text:
What is the difference between absolute and relative fitness?
It's seems to me that the definition of relative and absolute fitness is not that clear.

Absolute fitness[edit]
The absolute fitness (W) of a genotype is defined as the proportional
  change in the abundance of that genotype over one generation
  attributable to selection. For example, if  ${\displaystyle n(t)}$ is
  the abundance of a genotype in generation t in an infinitely large
  population (so that there is no genetic drift), and neglecting the
  change in genotype abundances due to mutations, then[4]
  ${\displaystyle n(t+1)=Wn(t)}$. An absolute fitness larger than 1
  indicates growth in that genotype's abundance; an absolute fitness
  smaller than 1 indicates decline.
Relative fitness[edit]
Whereas absolute fitness determines changes in genotype abundance,
  relative fitness (w) determines changes in genotype frequency. If N(t)
  is the total population size in generation t, and the relevant
  genotype's frequency is ${\displaystyle p(t)=n(t)/N(t)}$, then
  ${\displaystyle p(t+1)={\frac {w}{\overline {w}}}p(t)}$, where
  ${\displaystyle {\overline {w}}}$ is the mean relative fitness in the
  population (again setting aside changes in frequency due to drift and
  mutation). Relative fitnesses only indicate the change in prevalence
  of different genotypes relative to each other, and so only their
  values relative to each other are important; relative fitnesses can be
  any nonnegative number, including 0. It is often convenient to choose
  one genotype as a reference and set its relative fitness to 1.
  Relative fitness is used in the standard Wright-Fisher and Moran
  models of population genetics.
Absolute fitnesses can be used to calculate relative fitness, since
  ${\displaystyle p(t+1)=n(t+1)/N(t+1)=(W/{\overline {W}})p(t)}$ (we
  have used the fact that ${\displaystyle N(t+1)={\overline {W}}N(t)}$,
  where  ${\displaystyle {\overline {W}}}$ is the mean absolute fitness
  in the population). This implies that ${\displaystyle w/{\overline {w}}=W/{\overline {W}}}$, or in other words, relative fitness is
  proportional to ${\displaystyle W/{\overline {W}}}$. It is not
  possible to calculate absolute fitnesses from relative fitnesses
  alone, since relative fitnesses contain no information about changes
  in overall population abundance

That's good when we are talking about genotypes or phenotypes. But
when we are using models, e.g. fitness landscapes, how can we
translate that? For example, if I have a linear fitness landscape
(made with a linear function), then the "fitness" value that I find
with the model are "expected fitness" or $\widehat y$. Thus in this
case, it's the "fitness of all possible phenotypes, based on the
population fitness and phenotypic information". Are we calling this
relative or absolute?
When fitness, or one of its components, is calculate from a model
(say a mark-recapture model), which type of fitness is computed? In
Marc Kéry and Michael Schaub (2012) Bayesian Population Analysis using WinBUGS: A Hierarchical Perspective, they are showing models
to compute survival probabilities based on a recapture history.
Would that be relative or not?
What are the distinction of the 2 definitions, and are they too restrictive when we want to extend them to models that calculates the fitness of a all the individuals in a population?

See also, Endler, J.A. (1986) Natural Selection in the Wild.
On page 168 of the book:

Mean absolute fitness: $\overline {W} = [∑ƒ(X)W(X) ]/[∑ƒ(X)]$
ƒ(X) frequency of genotype or phenotype X
Absolute fitness: $W(X)$
Relative fitness: $w(X)= W(X) /\overline {W}$
Therefor, $\overline {w}(X)=1$

Relative fitness can also be measured with reference to a particular phenotype (or genotype), in which cas $\overline {w}$ is not necessarily 1; this is the most common method used for polymorphic traits. If the population is sampled twice (or more) within a generation so that individuals in the second sample represent a subset of those sampled in the first sample (as in a capture-recapture or cohort study), then absolute fitnesses can be calculated. Examples are the probability of surviving between samples, or the probability of mating. On the other hand, if samples are made without replacement, or if samples are made of juveniles and adults at a single time, then only relative fitness can be calculaqted; information on total numbers and mean fitness is lost (see discussions in O'Donald 1971, Horns and Harrison 1970, and Manley 1974).)

On page 42 of the same book:

Adaptedness and Adaptation. Adaptedness is the degree to which an
  organism is able to live and reproduce in a given set of environments:
  the state of being adapted (Dobzhansky 1968a,b). Adaptation is the
  process of becoming adapted or more adapted (ibid.). Unfortunately,
  adaptation.is also used in the sense of an adaptive trait (Lewontin
  1978), confounding the end product with the process (see also Dunbar
  1982). An adaptive trait is "an aspect of the developmental pattern
  of the organism surviving and reproducing" (Dobzhansky 1956, 1968a).
  There are problems in defining precisely what adaptednedd is so that
  it can be measured (Dobzhansky 1956, 1968a,b; Stern 1970; Lewontin
  1978; Dunbar 1982). One solution is to define it in the sense of
  absolute (rather than relative) fitness (Table 2.1). In this case it
  can be measured by the average absolute lifetime contribution to the
  breeding population by a phenotype or a class of phenotypes. It thus
  becomes intimately related to the actual (R) or intrinsic $(r_{m})$
  rate of increase, or "Malthusian parameter," and these have actually been used as measures of fitness for populations and species, though there are some problems (Fisher 1930; Dobzhansky 1968a,b; Dunbar 1982). Adaptedness has also been defined as the mean absolute fitness (Sober 1984). [...]

Bonus: I'm trying to recreate the equation from Lande and Arnold 1983. But it's not working. I don't know what is not correct (the line where you see     (mean.rel.fit = mean(w.relative.fit)), this result should give 1, but it's not in my case. I don't know why):
# W: Absolute fitness
# w: relative fitness

set.seed(12)
nb.data = 5000
y = rnorm(nb.data,10,2)
x = 1:nb.data

# This should look normal
hist(y,
     breaks = 30)

# To have a mean of 0 for phenotypes scale the phenotypes
z.raw = y
z = scale(z.raw,
          center = TRUE,
          scale = TRUE)

hist(z,
     probability = TRUE, # In stead of frequency
     breaks = "FD",      # For more breaks than the default
     col = "grey", border = "black")
lines(density(z),   # Add the kernel density estimate (-.5 fix for the bins)
      col = "firebrick2", lwd = 3)

# Normally distributed trait, Phenotypic distribution (normal)
p.z =function(z) {
  z.mean=mean(z)
  sigma = sd(z)
  1/sqrt(2*pi) * exp((-1/2)*((z-z.mean)/sigma)^2)
}

# This is not working! It's suppose to be normal
hist(p.z(z),
     breaks = 30)
rnorm(nb.data,10,2)

# Linearly distributed absolute fitness function
W.z =function(z) {
  slope = 1
  intercept = 0
  e=(z*slope+intercept)
  (e-min(z))/(max(z)-min(z))
}

# There is a linear relationship between trait z and Absolute fitness W
plot(z,W.z(z))

de = density(z,
             n = 600000)
require(zoo)
# If n = 600000 in the density function, then it should ~=1
sum(diff(de$x[order(de$x)])*rollmean(de$y[order(de$x)],2))

duplicated(round(z,1))
df.z = as.data.frame(table(round(z,1)))
values = as.numeric(as.character(df.z$Var1))
frq = as.numeric(as.character(df.z$Freq))
frqcy = function(len){frq[1:len]}

f = function(values)(W.z(values)*frqcy(length(values)))
(mean.absolute.fitness = integrate(f,
                                   subdivisions = 2000,
                                   rel.tol = .Machine$double.eps^.05,
                                   lower = min(z),
                                   upper = max(z))
)

# Relative fitness
w.z <- function(z) {
  W.z(z)/mean.absolute.fitness$value
}
(w.relative.fit = w.z(z))

# This should be 1
(mean.rel.fit = mean(w.relative.fit))

w.relative.fit
f2 = function(z)(z*w.z(z)*p.z(z))

(mean.absolute.fitness = integrate(f2,
                                   lower = min(z),
                                   upper = max(z))
)

Before answering, I suggest reading this SE post.

