text:
Why does the HPV vaccine not work on already infected people?
With my limited knowledge, I understand that the vaccine works by inserting fake HPV-like material in the body, thus inducing the immune system to build up defenses against it, so when the body is exposed to real HPV on the wild the immune system will be able to handle it.
That makes sense, however, why can't the body still build up the defenses when there was already an exposure? Specially when the HPV virus is "dormant" and undetectable.
EDIT: After the discussion with @Bob in the comments section below, the hypothesis is:

In an infected person whose immune system was able to clear the acute
  infection, the virus (single infected cells) is constantly trying to
  enter lytic cycle again, only to be defeated by the immune system
  (because one infected cell leaving dormant state alone might not be
  effective); and then when the immune system is compromised for some
  reason, the virus is successful into entering lytic cycle and then
  there is a new clinical infection.
If this is all truth, then the answer to the question is that the vaccine
  does "work" in the sense that the body still reacts correctly (by responding to the antigen)
  to it, but it is, in practice, useless because: 1) when the virus is
  dormant there isn't anything for the immune system to do; 2) when the
  virus strikes, the immune system was already exposed to it anyway, so
  it is generally able to fight and there is no need for the vaccine; 3)
  the infection will get clinical again only when the immune system is,
  for some reason, defective.
The whole point of the vaccine is to never let the virus infect many (or any?) cell in order to avoid this situation where it is always trying to come back - and will do, when the immune system can't fight it off for some reason.

Please, if some specialist can analyze and comment on that it will be awesome.
More questions around it:

Is there the possibility that, while in this "dormant/attack" cycle, every single infected cell is defeated over the course of time, meaning an actual "cure"?
How does the cell replication process impacts the 1) hypothesis? (Maybe it is not possible for the immune system to achieve a natural cure because the virus keeps constantly replicating.)
How "much virus" would be needed for a successful strike in a compromised immune system (and how much compromised that system would have to be to fail)?
If the virus acts locally, is it possible for the vaccine to help other still-not-infected sites? In other words: is the natural immune response from the first infection in, say, the anus, worth anything for a subsequent infection in, for example, the oropharynx?

My guess: since the vaccine would trigger the production of plasma cells that are able to detect surface antigens on the viral envelope. Once the virus has infected a cell, it has inserted its genes into the host genome, and therefore can not be detected. The other thing HPV does is "kill" the the cells surrounding it (creating a wart), thus hiding any infected cells that would be displaying surface - antigens.

Also, the damage to host's genes has already been done during the acute stage of infection, so vaccination afterwards won't prevent HPV-induced cancer. It may reduce the risk, though, if the next exposure will be to a different strain.

@Bob The immune system does not recognize the vaccine material as an antigen, because the virus has already inserted his genes in the host's genome? So what happens with the vaccine material if it doesn't trigger the immune system, it just lays there?

The immune system could still trigger a response to an HPV - however, the antibodies would only target viruses that are outside of the cells (eg. in the circulatory or lymphatic system.) It could not target it once it's inside the cell, and it can not target infected cells that have been enclosed by dead cell material (the wart).

@IMil Is this gene damage systemically relevant? I understand that HPV has local effect, thus vaccination afterwards could still work on non-infected areas of the body since there wouldn't be any damage?

@Bob I understand now, thanks. So, if the immune system of an infected person still recognizes the vaccine antigen and responds to it accordingly; and there is no wart; and there is no virus outside because the virus is hiding for, say, 10 years... Shouldn't the immune system be now prepared for the moment when the virus try to strike again in the future?

As your cells replicate, they also replicate the dormant viral-genes. So, when the cells finally do enter the lytic cycle, there will probably be a lot more viral components than there are antibodies - thereby allowing the virus to infect more cells. And furthermore, just because one infected cell leaves it's dormant state, does not mean that all infected cells will also leave the dormant state.

And I just want to throw this out there again, as I said in my first comment, I am only guessing. If I knew with 100% certainty, I would have submitted an answer. (I've never studied virology). But I feel like I'm probably somewhat on the right track.

@Bob So it is possible that what really happens is, in an infected person whose immune system was able to clear the acute infection, the virus (single infected cells) is constantly trying to enter lytic cycle again, only to be defeated by the immune system (because one infected cell leaving dormant state alone might not be effective); and then when the immune system is compromised for some reason, the virus is successful into entering lytic cycle and then there is a new clinical infection? This all is pure conjecture of mine.

I believe that you are now thinking about it in the same way that I am. I don't think HPV is particularly dangerous (aside from the increased cancer risk), so in most cases what you said is probably what happens. I wouldn't be surprised if just about everyone has some form of viral-infection. But, until your immune system is comprised, you'll probably never know.

@Bob If this is all truth, then the answer to the original question is that the vaccine does "work" in the sense that the body still reacts correctly to it, but it is, in practice, useless because: 1) when the virus is dormant there isn't anything for the immune system to do; 2) when the virus strikes, the immune system was already exposed to it anyway, so it is generally able to fight and there is no need for the vaccine; 3) the infection will get clinical again only when the immune system is, for some reason, defective.

@Bob This spawns other questions (maybe not answerable without practical research - or at all): 1) Can the vaccine at least strenghten the current immune system response that was naturally trained before? 2) Is there the possibility that, while in this "dormant/attack" cycle, every single infected cell is defeated over the course of time, meaning an actual "cure"? 3) Is there any way to detect dormant virus, even if very expensive? 4) How "much virus" would be needed for a successful strike in a compromised immune system (and how much compromised that system would have to be to fail)?

By the way, if it were possible to detect the infected cells and kill them, would them generally be too numerous for that strategy to be effective without side effects on the body, or the whole problem lies in the detection?

To your first comment: 1) Definitely; 2) Probably. Unless there's a chance that it was able to infect a cell undetected? I just thought of something - the virus infects the basal layer epithelial cells, so i dont think it enters circulatory system. That would mean that antibodies would need to detect the virus in the dermal region (underneath the basal layer). And since the virus would need to infect a cell superficially to the basal layer, I suppose there is a chance it goes undetected. So, once the cell is lysed, the immune system wouldn't be able to make a response. Is that how warts form?

2nd comment: 1) No. Immunity, is an all or nothing attack. When your immune system is activated, your body will produce as much antibodies as it can very quickly. 2) I believe so. I know that some people can have warts that disappear/appear for many many years before they never see them again. But does that mean that their body actually defeated the virus? Or is it going to come back in 15 years? 3) You would need to create a protein or RNA or something that can recognize the viral gene-sequence in the DNA. It would need to be very specific. Then you would need

To have this protein/RNA/whatever trigger destruction of only infected cells. 4) I have no idea lol - but figuring this out would answer #2 from the first comment

I think you should add an edit to your question with some of these things that we have discussed. And maybe someone else would be able to clarify where we might have gone wrong - this quite an interesting topic to think about.

I do wonder, though, why the rabies vaccine can be given after a possible infection.  AFAIK it's the only one that acts like this, and though animals (dogs &c) routinely get rabies vaccine, I've never heard of a human getting it unless bitten by a possibly rabid animal.

@jamesqf I realize this is an old thread, but you brought up a good point about the rabies vaccine. Just to clarify: The treatment is called "rabies postexposure prophylaxis" (PEP). It's a rabies vaccine series plus a dose of rabies immunoglobulin (antibodies targeted against rabies virus). Immunoglobulin is an essential part of the treatment, as it triggers a more rapid immune response than you'd see with vaccine alone. Also - it needs to be given before symptoms develop. Here's a link to more information. It includes a link to CDC guidelines:
https://www.medscape.com/viewarticle/877636

This is an excellent question, and it is actually being studied -- but for a different reason than your question suggests. HPV is a bit unique because there is some data showing that infected individuals can become "reinfected" with the same virus type, causing reactivation of the dormant/latent virus that they are already infected with. So the question in this case is whether administering an HPV vaccine to an already infected individual can help prevent (or minimize) reactivation of the latent virus.
Here's a journal article explaining some of this research. Please note that it is not standard medical practice to give HPV vaccine to already infected individuals. This work is still in the research phase, and is aimed at minimizing viral reinfection and reactivation:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006803/
Simply put, a vaccine only works to prevent infection with a specific virus. It is rarely effective in treating a virus once a person has become infected. The reason for this has to do with how the immune system responds to its first encounter and subsequent encounters with a particular virus:
When the body encounters a specific virus for the first time, the immune system mounts a "primary" immune response specific to that virus. A primary immune response triggers the body to produce virus-specific immune cells that can generate antibodies against that virus. The body continues to make these immune cells in small quantities even after the virus is eliminated.
If the same virus is encountered again later, these cells will proliferate and immediately start producing antibodies against the virus. Thus, the body can mount a much faster and stronger "secondary" immune response. This prevents the viral load from reaching levels that produce physical symptoms, so the person does not become sick (or at most they may have milder symptoms), and the immune system is to able eliminate the virus more quickly.
The purpose of a vaccine is to trigger a primary immune response. With a vaccine, the body is exposed to a weakened form of the virus, and a primary immune response is triggered without the individual becoming sick. When the individual encounters the real virus, the body immediately mounts a secondary immune response, which fights off the virus much more efficiently and quickly, and the person typically has no physical symptoms.
Here's a more in-depth explanation on the difference between a "primary" and "secondary" immune response. Most cell biology textbooks (and all immunology textbooks) will have an explanation of this as well. This is an important concept in understanding how vaccines work:
http://www.microbiologynotes.com/differences-between-primary-and-secondary-immune-response/
If a non-vaccinated person is infected with a virus, administering a vaccine generally has no effect. At that point the body is already mounting a primary immune response, so a vaccine would serve no purpose. Because a primary immune response is slower than a secondary response, when a non-vaccinated person gets infected the viral load is able to increase more rapidly than it would in a vaccinated individual, resulting in the physical symptoms typical for that particular virus.
What makes "chronic" viruses such as HPV and Herpes virus (including chicken pox) harder to eliminate completely is that these viruses enter a dormant/latent (lysogenic) phase. At that point they become "invisible" to the immune system. Even if the person is not visibly sick, they are still infected with the virus. If/when the active (lytic) phase is triggered, the viral load increases rapidly -- more rapidly than if it were a new viral infection. The body still mounts a secondary immune response, but typically this will not completely eradicate the virus. As long as any amount of the virus is in the lysogenic phase, it remains "invisible" to the immune system.
With some viruses (e.g., chicken pox virus, which causes shingles) if a vaccine is administered during the latent phase, this can help somewhat with making symptoms milder if/when the lytic stage is ever triggered. But this doesn't work for all viruses.
If a targeted antiviral medication is available (e.g., Tamiflu for influenza; Harvoni for Hepatitis C) this can slow down the proliferation of the virus, allowing the immune system to "catch up" and eliminate the virus. Antiviral medications aren't vaccines. They are designed to directly target the virus and interfere with a biochemical activity that the virus needs in order to proliferate.
Currently there is no antiviral medication available for HPV, although a few drugs are being researched. One drug in particular (ranpirnase) looks promising, but it is still in early clinical trials.

