as region: does California represent all of the US? What part of California?  What part of Ireland?  What's the humidity and average temperature of each region?  What are the agricultural regulations?
As far as cultural/methodical differences: how do you store the food in your homes? The quality of your cooling method? The way people in the household handle the food?

That's a fair point. I expected this answer because I didn't know how to specify the question. I appreciate the feedback.


text:
Can a brain be transplanted?
Is it possible to transplant a brain and would it keep the memory? If not, what would be the prerequisite to transplant one?

"Is it possible" has a carefully conditional "yes".  Do we have the expertise or technology to do it now? No.  One of the biggest difficulties is that nerve tissues (the connections between brain and rest of body) will take time to heal... time during which the brain cannot sufficiently give commands to the rest of the body to keep autonomic functions running.
Head transplants, however, have been "successfully" completed using monkeys.  The monkey lived for sometime after the transplant, but eventually died.  China has also been known to do a similar procedure with dogs.
Caution, this may be too explicit for some; I'm not sure ethics boards would allow it nowadays:
Monkey Head Transplant

was the spinal cord reconnected in the head transplant?  I think it was not?  regenerating the nerve connections in a useful way remains a major goal in medical science.

Sergio Canavero and collaborators are controversially claiming they may be ready to perform a head transplant on a human by late 2017. @shigeta Canavero have been having some success in fusing nerve cells using polyethylene glycol.


text:
Water potential in plants?
The concept of water potential in plants tries (and succeeds) to explain various movement and transports in plants. I have learnt that it can be though of being composed of various components like the solute (osmotic) potential, Matric potential, gravitational potential and the pressure potential. I know how to quantitatively determine the osmotic pressure and have worked with the chemical potential of water in solution and pure state. Can someone help me develop an intuitive understanding of all these components quantitatively? I am comfortable with basic thermodynamic treatments of chemical potential and already have an intuition of the osmotic component. Here is the basic definition regarding water potential. (Since this pdf is quite old, I am not sure whether the same definitions operate or rather are used now.)
EDIT:- As an example, we can derive the lowering of chemical potential of pure water on addition of solute and for the ideal case, the lowering turns out to be $RTln(X_a)$ (where $x_a$ is the mole-fraction of solute, $R$ is the gas constant and $T$ the absolute temperature) and this is defined as the osmotic potential or the solute potential. Next, the gravimetric component. We can intuitively understand that the water must flow from higher gravitational potential to lower and hence flow downwards. But I want to understand how can we assign a quantitative basis to our arguments in terms of chemical potential for differenf heights. Same way, how can we ascribe a mathematical (or chemical) basis to all the components of water potential including the turgor pressure and the matric components.

sadly this paper is behind a paywall - any other references?

I have a copy but I dont think we can share without uploading. Nevertheless, (http://en.wikipedia.org/wiki/Water_potential) wikipedia provides some minimal non rigorous definitions. See if that helps provide some quanlitative clarification of this concept.

could you add a couple of questions or issues you have - what sort of phenomenon or math puzzles you about water potential?  again there's several ways to go here.