I'm not totally convinced in this post. The definition on Wikipedia changed. It is no longer "the ratio between the number of individuals with that genotype after selection to those before selection". Also, it seems there is a confusion with the fitness components and the measure of fitness when looking at relative vs absolute. In my mind, the absolute fitness can be larger than 1 for sure.

Relative fitness is "relative" so that it's supposed to be between 0 and 1. That's a ratio.

The reason why relative fitness is between 0 and 1 is because it's in relation to the highest performing individual (genotype). You take the frequency of the best performer and divide all others by that value, where the highest performer has a relative fitness of 1 (because it's being divided by itself), and all others are less than or equal to 1. This process can also be considered as "normalizing" the dataset.

Exactly, so the relative fitness is based on the absolute fitness in which the most "fit" is used to bound the relative fitness between 0 and 1. It's not necessarily based on the most frequent (the most frequent genotype or phenotype is not necessarily the most fit...)

Relative fitness uses the genotype with the highest survival/reproduction rate for calculations. Whether or not this actually represents the "most fit" genotype, is another question all together, as you've pointed out. This is exactly why evolutionary biologists are much more concerned with relative fitness models. However, relative fitness is calculated using the genotype with the highest frequency count (the maximum survival/reproduction rate). See here for an example.


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Questions about what a productive cough actually is and where it comes from
When I'm sick with a productive cough, what is the stuff I'm coughing up, is it coming from my lungs, and if so how come it doesn't hurt a lot and trigger a violent cough like if I got even a single drop of water down the wrong hole.

When I'm sick with a productive cough, what is the stuff I'm coughing up (?)

If we're talking about a productive cough, you're most likely coughing up mucus, which is a thick (highly viscous) liquid that functions as both a lubricant to the internal behaviors of the body, as well as a defense against foreign particulates from getting too far within the body (e.g., breathing in dust through the nose and preventing it from traveling into the lungs).

is it coming from my lungs (?)

Mucus is produced all throughout the respiratory tract by mucosae. However, since you're talking about coughing up mucus (as apposed to it running from your nose), it's probably originating from the lower respiratory tract. So, yes!, it's quite possible that the mucus is coming from your lungs.

how come it doesn't hurt a lot and trigger a violent cough like if I got even a single drop of water down the wrong hole (?)

Hmm.. I think this is a bit more difficult to address. First off, as previously mentioned, mucus has a much higher viscosity than water does. Because of this, it could be that water more violently moves around while being coughed up, whereas mucus may remain more intact, thus causing less (increased) agitation.
It could also be that, because the trachea (the "wrong hole") isn't as accustomed to coughing as the esophagus is, then increased sensativity is experienced (relative to what's felt when coughing within the esophagus).

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If a ubiquitously ill species existed, would that more or less falsify evolution?
It is true that a lot of members of our, and most other species, suffer from cancer, but it is still not ubiquitous nor does it exist throughout the individual's life.
If a species existed, in which all, or almost all of its members suffered from the same pathology, and that pathology showed up and existed throughout the organism's life, and this pathology has always existed within the species, would that violate natural selection enough to consider the current body of theory of evolution falsified?
To be clear, it is recognized that natural selection is not the only process which occurs during evolution, but it is pretty safe to say that enough of our body of theory on evolution rests with the validity of natural selection that if natural selection were falsified, so would the body as a whole, and we would need to rework our theories.
Consider what is said in Evolutionary dynamics in structured populations.

An evolving population consists of reproducing individuals, which are information carriers. When they reproduce, they pass on information. New mutants arise if this process involves mistakes. Natural selection emerges if mutants reproduce at different rates and compete for limiting resources.

In other words, evolutionary dynamics implies natural selection. A violation of natural selection therefore would make the current theory on evolutionary dynamics less likely. Now, it could be that other processes are so powerful that they completely override natural selection, but to find a species in which natural selection has totally failed to weed out a near universal illness should present a problem for current evolutionary theory.

If the disease/illness does hinder the fitness of the species, natural selection has no pressure to stop it.

Although I think @Remi.b's points about selection not being the same as evolution clearly show that this question is misguided, you could argue that aging is a ubiquitous illness that has some selection benefits. Overall, though, this question sounds like it's intended as a trap.

I am not conflating natural selection with evolution, but if natural selection is falsified, then so would evolution, at least as we view it now, which means that our entire body of theory would have to be reworked.

@vasshu Natural selection is only one process by which evolution occurs. There is also genetic drift, gene flow, and mutation. Even if natural selection is falsified, it would not falsify evolution since there are other ways evolution occurs.

True, but natural selection is a consequence of evolutionary dynamics. To see it fail to function, even in one species, would present a problem.

The question is non-scientific and imprecise. The phrase "natural selection is a consequence of evolutionary dynamics" is either wrong or ill-defined. At best, the implication is backwards, and even then only a partial truth. Natural selection is merely the fact that different entities survive differently. This can contribute to evolution, if e.g. there is a mechanism for heredity. As for the question underneath, the answer is no. Evolution is limited by its substrates and environmental factors. That is why we still have cancer, age-associated diseases, etc... which are indeed near-universal.

The question is non-scientific and imprecise. The phrase "natural selection is a consequence of evolutionary dynamics" is either wrong or ill-defined.

I mean, I paraphrased a scientific paper on the topic, but sure. Okay.
As for cancer, etc, I specifically pointed out that I am not addressing conditions, such as aging, which are not necessarily able to be "weeded out" by natural selection. However, even in those situations, the affliction is not ubiquitous throughout most of the life of the organism. The organism does not start off elderly.

Very short answer
Evolution ≠ Natural Selection
Slightly longer answer
Evolution ≠ Natural Selection
You seem to equate evolution with natural selection which is the main issue. Various evolutionary processes may yield a population where all individuals suffer from a specific disease. It may not be an equilibrium state though but a state that may well last long enough to be frequently observed.
For example a bottleneck can cause a disease to reach an extremely high frequency if there was some deleterious recessive alleles in the parent population. A bottleneck is not a process that is encompass within the term Natural Selection but it is still an evolutionary process.
We actually have examples (incl. examples in humans) of populations where the prevalence of particular genetic disease is very high.
The existence of other evolutionary processes than natural selection does not violate the theory of natural selection
The existence of other evolutionary processes than natural selection does not violate natural selection theory. The theory of natural selection does not state that nothing but natural selection can affect a population's evolution.
If one were to think that the existence of genetic drift (another evolutionary process) would violate natural selection, then this person would also think that  the existence of wind that would affect an apple course falling through the air would violate the theory of gravitation.
What is evolution?
Your question comes from a misrepresentation of what evolution is about. You might want to have a look at a short and intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

I did not mean to equate the two, although our current theory of evolution is heavily dependent on natural selection. As for my understanding, I have a fair amount of bio behind me, including evolutionary biology and bio-archaeology.

You got close with the vague reference to diseases w/ high prevalence, but this is not the same as ubiquitous existence and expressed throughout the individual's life.

Can you please expand on diseases w/ high prevalence [..] is not the same as ubiquitous existence and expressed throughout the individual's life? I don't understand it. Do you mean high prevalence is not the same as prevalence of 1? You can have a prevalence of 1 and that would not change anything. Fixed deleterious alleles are really not uncommon.

Cancer, for instance, occurs in many individuals, but it is not something that almost every individual lives with for its entire life. It occurs within a fraction of the population for a fraction of the organism's life.

Evolution doesn't ensure a good quality of life, nor does it ensure a longer lifetime of a species's organism.. It only aims for the continued sustenance of the species in a changing environment.
What does being ill really mean?

Does it mean that the lifespan becomes smaller? No, an insect might have a smaller lifespan while being a very rapidly evolving life form.
Does it mean that the species would be pain-free while living? No, even humans are designed to endure chronic pain.