I believe the following paper discussing the lifecycle of HPV is of use for understanding at least some of the aspects of your question: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5394500/
Specifically:

Viruses like HPV have the capacity to form virions and become transmissible at some point in their natural lifecycles, but within tumors these infections are generally latent so that productive virus replication (also known as lytic replication) is either diminished or absent. Viral latency serves as an immune evasion strategy allowing the virus to hide from the immune system by turning off unnecessary viral proteins that might be sensed by cell mediated immune recognition. The virus persists as a naked nucleic acid, often as a plasmid or episome, which relies on host cell machinery to replicate whenever the cell divides. Viral latency should not be mistaken with clinical latency, which means asymptomatic infection (14).
The most favorable explanation for the connection between virus latency and tumorigenesis is that productively replicating viruses initiate cell death, the known cytopathic effect (CPE). Virus-induced CPE can be harnessed to kill cancer cells in viral oncolytic therapies, illustrating the anticancer activity of active lytic viral replication. Although CPE is often thought of as a virus-induced event, it is in fact a stereotypical and nonspecific innate immune response of cells to infection by many types of viruses. When latent viruses switch to producing virions, virus replication generates pathogen- associated molecular patterns from partially synthesized viral chromosomes, double-stranded RNAs and empty capsids that trigger cellular DNA damage responses and innate immune signalling. For some viruses, lytic replication generates a linear viral chromosome that can be recognized as a DNA fragment unless either the DNA ends are structurally hidden from DNA damage response sensors by encapsidation or these sensors are inactivated (14).

I think this addresses some relevant aspects of your question, namely:

why can't the body still build up the defenses when there was already an exposure?

It can and already has, see my answers to later questions. But it doesn't work on the already present viral infections because:

Is there the possibility that, while in this "dormant/attack" cycle, every single infected cell is defeated over the course of time, meaning an actual "cure"?

Not really, since the immune system cannot 'reach' or 'see' the HPV infected cells and thus isn't attacking them until they enter the reproductive phase.

How "much virus" would be needed for a successful strike in a compromised immune system (and how much compromised that system would have to be to fail)?

There probably won't ever be an exact number here but the paper I linked above does list some (obviously approximate) numbers regarding HPV activity:

After infection of wound basal cells, it is thought that there is a round of viral DNA replication that appears to be independent of the cell cycle and amplifies the viral copy number to around 50 to 100 copies per cell. The infected cell leaves then this primitive compartment and enters the transit amplifying proliferative compartment of the epithelium, where there is a phase of plasmid or episomal maintenance when the viral copy number remains constant and viral gene expression is minimal. In this phase of the viral life cycle of the high-risk HPVs, the expression of the potent oncogenes E6 and E7 is under strict control, and E6 and E7 transcripts of high-risk HPV types are hardly detectable in the proliferating compartment of the epithelium (10). When the infected keratinocyte enters the differentiating compartment, in the stratum spinosum exiting the cell cycle, then there is an extended upregulation of viral gene expression and viral DNA replication, with amplification of the viral copy number to many thousands of copies per cell, gross expression of the E6 and E7 early genes, and expression of late genes from the late promoter, leading finally to HPV formation

Lastly, you asked:

If the virus acts locally, is it possible for the vaccine to help other still-not-infected sites? In other words: is the natural immune response from the first infection in, say, the anus, worth anything for a subsequent infection in, for example, the oropharynx?

The answer to this, I believe, is that if you are speaking of an HPV vaccine of the same strain then it would likely not be useful, since your body's immune system would already recognize the same strain that it already has been fighting off, also in a different location. However, HPV has a couple of different strains and a vaccine for those might help with infections in different locations by different strains. Considering that vaccinations like Gardasil actually cover a lot more than 1 type of HPV, vaccination might still be relevant.
For a source that HPV vaccines cover more than 1 strain, see: https://www.cancer.gov/types/cervical/research/gardasil9-prevents-more-HPV-types and https://www.ncbi.nlm.nih.gov/pubmed/25693011
For a semi-source that already infected people might benefit from vaccination, see: https://www.cancer.gov/news-events/cancer-currents-blog/2015/hpvvaccine-multisite (note that this is from what I can tell pre-publication research presented at a conference and so it all seems quite preliminary).
I also found this paper to be informative on the topic of HPV and the immune system response to it, but it isn't open access so I cannot guarantee that you'll be able to read it. For the sake of completion, I'll still link it: http://dx.doi.org/10.1016/j.ygyno.2013.08.025


text:
Is it possible to determine the initial population given the final one?
It is possible to determine the initial population of, say, bacteria given a measure at a later time?
Let's say I use the logistic growth model
$$\dot N (t) = rN(t)\left(1 - \frac{N(t)}{K}\right)$$
and let's assume I know $K$. Let's imagine I have a mouse and I inject it with a dose of Shiga-toxin producing Escherichia coli (STEC). After 24 hours, the mouse dies, and I measure STEC with qPCR, obtaining a value of 20 million cells.
Can I calculate how many bacteria were in the initial shot, $N_0$?
And how many parameters do I need to know? For instance, let's say the mouse simply died some times after the injection. Can I know $N_0$ even if the absence of the time parameter?
How do I calculate $K$?
Is the logistic equation valid for live models? I understand it is good for chemostats, but is it valid for a mouse. Of course, a mouse can also reach saturation, since if $K$ is reached, the mouse dies, as in the example. Or is it a better description for bacterial growth in animals?
Thank you

can you link any study which shows quantification of bacterial numbers using qPCR. I just want to see how it is done.

The second here https://pubmed.ncbi.nlm.nih.gov/?term=bacterial+load+by+qpcr&ac=no&user_filter=Review&schema=none&size=100 explains also how to make the standard curve for the quantification...

For the logistic equation,
$$\frac{\mathrm{d}N(t)}{\mathrm{d}t} = rN(t)\left(\frac{K - N(t)}{K}\right)$$ the solution that allows you to calculate population population size at any time is:
$$N(t) = \frac{N(0)Ke^{rt}}{K - N(0) + N(0)e^{rt}}.$$ Looking at this equation algebraically with a set of knowns—$K$, $t$, and $N(t)$—and a set of unknowns—$r$ and $N(0)$—we see with this one equation that we have two unknowns, which are the intrinsic rate of growth and initial population size. So, the short answer is there is insufficient information to know the initial population size without additionally knowing the intrinsic rate of growth.
Hopefully this makes intuitive sense as well. If we know what the population size is, we just don't know how fast it arrived at that value. The intrinsic rate of growth could be small with a large initial population size on one extreme of the intrinsic rate of growth could be large with a small initial population size.
Calculating $K$ is problematic since $K$ is a maximum value. Better would be to use the original Verhuslt logistic equation, where the parameter $\alpha$ represents the decrease in population growth rate as a function of individuals added to the population:
$$\frac{\mathrm{d}N(t)}{\mathrm{d}t} = rN(t) - \alpha N(t)^2.$$
Note here that is the same if equation if $K = r/\alpha$. In the $K$ equation, $K$ is conflated as both a maximum and an equilibrium, which is never the case in real populations or any extension of the logistic model (e.g., including harvest or species interactions).
There are many single-species models of growth. The equation is valid, depending on what's done with it. The logistic equation is a generalized model that is elegant in the sense that is simple and has relative high qualitative explanatory value. But if you are looking to forecast population dynamics or look at bacterial populations among populations of mice, then there are many different and preferred approaches that are more mechanistic, predictive, and realistic. HTH.

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What is the mechanism behind cats' geolocating homing behavior?
Some cats, which are separated from their home, have the ability to travel back to their original home - even over long distances and land that they haven't encountered before. E.g., see the Time article on the mystery of the geolocating cat or the following blog entry.
Based on the material above there seem to have only been some suspected mechanisms a few years ago.