Added in the edit

Ok let me try to tackle this one - still could be off - let me know.
The book Chapter from UCDavis that is linked from your wikipedia page is a good reference I think. Overall the term 'water potential' will try to estimate an energy function that describes the behavior of water in a chemo-mechanical sense.
$\Psi_{total} = \Psi_{reference} + \Psi_{solute} + \Psi_{pressure} + \Psi_{gravitational} + \Psi_{humidity} + \Psi_{matrix}$
It looks a lot like a Hamiltonian expression of total energy that tries to see the water as a fluid.  The water potential is not the same as an energy equation for fluid dynamics which tries to understand the motion of a body of liquid and does not typically take into consideration chemical changes like solute in the behavior.
So first we are looking at a set of behaviors that the fluid experiences.  some of them treat the fluid as a body ( pressure, gravitational) others look at the potential for evaporation or diffusion (solute and humidity to some degree).  wetting of surfaces and surface tension (matrix).
The water potential is an equation broken down into a set of measurable or approximately measurable energy terms.  But like a lot of Energy equations, when  you are looking at a biological system, it is more often qualitative than a quantitated entity.  The general observation that surface tension decreases when temperature goes up, or when the solutes have higher concentration is used to make arguments of the mechanism of say physiology
Generally speaking looking at the magnitudes of the various terms you can see how influential they are and then try to focus the hypothesis into a test that can make a distinction about the mechanism with specific measurements.  The actual overall measurement of a water potential or any total energy is almost always intractable.  The difference in energy is what you might be able to measure, but in the case of the water potential, the measurement will usually be an observation, with some uncertainty that water is moving from point A to B and not elsewhere.
Take a look at this paper describing Drought Stress in Arabidopsis.  The water potential is cited as a critical element of drought response - and of course it should be.  But all this work here, with all the proteins acting to change the physiology of the cell, adjust the chemical potential (and therefore the osmotic potential) of the cell membrane, its hard to imagine how measuring a root system at all points would be possible.

Physical properties of the cell wall play a crucial role in the response of plants to water deficit (Bacon, 1999). Transcriptome analysis of pDr showed the repression of many expansin genes (Bray, 2004), while mild osmotic stress revealed the induction of expansin genes (Skirycz et al., 2010). Cell expansion in response to drought was characterized in the maize (Zea mays) root system as an adaptation to low water potential (Wu and Cosgrove, 2000).


text:
When can a virus modify DNA in every cell of a living organism?
I've recently heard about experiments with brain tissue, where a virus is introduced in a rats brain, causing a "glow when electric charge is present" protein to be created. This protein then helps to study the brain using optical techniques to detect this glow. As far as I understand, not all cells in the brain were affected by this virus.
It seems like this kind of "virus operation" on DNA is pretty powerful, so my question is : at which point in an organism's life can a virus operation be done in such a way as to affect the entire organism for the rest of its life?
In other words, will a virus is introduced into a young embryo(or sperm), affect all cells and stay with an organism until death? Can it be introduced later and still have "complete effect"?

Note that in the type of experiments you are referring to (for instance look for "in vivo optogenetics") you generally do NOT want to infect all of the neurons in the brain, but rather a very specific subpopulation. This is achieved by using various strategies, which essentially depend on the presence of specific DNA sequences in the virus or in the target neurons. Also, if you do this in adult animals, the virus will only infect cells around the site at which it has been injected.

The answer depends on two factors:

The type of vector (virus) you are using
How well your vector can be integrated.

The bottom-line is that there is no guarantee the vector will work even if you start from the embyro.
As far as I know, the problem of using vectors in general is that the vector you are using might not be integrated into the genome of the host. (Not necessarily get into the DNA, but just keep replicating during each S phase.) Therefore doing it earlier gives you a better chance to actually get them in the organism.
For example, there is a linear vector used in C. elegans that was injected into the oocyte even before fertilization. The cell later treats the vectors as broken DNAs and linages them so they could be pull to one side of the cell during mitosis. However, the huge chunk of vector DNA is mosaic. (i.e. only some of the cells in that worm have the vectors.) Other vectors like engineered HIV have better chance to integrate themselves.


text:
Do male animals visually perceive females as more/less attractive?
If we somehow remove pheromones, do animals experience a phenomenon similar to human "visual beauty" when looking at members of the opposite sex? For example, given a set of 20 female ducks observed through a glass panel, would male ducks attempt to court/mate with a small subset of female ducks first(more attractive ones), or is it based on some other criteria (most receptive, random, closest, fittest, pheromones, etc?)
If there is some "visual attractiveness selection criteria", is there a requirement of certain complexity of the brain and/or visual system for an animal before this phenomenon starts to occur?
I'm aware of the existence of this question: Why does sexual selection evolve beautiful features?, and my question deals with the members of the same generation, not long-term evolution.

One related idea is that they have found in some species of fish that, no kidding, a male being seen with other females is attractive to a female who see this situation. This makes some sense evolution-wise, I think. I am sorry but have no link.