All the things that contribute to not being "ill", are really just things which contribute to being able to have a faster and continuous sustenance. Long life means more chances of offsprings, being pain-free gives more time and ability to mate.
Hope this answers your question! First post. This thread made me join this exchange!

Evolution [..] defines continuous sustenance That is a little unclear but sounds pretty wrong. Selection (and other evolutionary processes) does not necessarily minimize the probability of extinction.

You are right, I should change that to "Aims to" rather than "Is defined by".

Even "aims" would be wrong. Evolution is not conscious being attempting to do anything. You could say "tends" to avoid the agent view of evolution but even then, it would be misleading. Evolution does not necessarily tend to minimize extinction probability nor does it tend to increase individual's lifespan (whatever you mean by sustenance). A genotype decreasing the group mean absolute fitness to its own benefit will be selected for.

Well, I think it is agreeable that Evolution(Even though it is a phenomenon) can be attributed to doing something. For example: The Cold temperatures in the high altitudes leads to a higher chance of rain.

Evolution refers to the change of allele frequency (and phenotypic traits) in a population over time. It does not do anything (sorry that sounds like I'm being a pain in the neck with definitions but it may be important for our discussion). There are particular evolutionary processes that cause those changes, such as natural selection and genetic drift for example. But genetic drift and natural selection do not necessarily lead a species to increase its probability of survival (or whatever is meant by sustenance in your answer).

The mechanics of evolution imply natural selection.

Welcome to the site and thanks for your answer :) It's probably better to say evolution due to natural selection tends to favor continuation of the species. But, this may not always be true; evolution can be very short-sighted [e.g. the giraffe recurrent laryngeal], and allow a trait that harms the population later e.g. due to environment change (say, allowing a koala's diet followed by a disease that wipes out eucalyptus trees). Further, as Remi noted, a trait that harms the group but helps the individual can easily be selected for.

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What kind of snake is this? Seen on Koh Lanta, Thailand
We had this snake in our bungalow on Koh Lanta, Thailand. From the reaction of the employees at the resort I can tell that it is venomous, but that's all I know. I am curious, does anybody know what species it is?
Thanks and cheers, Philip!

Are you able to provide an image showing the snakes head? That would make identification much easier. Currently I'm thinking it's a chinese rat snake (quite common in Thailand), even though you said the employees are acting like it's venomous. see here for image

If the resort is near a water body then it is highly likely that it is a keelback snake.
For determining whether it is poisonous or not it is extremely important to look at the scale pattern on its ventral side(belly). Unfortunately that is not visible here.


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Why aren't drugs delivered directly into arteries, rather than veins?
Normally when drugs are administered to the blood of a mammalian subject, it is done intravenously--the needle being inserting into a vein. One potential problem with this is that the veins contain the exhausted blood which is returning to the liver and spleen. This is potentially disadvantageous because these organs could absorb the drug or be damaged by it.
It would seem more advantageous to introduce a drug to the arterial system, such as the aorta, so that the drug flows outwards to all parts of the body before returning to the filtering organs of the body.
Is this type of drug administration a known procedure. If so, why is not more generally used?

Because of the risks of putting a needle in an artery. Additionally: After a few heart strokes the drug is distributed in the blood and it is going through the liver anyway, most drugs are processed there.

Seriously, the aorta? It's not accessible, and you don't want to mess with it. Veins are used because they are low pressure and low risk. You can't administer a drip into a high pressure artery; the blood would back up into the tubing; in fact, there is enough pressure in just the radial artery to push a plunger up as it fills the syringe. Also, it would keep bleeding as long as there was a needle or tube in it. Damaging a vein is no big deal, damaging an artery is. Finally, regarding metabolism, just give enough drug to minimize the effect of first pass metabolism.

Further, most IV drugs are given through easily accessed veins such as in the arm: these return to the heart before any pass through the liver or spleen. Unless you were trying to deliver the drug to the arterial circulation of that particular hand, it's going to circulate before it gets to the target organs. And if your drug is going to damage the liver, why don't you think it's going to be dangerous for anything else? The liver isn't particularly vulnerable, quite the opposite.

Although this is a fairly basic question, I realized three very active users here put our answers in comments. Let me summarize:
1) It is risky to poke holes in any artery, let alone the aorta. Arteries are full of blood under high pressure. When you poke a hole in one, there is always some risk of serious bleeding. You also have to push against the arterial pulsatile pressure, making it more difficult to administer slow drips of drugs, as is often done with I.V. administration: either you are going to get high flow during diastole with high pressure, or you are going to get backflow of blood into the catheter during systole, or both. On the venous side, there is a lot more collateral circulation, too, so in an emergency you can usually close most veins without severe effects. Some drugs can be toxic to the local vascular environment, as well, which is again safer in a vein should it occur. Note that for some special procedures, such as angioplasty/stenting, arterial access is necessary, but this isn't true for drugs. (Thanks @Chris and @anongoodnurse)
And the aorta? Depending on body fat and where on the aorta you want to target, you are talking about a needle inches long, poking into a vessel you can't see, after passing other organs and tissues, versus veins, some of which are specially located near the surface.
2) IV drugs aren't "delivered" specifically to particular targets in the first pass: they dissolve in the blood, flow around the circulation, diffuse in and out of tissues, and eventually partition according to their binding affinity, hydrophobicity, etc. Therefore, drugs are going to go through the liver anyways. In fact, many drugs are metabolized by the liver, and some aren't even delivered in their final active form: metabolism may be required for activity, and often the liver is involved. Essentially, if a molecule isn't stable enough to make a pass through the liver, it won't be a useful drug or needs to be given in a higher dose to account for the high rate of metabolism. (thanks @Chris and @anongoodnurse)
3) Further, most IV drugs are given through easily accessed veins such as in the arm: these return to the heart before any pass through the liver or spleen. Unless you were trying to deliver the drug to the arterial circulation of that particular hand, it's going to circulate before it gets to the target organs. And if your drug is going to damage the liver, why don't you think it's going to be dangerous for anything else?

The question is not just about human beings, but about any mammal.

@ImprisonedRhesus That changes little if any of my answer - which parts do you think are human specific?

Not all mammals have "arms" for starters. Also, when the researchers give me injections, they never put the needle in my arm.

Forelimbs might as well be arms in this context. Are you getting IV injections? The veins of the arm, or hand are by far most common. If there are other targets I presume that's either directly related to the research or they are not IV.

(Still none of this affects substantially my answer - unless you are getting injections into the veins in your digestive organs or spleen that drain to the portal system, none of the blood is going directly to the liver)

@ImprisonedRhesus - Vets often do use the veins in the animal's foreleg to administer IV meds; other meds are subcutaneous or intramuscular. In humans, IM usually involves the upper arm (deltoid area) for small amounts of drugs, the buttocks or thigh for larger amounts. IV could be any vein; before picc lines, we'd even use the veins of the scalp for neonates or between the toes for adults.

A couple of things to add:

(Most important) The 'exhausted blood' in the veins isn't going directly to the liver or metabolic organs - it's going directly to the heart, to be pumped through the lungs and then returned to arterial circulation. First-pass metabolism by the liver is a concern for oral delivery, since a substantial fraction of blood goes directly from the absorptive digestive tissues (e.g. intestines) to the liver through (IIRC) the hepatic portal circulation. This isn't an issue for drugs administered IV.
In addition to the relative safety of venipuncture vs. arteriopuncture, there's also the small point of pain. Arterial puncture is done when necessary - for example, when you need a sample for blood gas analysis. This procedure is quite painful. I have had it performed on me, and I have performed it on animals when I worked in veterinary practice. So in addition to venipuncture being safer, it's also much more comfortable for the patient/subject.
What you describe in your last paragraph is kind of done, although not into the aorta. When large boluses of drugs need to be given frequently, and/or the drug in question might seriously irritate peripheral veins, you sometimes see devices like a PICC line used - a percutaneous indwelling central catheter - or for shorter durations a temporary jugular central line. These are used to deliver the drug into the vena cava - the venous analog of the aorta, if you will. Just as in conventional IV administration the blood goes through the heart, through the lungs, and back into arterial circulation, but this time it's administered in a large enough volume of blood to avoid adverse effects of dilution (large/fast bolus) or irritation.