It is explained with path integration in behavioral neuroscience. Not only cats, but other mammals, birds and even insects use path integration to return to a starting point.
Here is a relevant excerpt from the book Beyond the Cognitive Map: From Place Cells to Episodic Memory (by A. David Redish):

Path integration is the ability to return directly to a starting
  point (sometimes called a home base or reference point) from
  any location in an environment, even in the dark or after a
  long circuitous route (Barlow, 1964; Gallistel, 1990; Maurer and
  Seguinot, 1995). Sometimes called dead reckoning, this ability
  has been shown in gerbils (Mittelstaedt and Mittelstaedt, 1980;
  Mittelstaedt and Glasauer, 1991), hamsters (Etienne, 1987, 1992;
  Chapuis and Scardigli, 1993), house mice (Alyan and Jander,
  1994), rats (Tolman, 1948; Alyan et al., 1997; Whishaw and
  Maaswinkel, 1997), birds (Mittelstaedt and Mittelstaedt, 1982;
  von Saint Paul, 1982), and even insects (Wehner and Srinivasan,
  1981) and arthropods (Mittelstaedt, 1983), as well as dogs, cats,
  and humans (Beritashvili, 1965).
Path integration in animals has been the subject of argument
  for more than a century, including a notable debate in 1873 between
  Alfred Wallace and Charles Darwin in which Wallace suggested
  that animals find their way back via sequences of smells
  and Darwin argued that animals must be using dead reckoning
  (see Wallace, 1873a, 1873b; Darwin, 1873a, 1873b; Nature, 1873;
  Forde, 1873; Murphy, 1873). The carefully controlled experiments
  of Mittelstaedt and Mittelstaedt (1980) and Etienne (1987) have
  demonstrated conclusively that this ability is a consequence of integrating
  internal cues from vestibular signals and motor efferent
  copy.

emphasis mine
Cats, dogs and rodents can use taxon navigation as well along with path integration. Here is a relevant excerpt from Neural compass or epiphenomenon?
Experimental and theoretical investigations into the
rodent head direction system (by Matthijs van der Meer):

“Internal allocentric” navigation. This type of navigation relies on a mapping of praxic commands to an allocentric spatial representation, allowing the animal to make a direct return to a home base after a complex outward path in the absence of cues, an ability referred to as path integration, discussed in detail in the next section. Returning by following an odour trail back, or navigating to a cue indicating the home base would be taxon navigation, but behavioural experiments have provided convincing evidence that rodents are able
  to do this without using external cues. As mentioned above, this ability requires some mechanism of continuously updating at least one’s directional heading (a “homing vector”) relative to the home base. This is an allocentric representation which does not need to be related to any external cues, unlike the next class of strategies; the reference point or direction can in principle be set to any location the animal desires.

emphasis mine
Further reading:

A connectionist model of path integration with and without a representation
of distance to the starting point (ROLAND MAURER, University of Geneva, Geneva, Switzerland) - Copyright 1998 Psychonomic Society, Inc.

Thank you for your great answer - and the introduction on a topic, I didn't know before! Happy that you getting the reward. For the sake of this Q&A site, I will accept the answer if the Beritashvili book indeed shows path integration in cat. As the above review appears to be the only place with a strong claim on path integration in cats, I'd like to assess, if there is direct support, or if there only is circumstantial support (which would still be sufficient to be listed in a focused review / book).

The book of Beritashvill (original source) does not speak about cats' geolocating behavior. - Nor does it establish a link between cats' geolocating behavior and path integration. - The source cited above, Beritashvill, talks about "image-based" behavior that can extend to non-visual cues. While Beritashvill makes some valid case for "image-based" behavior in cat regarding fear, the detailed experimentation on spatial orientation are with dogs. The only observation on cats is one experiment with a blindfolded cat, which can be conditioned to find food 2m away if carried in a box.

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What allows grass eaters to digest cellulose?
Scientists are saying that it was a small step for the Panda to move from a meat diet to a grass diet. The article only refers to differences in the Panda's skull, presumably for better chewing.
I've also heard that the Japanese are able to digest Nori because they have the right gut biome because Nori has been part of their diet and the appropriate bacteria has developed over time.
Does that suggest that if the cellulose of bamboo and other grasses were pre-chewed by mechanical means and the right bacteria were introduced into the human gut that we would likewise be able to digest grasses?
Related story

fresh foods contain the right bacteria, especially if they are fermented of left to get a bit old in the right way. taboulet and grass salad after a few days would contain colonies of bacteria that digest grass and taboulet.

There are edible varieties of bamboo, which are used in Asian cooking.

You might find the answers to a similar previous question interesting:
Human Digestion of Cellulose?
Summary of those answers: It seems that some humans do host cellulose-digesting symbiotic bacteria, and do digest some of their cellulose.  According to Cellulose and the Human Gut, finely ground cellulose with low lignin content is most readily digested by humans who host the right bacteria.

Note if you read the linked answer humans digest an insignificant amount of the cellulse they ingest. The problem  is the human gut is to short and has nowhere to house the bacteria to allow long term breakdown. bacterial digestion is slow.

Hi John.  You might find the paper I linked interesting.  In some cases - e.g. the digestion of cabbage in some individuals - it appears that up to 75% of the cellulose was digested.

The only paper you link is about tiny amounts of a single type of purified cellulose It does refer to a paper that has little to do with digestion, cellulose need to be broken down and absorbed, that study never controlled for large intestine breakdown which is not absorbed. this is why some animals like rabbits use coprophagia to digest cellulose.  Cabbage is also a domesticated crop with low fiber content.

No there is something else missing besides bacteria
humans often already have the right bacteria but they don't digest most of the cellulose they ingest because digesting cellulose with bacteria is SLOW. Too slow to keep up with normal mammalian digestion. You need a specialized gut that  either has a large complex stomach to keep recycling the cellulose in the system (foregut fermenters) or has large storage chambers to keep the cellulose a long time and allow it to be digested slowly (hindgut fermentation).
humans have neither. To make matters worse Humans have huge caloric needs compared to other animals of the same size. Brains are calorie hogs and our brains are so large they consume 1/4 of all our calories. That is 3 pounds of our mass consumes a quarter of all the calories we eat. honestly without the advent of cooking (which drastically improves the caloric availability of food) human brains could never have reached the size they did.
Further reading
More further reading

What about panda bears? Do they have said requisites?

Just barely, that would by why they have to eat so much compared to other herbivores,  bears already have a longer digestive track than humans, and the giant panda has expanded the stomach and intestines further. but they are still only able to barely survive. https://www.theguardian.com/science/2015/may/19/hard-to-bear-pandas-poorly-adapted-for-digesting-bamboo-scientists-find Note human have a much higher caloric demand than an bear of the same size our brains are calorie hogs.

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text:
If humans had cellulase would they be able to digest grass?
Cellulase is an enzyme capable of breaking cellulose. If humans were able to produce cellulase in our stomach would we be able to digest grass? If not, what more things would we need in order to digest grass?

Related: https://biology.stackexchange.com/q/59205/24354

No. Even for an herbivore, digesting grass, or plants to be more general, is hard, because they contain cellulose. Herbivores have different parts of a stomach, whereas humans only have one compartment, so in herbivores, the plants (or grass) enter the first part of their stomachs called the rumen, which contains a salty solution that breaks down cellulose, then, the herbivore will regurgitate the processed food, or cud, from the rumen, into their mouths, and break down the cellulose even MORE. The cud then enters back into the rumen and then digests as normal. So even if a human had cellulase, they would need a rumen, to break down the cellulose further.

But I have read somewhere (I can't find it) that some monogastric animals (with a one compartment stomach), specially small herbivores animals are able to diggest cellulose with a lesser efficiency than rumians animals. Futhemother cellulase, what another things have them to diggest it without a rumen?

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text:
If a dead animal is electrified, will it decay?
I was walking past some power lines today, and a flying fox (like a small furry bat, for those who don't know Australian fauna) had grabbed onto two adjacent power lines, closing the circuit, and as such died due to electrocution.
That got me thinking about whether or not the animal would decay in this situation. As far as I understand it, decay is caused by bacteria and other micro-organisms. Could they survive in this high-voltage environment? If not, will this poor flying fox be perfectly preserved until the next blackout occurs?

even if all the bacteria on and in the flying fox die, as soon as he hits the ground there will be plenty more organisms joining.

Environemental factors will degrade it (wind-water etc.). For the decaying part, good question sir. But from what I know, electricity will follow a certain shortest path inside the body to close the circuit. The rest shouldnt be electrified and bacteria will be alive.

@Always Confused "but never read about electrified environment". Bioelectrochemistry is actually a field of research. Microbes can exchange electrons with solid electrodes. If interested, you can search for Microbial Fuel Cells or Microbial Electrolysis Cells. Of course it's rather low voltages and currents, but still, there are a lot of exciting applications.

Degradation doesn't necessarily require bacteria to start. Death would stop oxygenation and feeding of cells, cell lysis would occur, and decomposition would start. add surviving/environmental bacteria and nature takes its course.