I have read that among human cultures, standards of beauty vary but all cultures want symmetry and asymmetry probably indicates some developmental/genetic disorder. I would bet that this symmetry thing also holds among non-humans. I also believe that visible signs of sickness will cause an member of non-human species to be ostracized, not just avoided as a potential mate.

There are numerous examples of visual attraction in animals. An absolute classic of an experiment, taught to most/all evolutionary biology students, is the widowbird tail length experiment by Andersson. He experimentally manipulated the tail lengths of male widowbirds at random. Some tails were made longer and some shorter. From this experiment Andersson showed that females choose males with longer tails more preferentially. Another classic example is the lek mating system where there is a bias in reproductive success towards attractive males, in some cases 10-20% of the males get 70-80% of the matings.

A lek is an aggregation of males that gather to engage in competitive
  displays that may entice visiting females who are surveying
  prospective partners for copulation. Leks are commonly formed
  before or during the breeding season. A lekking species is defined by
  the following characteristics: male displays, strong female mate
  choice, and the conferring of male indirect benefits. Although
  lekking is most prevalent among avian species, lekking behavior is
  found in a variety of animals such as insects, amphibians, and
  mammals

Beauty could be a an example of a an indicator trait:

Indicator traits are those that signal good overall quality of the
  individual. Traits that are perceived as attractive must reliably
  indicate broad genetic quality in order for selection to favor them
  and for preference to evolve.

I'm sure there are some studies in fish, likely guppies or zebra fish, which gave individual fish the opportunity to visually assess potential mates (placing tanks next to each other and observing courtship) which would be very similar to your hypothetical duck example. Despite often being a paradox, female mate choice is well documented. Further, male mate choice is now coming to light, even in species where female mate choice and male-male competition exists.
I don't think selection on "beauty" would require some kind of particularly special neural system, obviously some visual capacity is necessary for visual attraction and some basic neural pathways linked to that. I have done experiments myself in Drosophila simulans which looked at good gene benefits of mating with attractive males (indirect genetic benefits of female mate choice) and another which assessed precopulatory selection (female mate choice) for a secondary sexual character in the same species. Even in such a small-brained species there appears to be some degree of (partially visual) mate choice going on.

Those articles mention 2 examples of bird visual preference: a) better diet translates into more plumage pigment in some birds b) parasites dull the color of certain parts of plumage

@AlexStone Thanks, could you please include a citation on that quote you've edited in

I added the link

Absolutely.  Quality by appearance is sometimes a big part of mate selection and sometimes it is not.
The size and cognitive capacity brain is probably important but not always. Primates are closest to us and have most similar tastes to us, have varying levels of interest in mate appearance.  Most primates have a troupe dominance where a dominant male mates with all the females and sires as many offspring as he can before he loses his place on top.  Many smaller primates rely more on sperm competition and the females mate with all the males they can when they are in estrus - the offspring just emerge from the most competitive sperm.  Note I studied Sarah Hrdy a while ago.  I hear Robert Sapolsky is another great source of insight on primate/human behavior.
Neither of these modes are quite so focused on visual beauty as our culture is.  Other cultures are also not selective based on appearance, e.g. cultures where marriages are arranged would often consider the social and economic relationships between the families more than we do.  This is a broad generalization, but just to point out that just looking at someone to decide mate choice isn't as dominant as sometimes it feels.
But to look at some tiny brains I know that snakes often mate in gigantic balls of snake and mate choice is pretty indiscriminate, on the other hand, spiders where female choice is dominant, males will experience rejection.  This is a bummer for the males because they only often live long enough to offer to one mate.  Its probable that the females are not hungry or have recently mated with another male, but just an example to demonstrate that even small brained animals can be discriminating.

It would be interesting to know if an alpha primate male, while mating with all his females still shows stronger preference to some of them, and if so, what controls that attraction

Good observation.  There are definitely favorites amongst primates (i mean besides humans, who obviously play favorites).  Hrdy and Sapolsky's books have examples where females in the troupe are definitely favored recipients of mating behavior - younger females have an easier time producing offspring and so are favored just as they are with humans for instance.  There are also observations that female apes will break away from the alpha male for males who treat them better.