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what is the word origin of myelo- as in myelofibrosis or myeloma?
what is the word origin of myelo- as in myelofibrosis or myeloma? I know that these are plasma cancers originating in the bone marrow.

It's greek, and brings with it the meaning: "marrow", "spinal cord", or "brain". source

I'm voting to close this question as off-topic because it is about the etymology of words and not biology.

myelo- is from Greek related to the word for 'marrow'.
See also: http://www.dictionary.com/browse/myelo-
Most cancers are named in a similar matter, with the tissue of origin followed by the suffix "-oma": glioma from glial cells, sarcoma from the connective tissues/"flesh",

medical terms are mainly based on Greek and Latin words, myel(myelo) is a root which means bone marrow and it also can mean spinal cord , it depends on the word. in myeloma , myelo means bone marrow and oma is a suffix which means tumor just like lymphom( cancer of lymphatic system ).
ex: meylitis: inflammation of spinal cord , but , myeloma : cancer of the bone marrow

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Do human women smell different before they enter labour?
Surfing youtube I found a video where a cat shows a protective behaviour towards a pregnant woman soon to enter labour.
In the miriad of average (dumb) comments I found another person stating that her cat felt precisely (via olfactory means I guess) that her (the woman's - not the cat's) day had come to give birth and started acting weirdly.
Do mammals leave a clear olfactory footprint before labour? And is this footprint noticeable by cats and dogs?
Is this definetely myth? Is this something yet to study? or is this something well known?
If the latter is the case: is it based on the sense of smell? is there anything to read to study the topic?

There is plenty of anecdotal evidence of this happening. However, studies cost money, and knowing when a woman is about to go into labor is not a particularly compelling reason to spend a significant mount of money doing a controlled study. On the other hand, predicting a seizure or detecting a cancer has some significance, and those have been studied.

Ty for the feedback. Well... I guess a lot of women would disagree on that: knowing that "today it'll happen" might be more than useful - especially in emerging countries where people can't manage a thorough monitoring of the pregnancy. And given this, the compelling reason might have also an economic basis. But I get your point.

It is not a definite myth but is a subject of much debate. However, it may well be that it is from smell (olfaction). We certainly know that cats have a significantly larger number of scent receptors, being approximately 200 million, compared to the 5 million receptors humans have. Cats also have an organ called the Jacobson's organ found in many animals that helps to pick up scents even more, especially chemicals - hormones.
As an example, the primary hormone released to progress labour is oxytocin, which causes the body to perform homeostatic positive feedback (initial stimulus is increased until an end result). This begins when the baby's head puts pressure on the cervix, which triggers contractions. This in turn starts oxytocin release which speeds up both the frequency and intensity of the contractions.
This increased concentration of oxytocin could well be what the cat is smelling as animals are well known to detect human hormones such as adrenaline in situations of fear. Although oxytocin is usually present in the body even apart from childbirth, in the moments leading up to labour and just afterwards, the oxytocin concentration is at its highest concentration. The cat probably sensed the 'abnormally' strong smell and began to behave accordingly as it recognised it from instinct (cats release oxytocin in labour too).
It's still all very hypothetical though so I don't know of any authoritative investigations for you to have a look at – it’s one of those anecdotal subjects which has yet to have any concrete evidence.


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Why are certain animals much much bigger than other ones?
If you look at the following image:

The Argentinosaurus was the largest dinosaur that ever existed. If dinosaurs came through the process of evolution, and evolution is small changes in DNA and/or mutations, how can certain species by immensely bigger then others?
Even consider the blue whale. Why is it so much bigger then other  whales. None of the others even come close to it, and same as the Argentinosaurus.
I understand if some are "a bit" bigger, but this dinosaur was the length of 3, and really the question that I want to ask is that, can evolution really make someone/something that much bigger then it's kind?

can evolution really make someone/something that much bigger then it's kind? Downvoted and tempted to flag for closing as "Unclear what you're asking".  Obviously evolution can make bigger animals, because it has made bigger animals. What is the question here? Are you asking if titanosaurs were created rather than evolved? Are you asking how dinosaurs could be so large?

Could anyone please correct the typo in the last sentence: then should be than

There is much more size variation than you seem to acknowledge!
The blue whale is actually much heavier than the Argentinosaurus was (180 tons against 90 tons).
If you are impressed by size different between humans and some dinosaurs, then you will really be amazed to appreciate of how much size variation exist.
You currently spend one orders of magnitude (2 meters for humans and 30 meters for the Argentinosaurus). If you include all of life, including bacteria, you will spend 9 orders of magnitude from ~$10^{-7}$ meters for the smallest bacteria (I excluded viruses, viroids and prions) to ~$10^2$ meters for the blue whale and the sequoia trees.
Of course, size does not mean much. Do you mean, the longest, the heaviest, the tallest, etc... A fungi might actually well deserved to be recognized as the biggest living thing on earth (see The biggest underground living animal)
You might also want to have a look at How did the huge dinosaurs cope with gravity and loads on bones?.
Evolution misrepresentation
You said

evolution is small changes in DNA and/or mutations

Evolution has brought different lineages to have DNA sequences that differ drastically. Compare an angiosperm (say a dandelion) and a bacteria (say and E. coli), you will hardly be able to align any of their DNA sequence. They are genetically completely different.
The standard saying from layman people is to say that evolution occurs through small gradual changes. Over a long period of time, such small and gradual changes end up making organism that differ a lot. The most recent common ancestor between the dandelion and the E. coli lived about 3 billions years ago (maybe more).
Now, even the saying that evolution is necessarily very slow and go through small gradual changes is quite wrong. Specific mutational event can be extremely drastic and there are period of extremely high speciation rate in a given lineage. But all of this is a story for another time!
Coming back to size, you might want to have a look at the post Do large animals often evolve into smaller animals?.

Also, changing size really doesn't seem like it should require that much of a DNA change.  Very simplistically, looking at it as a software program, there would be instructions that basically tell cells "double N times then stop" during the growth process.  So a mutation that replaces N with N+1 doubles the size of the organism.

Why has this answer bin downvoted???

@cezar I think it is being downvoted (not me!) because it appears not to answer to the question. I think Remi.b tries to say that the size range is normal.

@jamesqf except just doubling the size on an animal will not work, the square cube law forcins parts to chang in size at diffrent rates to still remain functional.

Why there are so many big dinosaurs
In evolution there is something called preadaptation or exaptation that is adaptations that have benefit in one way that happen to have another benefit after another adaptation occurs. Consider the avian breathing system which evolved in small ground running animals turns out to also make their breathing work at high altitude, this was not part of the conditions the adaptation evolved in/for but is a side benefit that is exploited later. Because there are multiple solutions to an adaptive problem and evolution has no foresight, some groups will just happen start in a better position anatomically to evolve large size.
Compared to mammals dinosaurs start out with better preadaptations to large size. mammals have a lumbar region in which all the weight is supported only by the spine while dinosaurs have ribs from the neck all the way to the pelvis, this means the torso is far more rigid, if you grow very large this helps distribute weight more efficiently. The avian breathing system (in theropods and sauropods) scales better and doesn't loose efficiency as fast as the mammalian system, air sacs allow them to better compensate for the large dead air spaces caused by large size. Air sacs also allow bones to be larger for the same weight, sauropod bones are mostly hollow where as mammal bones are either solid (or filled with something just as heavy) so if they were the same size the mammal bones will be significantly heavier. Now this is not to say dinosaurs are completely superior, live births is a big advantage for large size, but the simple anatomical advantage dinosaurs start with just make achieving large size far easier.
Why size and fossilization vary
As for why animals vary in size it is the same reason they vary in so many other respects, different solutions to the same problem, how to get your genes into the next generation, the same factors that favor different diets or anatomies can favor different sizes. A rat and an elephant are drastically diffrent is size but both are successful body plans. You are mistaken that nothing comes cclose to these animals it is just that the ones that do are dead (in the case of whales) or didn't leave fossils, keep in mind only the tiniest sliver of a fraction of organisms ever fossilize. Only one Argentinosaurus fossil is known to exist, that does not mean that 95 million years ago only one Argentinosaurus existed. Fossilization is so rare that in a population of literally billions you might only leave one or even no fossil remains. The fossil record is like taking one random photograph in paris and trying to reconstruct france we know we are missing massive amounts of what was there but it is still incredibly informative compared to not having it.
Why does size vary.
This one is simple, because selective pressures vary, different pressures favor different things, and different condition create different costs. In whales for instance the fact Blue whales have to fast for part of the year encourages large stores and thus large size, that is just one factor favoring large size.  the largest whales and dinosaurs are not significantly bigger than their ancestors, the changes in each generation is minor and usually due to changes in different developmental triggers/regulators. Argentinosaurus is big nut it is comparable to other large sauropods.