Environemental factors would degrade it (wind-water etc.).
But from what I know, electricity will follow a certain shortest path inside the body to close the circuit. The rest shouldnt be electrified and bacteria will be alive.
Bacteria are indeed not resistant to high levels of electricity and would die of it. The current would need to traverse the Entirety of the animal to kill every single bacteria which is highly improbable. Leave one alone, it will reproduce fast.
From what I researched, a constant electrical current of the power of an electric line would cook the animal in a short time. The flying fox you saw probably didnt have live current traversing him anymore and died from a quick jolt (this is a guess only).
Even in the extreme case that 100% of the bacteria would die, the dead animal would be recolonized by bacteria really fast. Even in the wires, wind or animals would carry bacteria.
Power lines are probably protected from arcing this way through anything that could touch them. Imagine if they werent, trees touching them would burn, shoes you throw and hang on them would be calcinated etc.
Off-topic: Are you sure he wasn't only sleeping on his improvised power-line hammock ? :P
Sources:
Conduction of Electrical Current to and Through the Human Body: A Review
Effects of high electric fields on microorganisms I. Killing of bacteria and yeasts

https://www.youtube.com/watch?v=eczDpGiULLo

Note that that paper used 25 kV/cm (2.5 mega V/m - the si unit) - this is way way higher than all but the very highest voltage transmission lines. I think you will find that the reason is purely cooking (high temp) and then desiccation. Trees that touch powerlines can indeed burn and short out lines.

Let me first point out what is harmful about electric current:

alternating (ac) current in the range of 20-200Hz is dangerous, because (even for miliampere current values) it may interfere with the oscillations of heart, causing fibrillation and subsequent death, if the normal blood circulation is not restored within a short period of time. This is typically the cause of death in the domestic accidents associated with electricity (leaving apart falling form a ladder when getting shocked).
direct (dc) current is harmful only at high values, such as 1 ampere and greater. These are rare in domestic conditions, but not uncommon in industrial setting. In this case the current flowing through the body simply paralizes miscles, leaving the eprson conscious, but unable to release the wire. The harm results from being heated by currents, resulting in lethal burns.

Touching the electric power line certainly involves the ac effect, and in some cases may imply the dc effect as well. If the animal simply died from the heart fibrilation, the damage to its tissues due to the current is virtually non-existent, and it will decay normally. If the current was high enough to cause burns, then the current stops once the tissues along its path carbonize and stop being conducting. Burned tissue is inorganic matter, which is of little interest to micro-organism. However, anything that was not burned, will decay normally.
Some also these relevant posts:

Why does electric shock freeze up muscles?
Why does an electric shock contract the muscle?


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Are there any arboreal mammals which eat leeches?
Are there any tree-dwelling mammals which might be found taking a living leech and eating it?
(And do any hollow-dwelling birds of prey eat leeches?)

I'm not an ecologist, but doesn't arboreal mean they live in trees? Since leeches are found in water, where would an arboreal mammal find a leech? There are grub eating mammals in trees, and I assume if they found a leech they could eat it. And how are birds involved in this question?

I guess they could meet in the water? Even koalas are known to drink from streams or lakes. I was going to say that leeches are also known to climb trees to drop on their victims but apparently that's a myth.

Arboreals are known to have food that is easily available near their habitats...trees...leeches if available for consumption up there, would obviously be consumed!

First I'd like to point out that there are over 500 species of leeches. Most of them live in fresh water (nearly 90%), and so most tree-living animals would not come into contact with these leeches. Because of this a leech's biggest predator would be fish.

According to The New World Encyclopaedia the predators of leeches are fish, crayfish, turtles, birds, frogs, dragonflies, and damselflies. It states that many of their predators have also been their prey. Ecospark also adds snails and other insects to the list. Biokids also points out that leeches will eat other leeches.
Britannica cautions humans about swimming and drinking water with leeches in it. They can attach to internal cavities - such as the nose and throat and then the leeches can drop into the lungs and cause suffocation. In Asia, it is common for a domesticated animal to die in this fashion.
According to Animals.mom.me monkeys and other omnivorous animals will eat leeches that live on land, but land leeches aren't very common. After over an hour of searching various websites and information about leeches, there is no other source stating that mammals eat leeches.
However, it is possible to eat leeches. They did it on a television show called Fear Factor (video of the leeches being eaten linked). Before you go eating leeches though, remember these people were monitored both during and after ingestion of the leeches.
Short answer: There are no recorded mammals as predators to leeches, but it is known that pets have eaten leeches (as well as breathed them in). And humans are also able to eat leeches. It's all about if the leech is within grabbing distance when the mammal is hungry.


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How does lactulose cause the removal of ammonia from the colon?

Lactulose is also used to reduce the amount of ammonia in the blood of patients with liver disease. It works by drawing ammonia from the blood into the colon where it is removed from the body.
[Source]

How is ammonia removed from the colon?
From the quote above it sounds like ammonia removal must be some other mechanism than absorbing it into the blood, correct?

I'd imagine it would be defecated out.

@RoryM: Do you mean that ammonia would be dissolved in the liquid content of the stool? A stool with ammonia smell?

It's an interesting one, the BNF states that it "discourages the proliferation of ammonia-producing organisms" in the GI tract rather than pulling ammonia into the gut lumen, I'll perhaps write a full answer when my exams are out of the way :)

and from MRHA "Lactulose is used to
treat hepatic encephalopathy by reducing the pH of the colon causing ammonia to form
in the colon, thereby reducing blood-ammonia concentrations."

@RoryM: This sounds most logical to me so far! I believe if the colon pH is reduced then ammonia (that is alcalic) will be dissolved as ammonium ions, stay trapped in dissolved form and defecated. I would definitely accept your comments as an answer!

@RoryM: Also thanks for the sources. I found the BNF at https://www.medicinescomplete.com/. But how can I access the MRHA source you quote?

MRHA approval document though you can also just enter lactulose as a search term at mhra.gov.uk.

@RoryM Could you perhaps turn your comment into an answer? It seems like an interesting discussion and a valid answer. The question is on its way to deletion.

Excess nitrogen must be excreted by the body and can come from nitrogen in the diet (e.g. amino groups from excess amino acids) or nitrogen-containing compounds produced by bacteria in the gastrointestinal tract (GI tract).
Normally the liver and kidneys are involved in excreting ammonia ($NH_3$) and ammonium ($NH_4^+$) from the body. Ammonia can be toxic in high concentrations, but the body can detoxify it through conversion to other nitrogen-containing substances (i.e. urea) or excrete the ammonia itself.
Ammonia in the blood is freely filtered at the kidney glomerulus and can be "trapped" in the urine flow by accepting a proton to become ammonium (i.e. $H^+ + NH_3 = NH_4^+$) . Because of the positive charge the ammonium ion is unable to passively diffuse back across the tubules into the blood. This is one mechanism that ammonia is excreted. In the liver, the Urea Cycle (see any basic or clinical biochemistry text for more information) is a set of enzymes that converts most of the excess nitrogen in the form of ammonia to urea, which is a non-toxic, water soluble organic compound that can also be excreted in the urine. The body uses these processes to dispose of excess nitrogen from amino acids as well as ammonia that is produced as a by-product of bacterial metabolism in the GI tract.
Some patients with significant liver disease (e.g. cirrhosis from either NAFLD, hepatitis or any other liver-damaging disease) have lost the ability to convert all the excess ammonia to urea. In these patients, an easy way to prevent excessive nitrogen uptake in the gastrointestinal tract is by treating them with lactulose. Lactulose is a carbohydrate that that is not digestible or absorbable by the body, but is osmotically active (pulls water into the intestinal lumen) and acts to speed up intestinal transit. Since lactulose works by speeding up GI transit it makes you stool more frequently (which is why it is very useful for constipation). For liver disease patients, however, the lactulose acidifies (i.e. decreases pH) the lumen of the intestines and ammonia is protonated to form ammonium, which effectively traps it in the intestinal lumen. A lot of the excess ammonium can then pass into the feces and decrease the amount of ammonia that the liver needs to process. This is similar to the mechanism of ammonium in the urine as mentioned above. Additionally, lactulose also decreases the amount of GI bugs that produce ammonia containing compounds as well, which also lessens the amount of ammonia for detoxification by the liver. (Lactulose can also be used for a treatment for small intestinal overgrowth). These GI bacteria metabolize dietary amino acids and other compounds in the gut for energy metabolism, which liberates nitrogen-containing compounds that can be absorbed by the intestines.
Edit: Here is a link for a great reference on NCBI that explains the mechanism of action of lactulose.

This answer is good, but it could be still better with references.

Reference:  See "Mechanism of Action" - - https://www.ncbi.nlm.nih.gov/books/NBK536930/


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Why are red blood cells considered to be cells?
Wikipedia states that a cell is

the basic structural, functional and biological unit of all known living organisms. Cells are the smallest unit of life that can replicate independently.

It then goes on to state that

All cells (except red blood cells which lack a cell nucleus and most organelles to accommodate maximum space for hemoglobin) possess DNA.

Then why are red blood cells still considered cells, while they can't replicate? Is the definition on Wikipedia just a bad definition? Or are red blood cells wrongly considered cells, but remain so for historical reasons? Or are they considered cells for some other reason, such as this answer which states that red blood cells do contain a nucleus at some point?

that's why they are referred to as corpuscles

Many fully differentiated cells can't replicate: neurons, for example.

Animals such as birds and amphibians have nucleated red blood cells...

The most prominent other non-nucleated corupscules are platelets. If you consider why they aren't called "cells", you'd arrive at the conclusion that it's something to do with one RBC originating from one precursor by eliminating its nucleus, rather than one precursor producing lots of non-nucleated membrane bubbles (i.e. megakaryocytes). Then again, jargon calls platelets thrombo-"cytes" ;)

A very good question, and it is most likely because of the last option.  It had a nucleus for part of its life. After the RBC jettisons its nucleus, it still remains very metabolically active for approximately 3 months.  It maintains its cell membrane integrity, it metabolizes glucose, it interacts constantly with its environment, numerous cellular functions and structure remain intact...  It is extremely specialized for a primary purpose, and no longer requires the nucleus to provide more proteins.  It has limited capacity to heal from injury, so it has a limited life span.
Speculation:  I wonder if it might lose the nucleus early on so that when it is destroyed in the spleen at the end of its life as RBCs are, the spleen macrophages are not overwhelmed with additional processing of nucleic acids?  Macrophage type cells are already working hard in there to clear infectious agents and some immune cells from the blood.