In addition to the answers stated here, it is also important to remember that we, humans, are more guided by vision than many other animals. Therefore, the idea of separating an animal from a potential mate with glass would also inhibit other important mate selection criteria that other organisms use (calls, pheromones, nest tending, etc.).

You seem to be dissociating physical beauty from fitness. In fact, beauty can be taken as a measure of biological fitness. For a classic, if simplistic example, many male humans find large breasts attractive and beautiful, however, large mammary glands are also an indication of fertility and robustness that would imply the prospective mate would be a good mother.
Anything that we consider beautiful in a prospective mate can be interpreted in terms of fitness. Another classic example is symmetry. Humans are attracted to symmetrical faces and bodies. Since we are a symmetrical species, symmetry is an indication of fitness. In other words, lack of symmetry may indicate a developmental problem and by extension decreased fitness.
There isn't really a qualitative difference between the way we define attraction and the way other animals do. In both cases we have instinctive attractions to healthy and fit (in the evolutionary sense) mates. It is simply that our complex society has marked these choices as "aesthetics" while we call them "instincts" in other animals.

Since asking this question, I've learned that 97% of male mammals do not have concept of "beauty" and will mate with every female indiscriminately. These species do not have any paternal investment, so the males are not picky.
In other 3% of mammals (~100 species) and a lot of birds, there is a significant degree of paternal investment in offspring. Species that have developed a "pair bond" mating strategy, have males capable of perceiving "beauty" in females and become much more picky. Humans are a pair bond species.
On the other hand, because mammal females have high investment in their offspring, without the pair bond females go straight for the top alpha male to secure his DNA.
The 97% -3% number is quoted multiple times in this podcast on Evolutionary Psychology: https://hosts.blogtalkradio.com/beatyourgenes/2016/03/24/gender-dynamics-biological-differences-of-men-and-women
There's also this article on social monogamy in mammals that quotes 3-5% figure

Can you provide a reference to the numbers you refer to?

@fileunderwater I have added a couple links


text:
Laying eggs vs giving birth: is there a connection with internal vs. external ears?
I have heard that "The animals who have their 'EARS' outside their body give birth to their young ones and the animals who have their 'EARS' inside their body lay eggs." Is this true? Are there counterexamples?

Just to expand on @rg255's very good answer, you could make the same sort of claim using just about any characteristic that is more commonly found in mammals.
Giving birth to live young is a characteristic of most (see the platypus below), if not all, mammals. Therefore, you could make the statement about external ears (also more common to mammals) using any other mammal specific body plan. For example:

"The animals who have their 'TESTICLES' outside their body give birth to their young ones and the animals who have their 'TESTICLES' inside their body lay eggs."

I am pretty sure you will find that this is as true as the statement about ears.
As in all other debates about this kind of thing, the platypus comes along and complicates things. This beastie has no external ears (or external testicles for that matter), it has tiny ear slits instead and it lays eggs. So, even this extreme weirdo seems to follow the ears (or testicles) on the inside means eggs rule. However, it is a mammal, it produces milk that it will feed to its newly hatched young like all mammals (well, almost, it doesn't have teats and instead the young suck up their mother's milk through her spongy belly).
A more straightforward and well known example that directly contradicts the ears claim is the dolphin. Dolphin ears are small holes on the sides of their heads but they give birth to live young as do all sea mammals. In fact, I am pretty sure that all sea mammals lack external ears (and cetaceans at least also lack external testicles) but give birth to live young. So seals, sea lions, walruses etc also contradict the ears rule.
In conclusion, no it is not true that all animals with internal ears lay eggs.

Actually there is a lot of variation in testes among mammals (descended vs. undescended, scrotal vs. astrotal): http://biology.stackexchange.com/questions/559/why-do-some-mammals-not-have-testes-in-a-scrotum

@kmm ah, but can you name an animal with external testes that lays eggs :) ? Anyway, that was just a tongue in cheek example to highlight the arbitrary nature of the distinction mentioned by the OP.

on a similar tongue in cheek note... I can't think of any animals with testes that lay eggs or have a pregnancy ;)

@GriffinEvo stretching the definition of having testes, the male angler fish will attach itself to the female and wither away leaving, essentially, only its gonads attached which the female will use to fertilize her eggs. Strictly speaking, at that point she has both testes of a sort and lays eggs :).