WRT fossils, it's also much easier to recognize that you've stumbled across the fossil bone of an Argentinosaurus than of its rat-sized cousin.


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Beetle Identification - Oregon
My dad found it so I don't have a lot of good information, but it was probably about 2.5 inches, somewhat west of Portland, and was found on a sidewalk. I don't know the area so I can't say what habitats are there that it might have come from.

This is a long horned beetle.. currently trying to pinpoint genus and species.

I agree that overall appearance is very longhornish. However, I cannot get the shape of the pronotum to fit with the rest of the animal (when thinking about possible tribes/subfamilies) @Charles

Too bad that the tarsal formula cannot be seen in the picture, which could rule out several families.

I think this may be a male of Trichocnemis spiculatus (Cerambycidae, subfamily Prioninae). This species is known from Western USA/Oregon, based on this key: Screening Aid for the Cerambycidae of the Western U.S.A. (from Oregon Department of Agriculture). By overall appearance, this species fits well. However, females have more pronounced spines at the sides of the pronotum, which points to a male for the individual in your picture.

(picture from http://cerambycidae.org/taxa/spiculatus-(LeConte-1851), also more pictures at bugguide.net)


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What evidence do we have that dinosaurs were mesotherms?
They went extinct millions of years ago, so what is the evidence supporting the claim that they were mesotherms? And are there any examples of modern-day mesotherms?

There are some examples in the Wikipedia page.


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Understanding the concept of a "Place Field" and the difference between place cells and grid cells
I have 3 questions that are interrelated:

After reading the proper literature on the subject, my understanding of the place field is that it's a place in space to which an animal's place cell reacts by firing. Then there might also be another place in field to which the same place cell reacts by firing. Is this understanding correct?
1.1 Why is it called place "field," what does the "field" actually imply, etymologically speaking?
1.2. The Wikipedia Grid Cell Page says that:

By contrast, if a place cell from the rat hippocampus is examined in the same way (i.e., by placing a dot at the location of the rat's head whenever the cell emits an action potential), then the dots build up to form small clusters, but frequently there is only one cluster (one "place field") in a given environment, and even when multiple clusters are seen, there is no perceptible regularity in their arrangement.

So then what are those "clusters", i.e. I guess the place fields, are they the ones I highlighted in red on this picture (sorry, I am a very visual learner!) and also, why do they fire in clusters?

The Wikipedia Page has the following description of this picture but I am still not sure I am understanding it correctly:

Spatial firing patterns of 8 place cells recorded from the CA1 layer of a rat. The rat ran back and forth along an elevated track, stopping at each end to eat a small food reward. Dots indicate positions where action potentials were recorded, with color indicating which neuron emitted that action potential.

The first question stems from the second and the main one I am confused about: what is actually the difference between the place cells and the grid cells, in a layman terms (beyond the obvious structural differences, i.e. that the place cells are pyramidal neurons and the grid cells fire in a hexagonal pattern)?
In terms of their functional differences, is the difference mainly in the fact that the grid cells are theoretically responsible for path integration, whereas "The place cells are thought, collectively, to act as a cognitive representation of a specific location in space, known as a cognitive map" ( O’Keefe John, 1978 ).

What is the physiological or anatomical difference between.... Available from: https://www.researchgate.net/post/What_is_the_physiological_or_anatomical_difference_between_place_cells_and_grid_cells_in_the_hippocampus [accessed Aug 16, 2017].
O'Keefe, John (1978). The Hippocampus as a Cognitive Map. ISBN 978-0198572060.

Yes, that's correct. Mostly, place cells fire in different places in different contexts, and they don't necessarily share the same spatial relationship in different contexts (like in your picture, the "yellow" cell comes right before a "cyan" cell; those place fields wouldn't necessarily be adjacent in a different context.

1.1. "Field" is just a term that refers to a region of space. I'd say the Merriam-Webster definition closest is #6:

a region or space in which a given effect (such as magnetism) exists

1.2 The picture you have is probably a schematic, but what it depicts is a recording from several different cells. Each cell is assigned a color. Every time the cell fires a spike, there is a dot placed at the location in space where the animal was at the time of the spike. You let the animal run through the maze and get a record of lots of these points, and you see that they cluster together into place fields.
2&3 - These questions are getting to be a bit too broad and also you are only supposed to ask one question per submission, so I'll be very brief here. Grid cells are located in an entirely different part of the brain, the entorhinal cortex (part of neocortex), although this part does project to the hippocampus where place cells are found.
Grid cells fire in regular patterns in a spatial field, like in this image:
https://en.wikipedia.org/wiki/Grid_cell#/media/File:Autocorrelation_image.jpg
They also keep their relationship of firing locations relative to each other constant across contexts. You can think of them like a nested coordinate system.
Place cells do not do this. For a given environment, they seem to be somewhat randomly arranged relative to each other. Most likely, what actually happens with place cells is that if you could record from all of them, there would be a unique combination of cells active at any location, and this location could then be associated with other information like "I found food here."
Perhaps you could think about grid cells like a GPS location, but place cells are like a map marker.

the picture you've attached is the autocorrelation heatmap, and I have always been wondering, how are those maps usually generated for grid cells? I heard they use something like Gaussian process? But the what is correlated with what in that plot?

@Jen The x- and y- axes are space. It's an autocorrelation, so the process is that you iterate through each spike you observe, and call the place the animal is when that spike is fired (0,0); then you look at where the animal is when every other spike is fired, and mark an event at each spatial coordinate relative to that first spike. Then you do that for all the other spikes. A gaussian filter is just used to filter the data a bit, so you see blotches rather than just a bunch of dots.


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Evolution of dinosaurs
What did dinosaurs evolve from? Was it the reptiles that evolved from amphibians? I have been researching this but am very confused with who their direct predecessor was. Amphibians evolved from fish...reptiles from  amphibians...dinosaurs from reptiles (?)...and birds from dinosaurs. That is my understanding, but it could be wrong. How are dinosaurs related to reptiles? And if they did evolve from reptiles, which kind of reptiles (such as lizards, crocodiles, or turtles for example)?

Related: If dinosaurs could have feathers, would they still be reptiles?

Source of information
See the post The best free and most up to date phylogenetic tree on the internet? for info about how to find such information.
Generally speaking, you might be interested in an intro to phylogenetics such as the one provided in this answer for example.
Where are dinosaurs in the tree of life?
Dinosaurs fall within the Reptiliomorpha clade. Please note that Reptiliomorpha does not quite correspond to what we today call reptiles. Please see the post If dinosaurs could have feathers, would they still be reptiles?
Reptiliomorpha is the sister clade to Amphibia (from here) which contain all living amphibians.

If you look within the Amniota, you will find all of the following

Here, you see that turtles and mammals are an off-shoot of Diapsida. So dinosaurs are not mammals and there are not closely related to turtles. Now if you click on Diapsida you will find ...

the Archosauromorpha which contains all crocodiles, birds and dinosaurs. You can keep going to find Therapoda which contains many dinosaurs and birds. You can keep going like this for yourself and discover the entire tree of life!

Reacting to your sentences

What did dinosaurs evolve from?