I'd say it's much more likely eliminated simply to free up the space. The nucleus is a massive organelle and takes away lots of space the cell could fill up with haemoglobin.

I definitely agree with @Armatus about space being the likeliest explanation for the early loss of the nucleus. Also keep in mind that the total "nuclear flux" (and the processing load of the waste from that flux) would be the same whether the nuclei were lost early or lost late


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Is it better to take a half dose of paracetamol and a half dose of ibuprofen together rather than a full dose of either?
Recently, I heard on this health-related radio programme that it was better to take a half dose of paracetamol and a half dose of ibuprofen together, rather than the full dose of either one, for acute pain. Could anyone explain the reasons for this ? Could it be something along the lines of there being diminishing returns to higher doses, so you get more bang for the buck, as it were, for the first half of a dose than the second, but due to possible toxicity or drug interactions, two full doses are not recommended ?
In the same radio programme it was stated that caffeine also helps. Can anyone explain that ?

Welcome to Biology.SE! As stated in the FAQ, we cannot furnish medical advice on this site. I think this question is borderline on-topic for this site--as long as answers to this question focus on the biological reasons as to why some treatments may or may not be better than others, it should be fine, but if the discussion in any way deviates to discussing the clinical benefits of one treatment vs another, we will have to shut it down.

By "better" I take it you mean a more effective analgesic rather than better in terms of potential toxic effects, speed of onset/offset etc?

Hello and thanks for the welcome. I am not asking for medical advice - sorry if that was the impression I gave. I am curious from a scientific perspective. I am interested from both the efficacy and toxicity point of view.

It would help your point to remove the personal anectdote

a start for someone researching the answer: http://en.wikipedia.org/wiki/Analgesic#Combinations

Related: https://medicalsciences.stackexchange.com/q/4052/12704

There are many different reasons for an acute pain and inflammation (both directly via pain receptors, and indirectly via swelling etc.) plays not the least role in this phenomenon. Therefore the combination of a classic analgesic without anti-inflammatory activity (as paracetamol) with a strong anti-inflammatory agent (as ibuprofen) is a reasonable one and potentially alleviates the pain manifestations in more cases than a single administration of every agent.
You are right with you suggestion that the doubled dose could be dangerous: even though the complications of Paracetamol administrations are not often, they are very dramatic (acute liver failure) with rather pessimistic prognosis. This is why one generally tries to half the doses if combined with other similar-acting agents (historically paracetamol was for the long time a member of the non-steroid anti-inflammatory agents).
Caffeine is generally believed to be a pain reliever, especially as concerns the pains with migraine background (source). One review, however, points out that there are still not enough data to support this belief (source).

Whilst Alexander Galkin gives some great information, I think there's a fundamental reason why that particular pain relief strategy is best, and it hasn't been mentioned yet.
The reason is simply that when you take Ibuprofen or Paracetamol (a full dose) you can only take it once every 4 hours. However, the pain relief doesn't last for 4 hours, so if you take either or both together every four hours you will experience pain after the medication wears off and before you are allowed your next dose.
So instead you can follow either of two strategies:

Take a full dose of Paracetamol at 0 hours, 4 hours, 8 hours, as well as taking a full dose of Ibuprofen at 2 hours, 6 hours, 10 hours. This will give you less time when no pain medication is in effect. But if your pain is inflammation related you might want to keep the anti-inflammatory effects of Ibuprofen topped up, so you can...
Take a half dose of Paracetamol + a half dose of Ibruprofen every 2hours. This gives you a mix of pure pain relief and anti-inflammation and ensures minimum time when each medication has no effect.

I don't think human biology has to come into it (apart from the fact that you can take the two substances together with no ill effects), it's just a good pain-avoidance strategy.

Can you provide evidence that taking a full dose of paracetamol every 4 hours equals taking half dose every 2 hours? And that the pharmacokinetics of paracetamol are not influenced by ibuprofen?

The only reason why caffeine helps with migraine pain is because the pain is caused by expanded blood vessels and caffeine's effect is to narrow the blood vessels.
But how it helps with other types of pain I really  can't imagine.
And it depends what you state as "full dose". The dose that can harm your liver for adults is 4g per day, so if you have Paracetamol 500mg you would have to take 8 pills  to reach it. Would you possibly do it? If seeing pain doesn't go away after first pill .. ok, second one?

You should consider referencing your answers with appropriate sources where facts are not commonly accepted as fact.


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How much influence does toxoplasmosis have on personality and intelligence?
Latent toxoplasmosis affects up to 1/3 of the human population and up to 40% of the population in Australia.  I have heard that latent toxoplasmosis has many significant undesirable effects on personality, such as decreased novelty-seeking behaviour, and decreased intelligence quotient.
While these changes are statistically significant, I'm wondering if anyone knows the magnitude of these personality and cognitive changes, since a statistically significant result doesn't necessarily imply that there is a large difference in personality between those who are infected and those who aren't infected.  Also, can one succeed in an academic career path if one becomes infected with toxoplasmosis?

Do you have some sources for this wide-spread infection? Would be interesting to read.

Heaps of sources, have to go now, but i'll post later.  Just search on google or google scholar in the mean time if you want to.

@Chris in France pregnant women are routinely tested for toxoplasmosis, since contracting it for the first time during the pregnancy may pose risks to the child.

@Kenshin scientific research or simple interest in studying can be also characterized as a "novelty-seeking behaviors" ;)

I believe its the other way around - humans may engage in riskier and more novel behavior when infected... which is the most interesting part of the story.  Its not cut and dried, but I think its quite possible that risky behavior increases.
T. gondii is a parasite whose typical life cycle includes both mice and cats as hosts.  The transmission involves the mice being eaten by a cat.  Mice infected with T gondii will tend to lose some interest in being sheltered in close spaces and wander out into open spaces.  They also lose their fear of cats.   That is a permanent change even if the mice are cleared of the parasite.
Other animals, such as humans are secondary hosts - they can become infected by handling or close proximity to cat feces, who have a nearly 50% (45.6%) infection rate themselves. As a result toxoplasmosis is very common in humans.
Toxoplasmosis has been found to increase novelty seeking and increases risk seeking behavior at least in men.  Its been shown to contribute to higher automotive accident rates, schitzophrenia and suicide.

Thus, the men were more likely to disregard rules and were more expedient, suspicious, jealous, and dogmatic. The personality of infected women, by contrast, showed higher warmth and higher superego strength (factors A and G on Cattell's 16PF), suggesting that they were more warm hearted, outgoing, conscientious, persistent, and moralistic. Both men and women had significantly higher apprehension (factor O) compared with the uninfected controls.

The correlation between toxoplasmosis and lower intelligence is a matter of debate, at least in this review I cite.  Its still not clear whether it is a sociological correlation - do smart people just handle their cat poo more carefully or not at all? This more recent study shows that some factors might make infected humans more intelligent and some researchers see toxoplasmosis as a transformative factor in humans ability to generate and use technologies.
I do see those links suggesting less risky behavior too.  Some say that the increase in traffic accidents is related to lower muscular coordination for instance.  There is evidence on both sides, but looking at what T gondii does to mice, I would bet that some risk behavior will increase.  As such, I'd guess that researchers as such might have a slightly higher rate of toxoplasmosis, but maybe you will do a study and help figure this out!
That being said - anyone who tries to link a single phenomenon; host-parasite interactions; a drug; a gene; a mutation to a phenotype with a simple description is definitely oversimplifying.  The mapping from biological activity to english (or any other language) is hopefully conscious of the caveats of such talk.

Thanks for your answer shigeta.  I find it interesting because many of the links I had seen say it lowers novelty seeking behaviour.  http://www.sciencedirect.com/science/article/pii/S0301051103000759.  http://web.natur.cuni.cz/~flegr/pdf/toxonovelty.pdf

let me add a comment in the answer here - you are right of course, but its not a simple yes/no thing.  I'll be a little more clear about this.

It is my understanding that toxoplasmosis can increase productivity and the brain's ability to understand things. It is when there is a toxo flare that behaviors can become irrational and angry. Knowing this can help as well as being in touch with when you are experiencing a flare. Knowing what range you have, if its active, and what supportives you will need to get it under control should help.
The Revolving Therapies have the best chance of putting folks into remission according to the following information:
*Together with the result of the checklist, the significantly positive Toxoplasma LTT overruled the result of the antibody assays and justified prescribing a combination therapy from the beginning on. This resulted in a good amelioration of symptoms. When the effect of this therapy decreased after 10 days, the significant toxoplasma LTT result backed the decision for a Revolving Therapy, which finally led to a very good remission of all symptoms. *
https://en.toxoplasmachronic.com/2-faelle-mit-positivem-ltt?fbclid=IwAR2VknK1asw1OoWuedVpRi_TOGaxjDsf6LxWoLM7HKPfxZaHe3AIf1YI5N4


text:
Why do we have no enzyme to digest cellulose?
As we know, cellulose is the most abundant polysaccharide in nature. Why don't we have an enzyme to digest cellulose?

Evolution doesn't make everything perfect.