You are quoting from Imam Ali,

"The animals who have their 'EARS' outside their body give birth to
  their young ones and the animals who have their 'EARS' inside their
  body lay eggs."

And in short the answer is that is wrong. Giving birth to live young is called vivipary. When a species lays eggs it is called oviparity. There are other mechanisms too.

Ovuliparity: fecundation is external (in arthropods and fishes, most
  of frogs)
Oviparity: fecundation is internal, the female lays zygotes
  as eggs with important vitellus (typically birds)
Ovo-viviparity: or
  oviparity with retention of zygotes in the female’s body or in the
  male’s body, but there are no trophic interactions between zygote and
  parents. (Anguis fragilis is an example of ovo-viviparity.) In the sea
  horse, zygotes are retained in the male’s ventral "marsupium". In the
  frog Rhinoderma darwinii, the zygotes developed in the vocal sac. In
  the frog Rheobatrachus, zygotes developed in the stomach.
Histotrophic
  viviparity: the zygotes developed in the female’s oviducts, but find
  their nutriments by oophagy or adelphophagy (intra-uterine cannibalism
  in some sharks or in the black salamander Salamandra atra).
Hemotrophic viviparity: nutriments are provided by the female, often
  through placenta. In the frog Gastrotheca ovifera, embryos are fed by
  the mother through specialized gills. The lizard Pseudomoia
  pagenstecheri and most mammals exhibit a hemotrophic viviparity.

Though it is true that most typically we would associate egg laying with animals with ears "inside" such as birds and snakes, there are some examples that are not this way. Boa constrictors are one species which gives birth to live young rather than laying an egg and being a snake their ears are 'inside their body'. However I should point out that this is Ovoviviparity, not viviparity. For an example of a lizard with viviparity see the Pseudomoia lizard genus.

Good answer +1. Although there are some counterexamples, there is still quite a high correlation between having ears inside/outside and being oviparous or viviparous. So why is there a correlation? It is certainly only due to phylogenetic correlation. If one make a study and decorrelate the effect of phylogeny, he would, I guess, find out that there is no significant correlation between ears position and viviparity/oviparity.

@Remi.b I agree, it is likely just a correlational relationship, rather than causal, but perhaps environments/lifestyles where external ears are less useful (e.g. underwater for reduced drag) are also typically less favourable to the birth of live young. I can imagine a bird doesn't want ears because they cause drag and wants to lay eggs to reduce the time it spends carrying the weight of a chick(s) - I'd imagine a pregnant bird would suffer from the extra weight when trying to fly.

@GriffinEvo Kindly excuse me for though people liked your answer more than that of anyone else but may be because of my lack of knowledge, I found terdon answer rather good and easy to understand be to accepted.

Internal or external ears is Not Relavent to an animal giving birth or laying eggs...
Examples
Sea Lions - External Ears - Live Birth
Seal - Internal Ears - Live Birth
Sharks - Internal Ear - Eggs (Oviparous), Live Birth (Viviparious), and Egg cases in mothers womb hatch producing young that feed on siblings before a live birth (Ovoviviparious)
Dolphins - Internal Ears - Live Birth
Frogs - Have an external ear drum - Lay Eggs
Exhidna (mammal) - Internal Ears - Lay Eggs
There is no relation to animal ears being internal(inside)/external(outside) to laying eggs or giving live birth.
I am a Biologist having worked at with a large variety of animals (egg layers and live birth) for 14 years. Feel free to ask any questions you may have. And by all means please do your own research to see the information I've provided is accurate.
Great Inquary, I hear of lots of fun facts to remember things...some true,  some not
True Fact...
You can SEE a SEA Lions ears but
A SEALS ears are SEALED up