When asking this question, please do not forget that no species evolved from an extant species. If this is unclear to you, you should have a look at this post.

Was it the reptiles that evolved from amphibians?

Well... the term reptile is a mess because it does not represent a monophyletic group (see this post). If you do not understand the term monophyletic, then you should have a look at this answer.

Amphibians evolved from fish...

Well... sure. However, fish is also not monophyletic so it is misleading. Also, I am afraid when you say "Amphibians evolved from fish" that you are thinking of modern extant fish which would be wrong.

reptiles from amphibians...

Nope, this is wrong. Reptiles and amphibians are sister(-ish) clades.

dinosaurs from reptiles (?)...

This is more or less true although again, do not think of modern reptiles and also, reptiles is a mess because it is not a monophyletic group. But Dinosaurs are Reptilia

and birds from dinosaurs.

Yes, this is pretty much true.
Note generally though that it is misleading to say "birds evolved from dinosaurs", "humans evolved from apes" and "mammals evolved from vertebrates". It is more correct to say "birds are dinosaurs", "humans are apes" and "mammals are vertebrates". I would be even better to use the latin names to avoid confusion with misuse of these words in the popular culture.

Nice answer!...

When you say no species has evolved from an extant species, why is that? Wouldn't the Galapagos finches have evolved from an extant species of finch in South America? Meaning that they did indeed evolve from an extant species? (I did read the linked post, but I am still a bit confused)

@Hawkeye The sentence you are referring to is followed by "If this is unclear to you, you should have a look at this post".  This post would also give you a good explanation.

@Remi.b If I am understanding the linked posts correctly: No species has evolved from an extant species because the species has also been evolving and is now different, no matter how slight. Am I thinking of that correctly?

@Hawkeye Yep pretty much! Good job!

Thanks for the informative answer! Just a few questions to make sure I properly understand it. At some point in time, Reptilia divided into Anapsida and Romeriida. Turtles are included under Anapsida while dinosaurs fall under Romeriida. So they are related, but one is not the ancestor to another. Is this correct? Dinosaurs and turtles are more related than dinosaurs and members of Amphibia but less related than dinosaurs and birds. Your anwser cleared a lot of things up, but I just want to make sure I grasp the concept

You got it! It feels good when the OP fully gets it! Good job @Vanessa! Note that tolweb.org (the reference I used) is a little bit updated. OneZoom.org is a bit better (see the tetrapods here). There are a few changes what you just expressed remains true.

If you check wiki you can find that dinosaurs evolved in the clade of Archosaurs. Crocodiles and birds are still living representatives of the Archosaurs. The most recent common ancestor of birds and crocodiles, was also the ancestor of the dinosaurs and was a reptile.


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Is there a biological urge to have children in women?
Searching information about this subject often leads to personal stories from women making the choice to live childfree and women stating they either always wanted to have children or experienced a sudden 'baby fever'. Often this baby fever is understood to be a biological urge.
In this article a link between hormones and the need for own offspring is made a couple of times, but also contradicted.

In  the  context  of  evolutionary adaptedness, all women were exposed
  to babies and infants, and the ‘default’ setting for the female  body
  is  to  have  experienced  both nurturing  and  pregnancies  by  the
  early  twenties. Rotkirch therefore suggests that longing for a baby
  develops out of hormonal changes evolved to prepare women for
  motherhood. These might be triggered by falling in love; the ‘nesting’
  behaviour associated with settling down; exposure to infants or the
  aging process. Conversely, however, Kravdal has found evidence in
  Norway of a demographically significant cohort for whom reproduction
  and finding a long-term partner and ‘settling’ down’ are quite
  exclusive (Kravdal 1997).

In the same article, the effects of hormones on human intercourse and attractiveness between men and women is briefly explained. However, to me it seems that the urge to have sex is something different from the urge to have babies or to become a parent. I would like to know if there are hormones or other biological changes in women that cause something like 'baby fever' or if it is rather more of a more psychological or social environment phenomenon.
Other relevant articles are often not accessible to me or prove too difficult to understand with basic biology knowledge.

Interesting though this question is, do you really think you will obtain a definitive answer? What would that be? That it has been shown by experiments on a large statistical sample of human subjects that injecting a cocktail of defined compounds leads their having more children than a control group injected with a placebo? I think you are left with individual anecdote or subjective opinion.

I was not thinking along the lines of a individual anecdote, those are easy to find anywhere. I was hoping there perhaps might be a study that shows something along the lines of increased hormones when women are subjected to children, other women having children or simply aging. Or a test that shows brain activity when testsubjects are exposed to images relevant to nurturing a child. Testing whether that happens seems doable to me.

Also, a definite 'No, this has not been proven and/or is impossible to research on a large scale because A and B' would be an answer that would clarify things.

The biological urge to find a mate means that an innate desire for children is unnecessary. Having sex with a partner pretty much guaranteed children before contraception was available.
It's hard to imagine why an urge to have children would exist, but that's not the same as saying it doesn't -- but I also can't imagine how you'd be able to pull apart biological vs social pressures in such a complex and core part of being human.

This is an argument but not an answer backed by facts in terms of SE Biology. "is unnecessary", "It's hard to imagine". The simple reason is that it is not really a question that it is suitable for SE Biology and therefore one that one is advised not to answer in the help.

Fair enough, would this have been appropriate as a comment?

— yes I think so.


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What is happening to this tree?
I was walking down to my mailbox when I saw this tree:

And by the looks of the branches, the tree seems to be dying because it has no leaves.  What is happening to the tree?

Look like ther's both crust and brackets. Fairly underdeveloped thus far. Could be just as you said - the tree is dying - or, is suffering from a disease. I'm definitely no arborist, but I don't think I'm too far off either.. Where do you live? Also, would it be possible to provide a picture of the entire tree? Thanks.

They may be lichens or some other fungi.

The tree is dying.  From what you say, it has no leaves wduring a time it should, it has saprophitic growth along the trunk; it looks like there's a crack in the bark on the right, and there are shoots coming up from the base of the trunk, the last hurrah from the tree to try to regenerate.
Trees send up suckers as a reaction to stress (like slowly dying). If you cut the trunk in such a way as to discourage rot, it will likely be replaced by this shrubby growth if the roots are sound. Some loggers use this as a way to quick-start new lumber trees.


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Role of ATP and AMP in functioning of Phosphofructokinase
I know that when ATP is more then it inhibits PFK and hence regulate the number of ATP. But how does PFK reactivates itself? Is it due to removal of ATP from allosteric site that just reconfigures the enzyme back to normal functional state, or does binding of AMP (after ATP removal) does that?
To clear the meaning,
PFK+ATP= (inactive PFK+ATP)
So is it (1) or (2)?
(1) (inactive PFK+ATP) => (Active PFK)+ATP
(2) (inactive PFK+ATP) => (Inactive PFK)+ATP removed => (Inactive PFK)+ attached AMP => (Active PFK) + removed AMP

This is clearly explained on the Wikipedia page for glycolysis under the heading Phosphofrucokinase. AMP is an allosteric activator of the enzyme and ATP competes for binding at the same site but is not an activator.
You should think of the interaction between the two regulators in terms of reversible binding of both: since they compete for binding at the same site the proportion of the enzyme with bound AMP will go down if [ATP] goes up, for example.
Neither of your proposed schemes is   correct: the enzyme is more active with AMP bound and less active with ATP bound. The idea that AMP binds, activates, then wanders off is wrong.

I know that when ATP is more then it inhibits PFK and hence regulate the number of ATP.

This is correct. High levels of ATP cause an inhibitory effect on PFK, specifically brought about by ATP binding to an allosteric site on PFK. By ATP binding to the allosteric site of PFK, the energy state of PFK significantly increases. Illustrated below are the active and allosteric sites of PFK that ATP (and AMP) interact with.

When ATP allosterically binds to PFK, the rate in which it also binds to the active (catalytic) site(s) of PFK drastically decreases (which is due to PFK already having such a high energy state).