I removed the line about evolution making things perfect. It is obviously wrong. Try watching an albatross land for example and tell me that they're perfect.

The question is really: "Why can't humans OR bacteria easily digest cellulose". It's very hard! Ruminants need a large, specialized bioreactor and to chew food for hours, "ordinary" gut-and-microbes won't do. If a bacterium found a quick, efficient way to digest cellulose it and it's animal host(s) would mow down forests (until trees evolve another defense that is).

While it's true that cellulose is full of calories, it's very difficult to get the calories out.
Symbiotic bacteria take ages to digest cellulose, and as a result animals that digest cellulose with specialized symbiotic bacteria have a huge gut to house them in.
It's likely that the reason humans can't digest cellulose is because mammals generally can't. And mammals generally can't because it's way too much work, and we don't need to.

"mammals generally can't"?

Even ruminants that eat grass and so on mostly just let bacteria eat the cellulose then digest the bacteria.

Are there animals who can digest cellulose without the help of bacteria?

Some termites, but I think that's it.

@Resonating imho your answer would improve, if you incorporated your comments.

This seems one form of a common question about evolution.
That being: "Trait X would seem to be an advantage, so why can't organisms adapt to X?
That is, why don't we have all traits that are advantageous at all?  Why not just digest cellulose, but maybe why not lignin as well?  Why shouldn't we photosynthesize our own food?  What about sonar as well as eyes?  We know that some living thing can do all these things.
The answer, somewhat mentioned elsewhere here, is that some advantages are not enough for the adaptation to take hold.  You have to consider that there is a cost to each such ability as well.
Cellulose is energy poor and any animal which relied on cellulose would have to specialize in cellulose metabolism to the point that they might not compete against fellow animals that got their food from other sources like meat or vegetables.
thanks for the comment below:  addendum:
energy poor in this case is a combination of how common the material is, how advantageous it is to digest (woody plants don't grow back very quickly once you eat them up).  i don't know why i wrote that there are not cellulases.  there are plenty of them and we use them a lot but they tend to be from slow growing fungi...
if you want to follow your question to the conclusion : "celluose digestion is a huge advantage in all respects" then the question is why aren't they in every bacteria that grows around plants?  because evolution is not how cellulases are created?
in fact woody plants include other materials supporting their structure to prevent this eventuality.  lignin is a non carbohydrate semirandom fiber based on phenols that is indeed very slow to digest and difficult to get at with an enzyme... at the moment it does seem to be enough to prevent plants and paper celluose from dissolving and being eaten...

You make a good point. I think these questions also come from the wrong perception (which was evident in the original version of the question) that evolution is finalistic towards making a species "perfect".

we make the same mistake when we buy cars too - a V8 2 ton pickup with back seats and i'll have the perfect car - it can do anything! But in biology a tiny fly is perfect and so is a rock clinging piece of lichen...they just do what they need to do well enough

shigeta, I agree with nico, evolution does not make things "perfect". Not by a long shot. Living organisms are a mess, riddled with hopelessly inefficient mechanisms. Think Rube Goldberg machines. It's nowhere close to what a decent designer would have come up with, but it's what you get from random mutation + selection. This more general question probably deserves an answer in itself ...

there's lots of shades of meaning here, which is definitely interesting to talk about.  Organisms are so optimal for selected traits that they amaze and astound us - better than we can design ourselves in many cases.  Where selection has not had as much pressure (e.g. long life, resistance to damage and disease, empathy, speed, intelligence) it can seem that they are strangely vulnerable.

"Cellulose is energy poor" Excuse me? You're basically saying glucose is energy poor. You should specify that it's "energy poor" in the sense that it's resistant to enzymatic breakdown or something (I don't know if that's the actual reason, it's just what I'm assuming based on other answers in this thread.)

energy poor in this case is a combination of how common the material is, how advantageous it is to digest (woody plants don't grow back very quickly once you eat them up).  i don't know why i wrote that there are not cellulases.  there are plenty of them and we use them a lot but they tend to be from slow growing fungi...

Why don't we have any enzyme to digest cellulose?

Why should we?  We don't use it as a source of energy so why bother?  Even animals that do "digest" cellulose, like ruminants, only do so because of symbiotic bacteria; it would be a poor system indeed in which every organism utilized the same resource.  We occupy enough of the food chain as it is.


text:
How does the microbial environment in your gut initiate?
Clearly, a zygote does not harbor any microbes. As it develops, and the alimentary canal tissue is differentiated, I logically assume that there is still no microbial activity in the fetus's gut. I'm thus also assuming that the commencement of microbial activity in the intestines occurs after birth, but when, and how?
Do newborn babies just happen to ingest only certain e.g., E.coli strains? Is the gut a selective environment in which only certain E.coli strains develop?
Are there any mechanisms to ensure that harmful bacteria do not initially reside in the gut? Is a newborn's digestive tract particularly unstable and ineffective until the proper microbes are established?

The gastrointestinal tract of a normal fetus is sterile. During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. Immediately after vaginal delivery, babies may have bacterial strains derived from the mothers' feces in the upper gastrointestinal tract.[15] Infants born by caesarean section may also be exposed to their mothers' microflora, but the initial exposure is most likely to be from the surrounding environment such as the air, other infants, and the nursing staff, which serve as vectors for transfer.[16] The primary gut flora in infants born by caesarean delivery may be disturbed for up to six months after birth, whereas vaginally born infants take up to one month for their intestinal microflora to be well established.[citation needed] After birth, environmental, oral and cutaneous bacteria are readily transferred from the mother to the infant through suckling, kissing, and caressing. All infants are initially colonized by large numbers of E. coli and streptococci. Within a few days, bacterial numbers reach 108 to 1010 per gram of feces.[16][17] During the first week of life, these bacteria create a reducing environment favorable for the subsequent bacterial succession of strict anaerobic species mainly belonging to the genera Bifidobacterium, Bacteroides, Clostridium, and Ruminococcus.[18] Breast-fed babies become dominated by bifidobacteria, possibly due to the contents of bifidobacterial growth factors in breast milk.[19][20] In contrast, the microbiota of formula-fed infants is more diverse, with high numbers of Enterobacteriaceae, enterococci, bifidobacteria, Bacteroides, and clostridia.[21][22] By the second year of life, the fecal microflora resemble that of adults (wiki source).

The initiation of gut flora come from maternal cervical and vaginal flora (Bezirtzoglou, 1997)1. These predominantly include facultative anaerobes (e.g., Staphylococcus, Enterobacteriaceae and Streptococcus). Birth by caesarean section can cause problems because these bacteria are not passed on in the  usual manner.
Vael et al. (2011)2 found an association between early gut flora and obesity later in life

High intestinal Bacteroides fragilis and low Staphylococcus
  concentrations in infants between the age of 3 weeks and 1 year were
  associated with a higher risk of obesity later in life.

suggesting that monitoring or alterations of gut flora might be effective in reducing rates of obesity.
Bezirtzoglou E. 1997. The intestinal microflora during the first weeks of life. Anaerobe 3:173-177.
Vael, C., Verhulst, S.L., Nelen, V., Goossens, H., Desager, K.N. 2011. Intestinal microflora and body mass index during the first three years of life: an observational study. Gut Pathog 3: 8.


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Introductory literature for synthetic / systems biology
I am a computer engineer (MSc in Computer Engineering) who's looking to switch into the field of synthetic / systems biology. I have a comprehensive layman's understanding of evolution, genetics, transcription, etc, but my academic studies have been in the areas informatics, computer science, computer engineering and mathematics.
Does anyone have a good recommendation for standard literature in the field, to get me up to speed?

An Introduction to Systems Biology By Uri Alon.

Systems Biology
Wingreen & Botstein who run the graduate systems biology course at Princeton wrote a paper about how to teach the subject (Wingreen & Botstein, 2006). In the paper they highlight the key concepts they think are crucial to understanding modern systems biology, and they teach the course through discussion of seminal papers in the field.
Here's the reference...
Wingreen, N. & Botstein, D. (2006) Back to the future: education for systems-level biologists. Nature Reviews Molecular Cell Biology. 7 (11), 829–832.
The paper is unfortunately not open access, so for those who can't access the paper  edit: @uvesten found a free PDF copy! I have listed their choices below, along with the key concept they think each provides...
Robustness (i.e. retaining function despite fluctuations)
Barkai, N. & Leibler, S. (1997) Robustness in simple biochemical networks. Nature. 387913–917.
Evolutionary perspective
Eisen, J.A. (1998) A phylogenomic study of the MutS family of proteins. Nucleic Acids Res. 264291–4300.
Microarray analysis (and more generally, the importance of data visualisation)
Eisen, M.B., Spellman, P.T., Brown, P.O. & Botstein, D. (1998) Cluster analysis and display of genome-wide expression patterns. Proc. Natl Acad. Sci. USA. 9514863–14868.
Individuality of elements in a system:
Elowitz, M.B., Levine, A.J., Siggia, E.D. & Swain, P.S. (2002) Stochastic gene expression in a single cell. Science. 2971183–1186.
Maximum likelihood
Felsenstein, J. (1981) Evolutionary trees from DNA sequences: a maximum likelihood approach. J. Mol. Evol. 17368–376.
Ultrasensitvity
Goldbeter, A. & Koshland, D.E. (1981) An amplified sensitivity arising from covalent modification in biological systems. Proc. Natl Acad. Sci. USA. 786840–6844.
Biophysical modelling
Hodgkin, A.L. (1958) Croonian Lecture, ionic movements and electrical activity in giant nerve fibres. Proc. R. Soc. Lond. B. Biol. Sci. 1481–37.
Specificity
Hopfield, J.J. (1974) Kinetic proofreading: a new mechanism for reducing errors in biosynthetic processes requiring high specificity. Proc. Natl Acad. Sci. USA. 714135–4139.
Random processes and distributions:
Luria, S.E. & Delbruck, M. (1943) Mutations of bacteria from virus sensitivity to virus resistance. Genetics. 28491–511.
Stable switching between states:
Novick, A. & Wiener, M. (1957) Enzyme Induction as an all-or-none phenomenon. Proc. Natl Acad. Sci. USA. 43553–566.
Sequence similarity
Smith, T.F. & Waterman, M.S. (1981) Identification of common molecular subsequences. J. Mol. Biol. 147195–197.