But how does PFK reactivates itself? Is it due to removal of ATP from allosteric site that just reconfigures the enzyme back to normal functional state, or does binding of AMP (after ATP removal) does that?

Well, it doesn't reactivate itself! Instead, AMP directly competes with ATP to bind to the allosteric site(s) of PFK. When this occurs, the binding of AMP causes the energy state of PFK to then again lower, which in turn promotes the binding of ATP to the active site(s) of PFK. It is this ongoing ratio of allosteric AMP:ATP binding to PFK that regulates PFK during this stage of glycolysis.
National Center for Biotechnology Information, U.S. National Library of Medicine

The allosteric effectors of PFK change the affinity of the enzyme for F6P not for ATP - your reference mentions this. And that's what your second Figure relates to: it doesn't say anything about ATP binding at the active site, it shows that ATP reduces the rate of reaction at any given concentration of F6P.

@AlanBoyd Ah, yes, my mistake. I'll make the appropriate edit. Thanks for pointing this out.

'ATP doesn't "attach and then come off" of PFK' -- this sounds the off-rate for ATP is zero (irreversible binding) which is probably not what you meant to say ...

@Roland Thanks for pointing this out to me.. I'll be sure to make the appropriate edit here shortly. :)


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Limitations of Gibson Assembly method
Why is the Gibson assembly method limited to ~8 fragments and what can be done to raise this limit?
Why is the method called "seamless" and what are the advantages compared to annealing complementary fragments and using polymerase and ligase?
Thank you

The technique isn't limited to 8 per se, it's just for every additional fragment you want to add, you require an additional joining event to occur. Eventually, your cloning efficiency will just bottom out, and you'll get no positives. Assembly of >8 fragments is possible though - I know a few people who have managed up to 15 or so, though the efficiency again is hugely fragment-length dependent (small fragments are easier than large ones).
To increase the number of fragments, you can try step-wise assembly, sticking subsets of fragments together to make progressively larger ones, or optimise your fragment ratios and overlap lengths. This is a bit of a 'dark art' though - it would be a lot of trial and error with lots of potential variables.

The technique is called 'seamless' as it, in theory, leaves no scars (deleted or inserted bases). NEB has a great page explaining it, but this figure basically summarises:

There would be nothing stopping you going and annealing fragments and then extending them, but this is more like a "joining PCR", and Gibson assembly is designed to mitigate the need to do this. Joining PCRs are very tricky to get working, especially if your fragment sizes differ significantly. The Gibson mastermix contains enzymes in compatible buffers with all the necessary cofactors to allow them to work together.


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What type of lizard is this?
The photo was taken in southern Florida.

It may be green anoles (Anolis carolinensis). They are harmless I think...

Definitely a green anole. Very common in FL. Also called chameleon because they can change color from green to brown, and back again!


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Can DNA methylation induce breast cancer?
What is the role of DNA methylation in breast cancer? DNA methylation is a process by which methyl groups are added to the DNA molecule.
In the September 2015 paper The Role of Methylation in Breast Cancer Susceptibility and Treatment published in Anticancer Research, Pouliot, Labrie, Diorio and Durocher write:

DNA methylation is a critical mechanism of epigenetic modification involved in gene expression programming, that can promote the development of several cancers, including breast cancer. The methylation of CpG islands by DNA methyltransferases is reversible and has been shown to modify the transcriptional activity of key proliferation genes or transcription factors involved in suppression or promotion of cell growth. Indeed, aberrant methylation found in gene promoters is a hallmark of cancer that could be used as non-intrusive biomarker in body fluids such as blood and plasma for early detection of breast cancer.

In addition, Pouliot, Labrie, Diorio and Durocher state that:

DNA methylation is a reversible mechanism that occurs most commonly with an addition of a methyl group in the fifth position of the pyrimidine ring of cytosine on CpG sites within the genome. Human DNA methylation is introduced into the sequence of nucleotides by enzymes of the DNA cytosine methyltransferases family including DNMT1, DNMT3A, DNMT3B and DNMT3L (6).
The DNMT1 protein methylates newly-synthesized strands prior to chromatin packaging and is localized to the replication foci during the S-phase. This highly expressed enzyme is mainly responsible for maintenance of the methylation pattern during replication (7). An increased expression of DNMT1 is observed in many types of cancers and this overexpression is associated with cellular transformation, while reduced DNMT1 expression levels seem to be associated with a protective effect (8, 9).
The DNMT3A and -B proteins allow de novo DNA methylation activity in vitro, without distinction between unmethylated and hemi-methylated DNA (10). In particular, the expression of DNMT3B is elevated in several human cancer types, while its suppression results in tumor cell apoptosis (11, 12). Indeed, inactivation of the TSG Ras association domain family 1 isoform A (RASSF1A), through promoter hypermethylation triggered by up-regulation of DNMT3B, is a common event in numerous cancers or tumor types (13). Several studies suggest that DNMT3B plays a predominant role over DNMT3A and DNMT1 in breast tumorigenesis, given its overexpression in breast cancer tissues compared to DNMT1 and -3A (14). Although DNMT3L has no catalytic activity on its own, this enzyme promotes the activity of DNMT3A and -B by increasing their binding capacity for the methyl group donor, S-adenosyl-L-methionine (15).
In mammalian tissues, DNA methylation occurs in CpG dinucleotides, and clustering of these elements in the 5’ regulatory regions of approximately 60% of genes are referred to as CpG islands (16). Unusual methylation of these CpG islands may lead to silencing of certain genes involved in key proliferation and apoptosis pathways such as TSGs, DNA repair and hormone receptor genes, as well as genes that inhibit angiogenesis (17). Two different DNA methylation mechanisms lead to transcriptional gene repression: CpG dinucleotide methylation inhibits the binding of transcriptional factors to their promoter regulatory elements; and methylated cytosines enhance the recruitment of methylated binding domain proteins, which inhibit binding of transcription factors through inactive chromatin configuration state around the genes (18). On the other hand, ten-eleven translocation (TET) proteins such as TET2 can remove DNA methyl marks and trigger re-expression of silenced genes. Of interest, TET2 has been shown to be mutated and therefore inactivated in many types of cancer (19).
In addition, growing evidence suggests that methylation of regions located upstream of CpG islands, called CpG island shores, as well as intragenic sequences, are also important for regulation of gene expression and can be involved in disease development and progression (20, 21). Generally in normal cells, gene promoters are unmethylated, while gene bodies and intergenic regions are methylated.

How do you analyze DNA methylation data generated from the EPIC array from Illumina as described here,   https://www.illumina.com/products/by-type/microarray-kits/infinium-methylation-epic.html?

Analysis of DNA methylation can be assessed through different methods including bisulfite conversion. This can be performed in combination with real-time methylation-specific PCR and specific primers to amplify CpG islands of a panel of selected genes (2). A genome-wide approach with high-throughput sequencing can also be performed using bisulfite-converted DNA from different non-invasive biological sources such as whole blood, serum and plasma.

The rapidGSEA method described in https://bmcbioinformatics.biomedcentral.com/articles/10.1186/s12859-016-1244-x takes five default arguments and three optional arguments rapidGSEA <- function(exprsData, labelList, geneSets, numPermutations, metricString, dumpFileName="", checkInput=TRUE, doublePrecision=FALSE) {...}
metricString denotes the local ranking measure (one of the following) and
numPermutations denotes the number of permutations in the resampling test.
If metricString denotes the local ranking measure we are requesting that rapidGSEA use when it is invoked, which metricString value listed below should I choose so that rapidGSEA properly analyzes DNA methylation data generated from the EPIC array from Illumina ?
naive_diff_of_classes
naive_ratio_of_classes
naive_log2_ratio_of_classes
stable_diff_of_classes
stable_ratio_of_classes
stable_log2_ratio_of_classes
onepass_signal2noise
onepass_t_test
twopass_signal2noise
twopass_t_test
stable_signal2noise
stable_t_test
overkill_signal2noise
overkill_t_test

I finally found the answer to the question, " If metricString denotes the local ranking measure we are requesting
that rapidGSEA use when it is invoked, which metricString value should I choose so that rapidGSEA operates
in a manner most closely resembling fgseaL?"
Please read this great article in May 12 2017 BioMed Central (BMC) Bioinformatics article titled
 with the
URL, https://bmcbioinformatics.biomedcentral.com/articles/10.1186/s12859-017-1674-0
Also, please read this blog , "Diving into Genetics and Genomics: Gene Set Enrichment Analysis (GSEA) explained."
with the URL http://crazyhottommy.blogspot.com/2016/08/gene-set-enrichment-analysis-gsea.html
After reading these two articles, my choice for the best rapidGSEA local ranking measure is
Minimum Significant Difference(i.e. MSD) because it has the best overall false positive rate(i.e FPR) for larger sample sizes.
Finally, it is important to realize that fgseaL's phenotype labeling principle cannot be emulated by GSEA  or rapidGSEA with any of it's sixteen possible ranking metrics.
Thank you.