Synthetic Biology
A good place to start in this subject is the Synthetic Biology network:

Syntheticbiology.org
iGEM.org
BioBricks.org

With some google-scholar-fu I found this link: http://www.princeton.edu/genomics/botstein/publications/2006_Wingreen_Back.pdf Is that the correct article?

That's the one, good job finding a pdf :)

Downvoters should have to leave comments. How can I improve the answer? Simply downvoting without commenting is not a positive contribution.

And http://DIYBio.org!

I have a similar background (CS switching to systems biology) and I learned a great deal by reading "Systems Biology: A Textbook" by Edda Klipp et al [1]. It's a very good overview of different sub-areas and it's written in a way that's friendlier to a technical mind than most other bio-related books (i. e. concise, to the point, not shy with formulas). The section about experimental techniques is a real treasure, at least for me getting used to the ways in which we can look into cells was the biggest challenge.
Another text you might look into is "An Introduction to Systems Biology" by Uri Alon, but it's very dynamic modelling-oriented and will give you less of an overview.
[1] http://www.amazon.co.uk/Systems-Biology-Textbook-Edda-Klipp/dp/3527318747/ref=sr_1_1?ie=UTF8&qid=1339413559&sr=8-1
[2] http://www.amazon.com/Introduction-Systems-Biology-Mathematical-Computational/dp/1584886420

There is a recent published book, from Garland Science for systems biology
http://www.garlandscience.com/product/isbn/9780815344674
and a clasic textbook: Physical Biology of the Cell
http://www.garlandscience.com/product/isbn/9780815341635

I've been working to prepare a synthetic biology curriculum for non-biologist and have found a great resource in Prof. Scott Mohr's (BU, Chemistry) "Primer for Synthetic Biology" available here:
http://openwetware.org/images/3/3d/SB_Primer_100707.pdf

Many people switch to systems biology from a math/physics/computer science background and may need a cell biology textbook to update them on general biology knowledge.
*For molecular biology knowledge:*A comprehensive and reliable biology text on the graduate level is "Molecular Biology of the Cell" by Alberts:
http://www.amazon.com/Molecular-Biology-Cell-Bruce-Alberts/dp/0815341059/ref=sr_1_1?ie=UTF8&qid=1361575051&sr=8-1&keywords=molecular+biology+of+the+cell
*For biochemistry knowledge, especially related to metabolic pathways:*A more Biochemistry focused textbook is the one by Voet&Voet, which is very comprehensive:
http://www.amazon.com/Biochemistry-BIOCHEMISTRY-VOET-Donald-Voet/dp/0470570954/ref=sr_1_1?s=books&ie=UTF8&qid=1361575189&sr=1-1&keywords=voet+biochemistry


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Are there dog breeds that are so far apart genetically that they can't produce viable offspring?
Obviously, a very large dog would have difficulties mating with a very small dog and vice versa.

But putting that problem aside (using, say, insemination), considering the large variation of dog breeds, are there any two breeds that are so different genetically that they can't produce viable offspring together?

Isn't that what distinguishes species from breeds/races? Whether they can reproduce with each other?

Wolves can breed with dogs, still they are considered different species.

@Zano: wolf and dogs are the same species (canis lupus), different subspecies (canis lupus familiaris vs canis lupus lupus). Dogs are domesticated wolves.

@nico: Fair enough.

I think many people believe that "species" is a clear boundary between organisms. This is NOT the case. And dogs and wolves absolutely breed and produce viable offspring.

I actually found some sort of reference for this.  Apparently in the case of a beagle and irish setter pairing, they had a lot of difficulty in producing pups, but as breeds have a lot of genetic quirks, this might be due to a genetic accident; this is probably a case of mutual infertility rather than speciation.  There are probably mutations in their genomes which are causing non viability in the pups the way that it does with some human parents who have difficulty having children - an immunological incompatibility or traits which cause most offspring non-viable.
In fact the discussion points out that the species designation does not always mean they cannot produce offspring, but simply do not.  Coyotes and wolves will produce offspring too if they are encouraged to do so, but are competing and antagonistic in the wild and so never do mate in practice.
So the answer is probably no. (the beagle/setter pups did show up, but with a much smaller litter than usual with just 2 pups).

I was looking for something like this. The definition of species was never an issue as far as I was concerned.

The domestication of Canis lupus (which gave Canis lupus familiaris -> dog) has given rise to a great morphological diversity from a common genetic material.
Some dog breeders might tell you that when the male is from a much larger breed than the female, mating is difficult, and delivery will probably happen by C-section. I have heard it but do not have very serious sources.
This is the closest I can think of something which would represent a reproductive isolation which might give rise to speciation if these breeds of dogs were left to chose their mates.
Some breeds of dogs have been selected for such morphological traits that 80 % of births happening within their breeds are delevered by C-section anyways. It is the case of the boston terrier and both the french & english bulldogs (source in French : Lignées, n° 3, septembre 2010 - SFC (Société Francophone de Cynotechnie)).
Dogs and wolves do not have different numbers of chromosomes, as is the case between horses and donkeys which do not produce a fertile offspring for example. Dogs and wolves are not considered separate species. They do interbreed and their progeny is viable and fertile.
Note however that how species are defined is still a matter or debate, and that the use of the criterion of reproductive isolation is an indicator people use among others.
See for example the Green Frogs complex.

There are in fact a few dogs that cannot breed.
African (spotted) painted dog, cannot breed with Dingos, nor wolves.
They are too far apart in the evolutionary line to produce viable offspring.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

African wild/spotted/painted dogs/wolves are a completely separate genus (Lycaon) from ordinary dogs (Canis), so are not dogs as such, rather just another member of the Canidae family, so not expected to be able to interbreed. Much like humans (Homo genus) can't produce offspring with a chimpanzee (Pan genus) even though we are in the same family (Hominidae) and even within the same subfamily Homininae.


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What is it called when one human eye is seeing brighter color than the other?
What is the name of a phenomenon where one of the human eyes is seeing brighter/more saturated color than the other? I can observe the same object from the same position while alternating which eye is closed, and there's a visible difference in the saturation of color. Like one color is more pale than the other.
Here's an example of what the difference looks like between image perceived by two eyes:

Interesting question; I've also noticed this but it's been that way my entire life. ♂

here is forum discussing similar effect ,
where as similar problem which leads to double vision is single eye is called monocular Diplopia.
There are two possible causes discussed in that forum. One is a cataract or an early indication of a cataract, for which a vision specialist visit is recommended.
Another solution is much simpler one of the pupils is more dilated than the other:

The way your eyes see colors changes throughout the day, not dependent
  only on external conditions. Try this: gently press the palm of your
  hand against one eye (closed), for about a minute; leave the other eye
  open during this time (feel free to blink, of course...). Now, look at
  the world with one eye covered (for a couple of seconds), then the
  other — the eye you help closed will see things as quite more
  saturated, partly because you've fostered its pupil to dilate in the
  time during which it was shut. I recall being confused by this when I
  first started noticing that, upon awaking, either eye would see colors
  differently from the other; simply, the eye rested on the mattress
  would be seeing colors with greater saturation.

Could you add some details to your answer useful to the questioner, in case that link goes away in the future?

I also noticed this phenomenon after laying on a mattress with one side of my head against the mattress. I don't recall which side had most brightness, but the answer sounds correct

So is it because our eye needs time to adjust back to the standard brightness or is it connecting to the "pressing"? (I suspect covering the eye is sufficient)

The phenomenon in question is anisochromatopsia, however this term is rarely used. This phenomenon is always present, however it is rarely mentioned subjectively, while objective color testing will reveal it easily.
In pathologic state, the term Color Desaturation is being used defining that the previous status of color vision has changed to "abnormal" one. The causes to this change could be multiple, for example the most common one Optic neuritis in Multiple sclerosis.


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Are there any pathogenic archaeans?
Most textbooks seems to restrict pathogens to the domains bacteria and eukarya. Are there any pathogenic archaeans?

To date, there isn't a single species that may be considered pathogenic to animals or plants. There are archeon who live in association with animals (in the case of human, they have been found in the gut microbiota aswell as certain skin surfaces) that are mainly methanogens. This could lead to think that archaons could produce "pathologic farting", but that condition has never been described.
In the case of ascidians and other marine invertebrates, some archeon have been found living in symbiosis, with the microbe aiding the animal by means of nitrogen fixation. One could think that, since they're able to live inside the organisms, they could behave as opportunistic pathogens, but none has been described.
Furthermore, it actually exists at least one known species who could be classified as parasitic, the nanoarchaeota Nanoarchaeum equitans, which has been described as a symbiont of some hyperthermophilic archaeon. Despite that description as symbiont, Nanoarchaeum cannot live by its own, while its companion does. Moreover, its genome contains the typical traits associated to parasitism, with great reduction in genome size and loss of many key pathways and cell functions, including methabolic pathways an even some key components of its transcriptional and translational machinery. Since there is no known function of the Nanoarchaeum itself, it should be considered as a parasite.
However, the lack of evidence may be biased, since few people has used metagenomic approach to look for archeon in clinical samples, and some rare cases may be found in the future.

I have to disagree with the comment "Since there is no known function of the Nanoarchaeum itself, it should be considered as a parasite." It is an obligate partner of its Ignicoccus host, and genome reduction occurs in beneficial symbionts as well.  There is currently no evidence either way, so it should not be assumed to be one way.  In the original papers on its discovery it was shown that Ignicoccus growing with Nanoarchaeota reached the same cell densities as Ignicoccus alone.  It is quite possible that in their natural environment nanoachaea play a positive role in the symbiosis.

Actually, there exist at least one reference to a negative effect of Nanoarchaeum towards its host. Jahn et al (2008) describes that single Ignicoccus cells wich had more than two Nanoarchaeum cells attached were unable to grow, while those with two or less could form a colony.
It's true that there isn't strong evidence to considere Nanoarchaeum as a parasite in the traditional sense, provided this is the only reference I have found to a negative (or positive) effect of this archeon. It's also true that even traditional symbiots such as micorhizic fungi can be harmful in certain conditions, and because of that, this lonely example wouldn't be representative. However, untill this reference there were the same evidence to consider this archaeon as a symbiot or as a parasite, and for unkown reasons the first hypothesis was assumed by default. This results sugest that Nanoarcheum is potentially harmful and, since there still isn't any evidence that demostrate that Nanoarchaeum has any benefit, I strongly believe the consideration of a putative parasite should be encouraged and used as the default hypothesis.
Some authors prefer to use the term "intimal association", and they define it as "a highly specialized system combining characteristics of symbiosis, commensalisms, and parasitism" wich tries to be something neutral beween the two hypothesis. However I find that expression unnecesary, confuse and with an strong lack of meaning; mainly because that kind of relationship can be described with classical ecologycal terms.

The conclusion to the paper you are referring to states: "However, the fact that I. hospitalis and N. equitans build a stable coculture without sustained damage to the Ignicoccus population clearly distinguishes N. equitans from the bacterial parasites mentioned above. Therefore, we propose that the association of I. hospitalis and N. equitans represents a highly specialized system. Consequently, assignment to the classical category of symbiosis, commensalism, or parasitism might not be possible even in the future."  It is confusing, but thats the nature of the system.

I agree that their isolation experiments are interesting, and point towards a negative interaction, but their data shows that: "N. equitans had no inﬂuence on the doubling times, ﬁnal cell concentrations, and growth temperature, pH, or salt concentration ranges or optima of I. hospitalis."  This does not seem like the characteristics of a parasitism, and I don't think there is a reason to choose a default when there isn't enough data either way.  For others: http://jb.asm.org/content/190/5/1743


text:
Do lions crabwalk?
Cats turn sideways arch their back and puff their fur, to apppear bigger, when trying to intimidate someone. Do lions do that? What is the largest feline that does that?

As apex predators who can also run away if necessary, it would seem to be an unnecessary tactic.

with a mane turning sideways might actually make you look smaller.


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What is the difference between an antibiotic and an antibacterial?
Concerning medicine, what are the differences between antibiotics and antibacterials?

An antibacterial is any compound that will kill or at least slow down the growth of strictly bacteria, a domain of prokaryotes.
An antibiotic is often used synonymously, but denotes a compound that kills or slows down the growth of any cellular pathogen, prokaryotic or eukaryotic. So, certain antibiotics can kill bacteria, fungi and parasites but antibiotics have no effect on viruses and prions.

Just to add to your answer: bacteriostatic agents slow down the growth of bacteria, whereas bactericidal agents kill it.

Waksman defined antibiotics as being produced by other living organisms. http://www.acs.org/content/acs/en/education/whatischemistry/landmarks/selmanwaksman.html

Can resistance form from anti bacteria from people using soaps etc to clean bathrooms or kitchens. I only ever hear resistance being due to poor use of anti biotics not anti bacteria?

The word antibiotic refers to metabolic products (chemical compounds)
 of one microorganism that has detrimental or inhibitory effect to another microorganism. These are kind of chemotherapeutic agents used for treatment of infectious disease or disease caused by proliferation of malignant cells.Although some are prepared synthetically but most of them are prepared by microbial synthesis for commercial purpose. The treatment of one antibiotic differs from another by its mode of action. Antibiotics also can have broad spectrum and narrow spectrum of action and it is also possible that out one antibiotic is more active than other antibiotic against a particular pathogen and the effect is more impressive. Antibiotics can be antibacterial ( only and only against bacteria, either inhibition, destruction or suppression of bacteria. E.g. Bacitracin), same way some antibiotics are antifungal like Nystatin and some may show antitumor activity anthramycin. Antibiotics sometimes also have non-medical use like growth stimulants in poultry and live-stock feeds.
Whereas Antibacterial agents are those agents which "specifically" show their action against bacteria. (broader spectrum of action than antibiotic) They can act bacteriocidal (agents which kill or destroy bacteria) or bacteriostatic (agents which hinder the normal growth and reproduction of bacteria without killing them). Antibacterial agents can be  metabolic compounds of microbes (antibiotics), they can be physical agents like radiations, heat (at particular temp that can kill only bacteria) or antibacterial agents can also be chemical by nature like alcohols,halogens (Iodine, chlorine, chlorine compounds).
So we can say that antibiotics can be antibacterial agents but all antibacterial agents need not be antibiotic.

Could you add references?

http://amrls.cvm.msu.edu/pharmacology/pharmacology and chapter 24, Antibiotic and other Chemotherapeutic agents from the Microbiology book  by author Michael J. Pelczar, JR.

Antibiotics are a broader range of antimicrobial compounds which can act on fungi, bacteria, and other compounds. Although antibacterials come under antibiotics, antibacterials can kill only bacteria.
Penicillin was the first discovered by Alexander Fleming antibiotic and antibacterial.
There are certian classes of compounds which are bacteriostatic, which will not allow bacteria to grow (Ampcillin kills dividing cells) in number.

Could you clarify the middle sentence ("Penicillin was..."), it's ambiguous and I wasn't sure what to make of it.

Penicillin was discovered by a Scottish scientist and Nobel laureate Alexander Fleming in 1928. Later Selman Abraham Waksman discovered another antibiotic named Streptomycin.

Yes, thank you, I meant it's confusing whether it was the first discovered by him or the first discovered.  I don't believe it was the latter.


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When did the most recent common ancestor of all living domestic dogs live?
Wikipedia provides a very detailed page on the origins of the domestic dog, but this fact does not seem to be present there. Google searches for terms such as "most recent common ancestor (MRCA) of dogs" didn't reveal any authoritative sources.

As Remi.b points out, the where and when of the ancestor of the domesticated dog is not well known.
Based on a review by Morell (2015), the ancestor of the domesticated dog (canis familiaris) was a now extinct wolf that gave rise to Fido 11,000 to 16,000 years ago. The author bases this conclusion mainly on data from Freedman et al. (2014). Interestingly, Freedman et al.'s data indicate that it was not the Gray Wolf (Canis lupus) that gave rise to Fido, which was long thought to be the one and only ancestor. The ancestral extinct wolf is thought to have give rise to present-day dogs, Dingoes and the Chinese, Israeli and Croatian wolf. The Golden jackal split off earlier, around 400,000 years ago.
Complicating the search for Fido's ancestor is the widespread occurrence of wolves and dogs, which makes it difficult to pinpoint the location of origin. Indeed, there is indication that canids were domesticated not once, but multiple times at different places, just like the domesticated pig was domesticated twice. Moreover, there is indication of gene flow between wolves and dogs after Fido split off, further blurring the available evidence (Morell, 2015).
A recent 2015 special issue on dogs and cats in Sci Am may shed more light on this, but I have to get to that. Will update this answer if appropriate!
References
- Freedman et al. Plos Genetics; 10(8): e1004631
- Morell, Sci Am (2015): 313(1): 60-7

From the wikipedia article you linked:

The origin of the domestic dog (Canis lupus familiaris or Canis familiaris) is not clear. Whole genome sequencing indicates that the dog, the gray wolf, and the extinct Taymyr wolf diverged at around the same time 27,000–40,000 years before present.

They cite Skoglund et al. 2015.
It seems that divergence between the grey wolf and the dog started at Taymyr (northern Russia) about 27,000–40,000 years ago. Therefore, the MRCA of all dogs and grey wolf today would have lived about 27,000–40,000 years ago. Tito et al. 2013 estimated canids fossils found in Europe were 39,000 years old. We currently don't have a better accuracy and we are not able to date the MRCA of all dogs with more accuracy than the MRCA of grey wolves and dogs.

Your answer tells us about the most recent common ancestor of of the grey wolf, dogs, and the extinct Taymyr wolf. My question asks about the most recent common ancestor of all living dogs. Although related questions, I do not believe they are identical.

You are right, I was a little inaccurate in my answer. I added another study showing evidence of canid fossil found in Europe. With this (and many other findings shown in the wiki article) we understand that we don't have the sufficient fine scale to date the MRCA of all dogs more accurately than the MRCA of grey wolves and dogs.

authors: user1205901 - Слава Україні