Can you please use > at the start of your quotations and link to the primary sources (not every cited papers in the quotation, but at list the source you quote)?

@Remi.b The source I quote from is the September 2015 paper "The Role of Methylation in Breast Cancer Susceptibility and Treatment" published in Anticancer Research by Pouliot, Labrie, Diorio and Durocher.

@canadianer, Thank you for the very nice edit just now.

I'm voting to close this question as off-topic because this is not a question it is a review inviting a discussion. If you cannot answer your own question after so much reading you can hardly expect a simple definitive answer here.

@David,I just found this article https://github.com/gravitino/cudaGSEA/blob/master/cudaGSEA/man/GSEA.Rd which answers my question,Thank you

Okay I'll try to put together a quick answer.
First: 'How do you analyze DNA methylation data generated from the EPIC array from Illumina'
The most common method to analyse DNA methylation is based on bisulfite conversion of DNA. This chemical converts the base cytosine (C) to uracil (U), which 'reads' the same as thymine (T), but it only works on non-methylated cytosine. When you want to know which bases in your DNA are methylated, you split your sample in two parts, do the bisulfite conversion on one and then sequence both. The C/T differences in the sequence then tell you, which C's in your sequence were methylated.
The Illumina arrays are special sequencing methods, that do not look for all sequences in a given sample, but only check specific ones (usually some genes of interest). For methylation analysis these chips allow the sequencing of the two versions (normal & bisulfite converted) of each region of interest separately.
Now: 'Can DNA methylation induce breast cancer?'
In principle yes, but it is very unlikely/almost impossible to be the only factor. A cancer forms only, if a whole range of cellular functions (esp. growth) are abnormally regulated and if the various control mechanisms intended to prevent this fail. Therefore most cancers have hundreds to thousands of mutations and some of these might also be abnormal DNA methylation patterns or regulation. Further details of how DNA methylation can affect which genes are active or repressed is also discussed in these questions.

Could you please select the rapidGSEA * gene set enrichment analysis * metric string value shown at the bottom of the original question which most properly measures the statistical significance of rejecting the null hypothesis where we are comparing a normal healthy control group of subjects with a group of subjects diagnosed with a distinct category of breast cancer? Thank you.


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Confirming exon shuffling in a gene
I'm trying to confirm that the sequence of a novel gene is derived by exon shuffling between several different genes. I have the promoter sequence, gene sequence, and mRNA (with defined exon/intro boundaries). I've tried performing several database searches with the sequences, but each search produces a set of different unrelated hits. How would one go about using this info to confirm the exon shuffling hypothesis? Any tips are appreciated. Thanks!

please avoid cross-posting across Stack Exchange platforms: https://bioinformatics.stackexchange.com/questions/2323/how-to-confirm-exon-shuffling-in-a-gene

It's not clear what is 'several database searches with the sequences'. The most obvious solution is blasting your sequence so you can see which part can't be aligned and then blasting the rest. You can choose different implementations (megablast of blastn) and play with algorithm parameters because it may not work for you as-is. But it will work as-is if you'll blast exons separately. This way you can identify origin genes.


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Please identify this bird
Please identify this bird? There are bright red feathers at the bottom of its tail. What do we call these feathers?

update:
Location is North India. Temperature is around 35° C.

Can you provide an approximate location where you saw this bird?

The bird resembles a Red-vented Bulbul (Pycnonotus cafer), a native of the Indian subcontinent but common as an invasive species in many other regions. Some location information would be very helpful in providing positive ID.

@bshane Excellent! The image is of bad quality, the bird's head can't be clearly seen, there is no location information, and yet you guessed so accurate. This should support your answer: https://yandex.ru/images/search?text=Pycnonotus%20cafer&stype=image&lr=213&noreask=1&source=wiz

Thanks, @cezar. These were briefly reported as an invasive species around my home a few years ago, and the Ministry of Primary Industries was desperately trying to track them down before they could breed and become a pest. I never saw any, but the ID appears to have stuck with me.

Location is North India. Temperature is around 35° C. I took the picture from a long distance with camera zoom to fullest. After 1st click, bird flew away.

I am hesitant to provide 'positive' ID without location information, but this bird strongly resembles a Red-vented Bulbul (Pycnonotus cafer). The species is native to the Indian subcontinent, but is a common invasive species in many other parts of the world.

Key identifying features, with features visible in the photo given in bold (description from NZBirdsOnline):
Red-vented bulbuls are slim, starling-sized songbirds with predominantly dark plumage. They are typically bold and conspicuous, with repetitive, monotonous calls. Their slim build and curved bill are reminiscent of a honeyeater (e.g. bellbird or tui), although they are not closely related. The two most distinctive identification features are a small erectile crest on the crown (giving them a square-headed Roman helmet look when the crest is raised) and the diagnostic bright red patch between the base of the legs and the undertail. The head, hindneck and upper breast are glossy black, with a circular brown patch over the ear. This dark hood becomes streaked or scaly on the lower breast and merges into the pale grey belly. The upper wings and mantle are mid-brown with pale margins when in fresh plumage, creating a scaly appearance. The rump is white, and the tail is long and blackish with a prominent white tip. The bill, eyes and legs are dark. The sexes are alike, although males are slightly larger. Juveniles are dull brown with an orange or pinkish (cf. red) vent.
The red feathers around the vent do not have a special name - you can just call them 'the feathers around the vent'.
edited for the addition of location information
As the photo was taken in Northern India, the bird is almost certainly a Red-vented Bulbul. The Red-vented Bulbul is common throughout India, and there are no similar species in the range that could easily be confused with this species.

the "bright red patch between the base of the legs and the undertail" refer to "bright red feathers"? can we refer to them as "undertail coverts" too?

On any other bird I would say yes, but 'coverts' is partially a functional term, meaning feathers which smooth the surface transition between body and flight feathers. In the case of the Red-vented Bulbul, the red feathers stand apart from the tail, rather than smoothing the transition. I may be being overly picky, but I don't think we can use the term here.


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Please explain this notation MW around 9 MDa
I am a computational science student and was reading about the structure of Pyruvate dehydrogenase (PDH).
link to article
The article mentions "PDH is a large complex (MW around 9 MDa) consisting of multiple copies of three enzymes."
What does MW around 9 MDa denote ?
I am not a regular student of biology but rather an engineering student so please try to provide simple explanations.

MW is Molecular Weight, or the mass of 1 mole of the protein. 9 MDa is 9 million Daltons, and 1 Dalton is 1 gram per mole. So a mole of PDH is about 9 million grams.

One Dalton = 1.66×10⁻²⁷ kg and one mole = 6.023 10²³ molecules.

The molecular weight of PDH enzyme is approximately 9$\times$10$^6$ gm/mol
The Dalton (or atomic mass unit (amu) ) is a unit of mass defined as 1/12 weight of carbon-12 atom in  ground state.
1 Da  = 1/12 m(12C)
The number of atoms in 1 mole is Avogadro's number (6.023 x 10^23) so weight of 1 carbon atom is   =   (12/ 6.023 x 10^23 ) g
This means 1Da (1 amu)  = 1/12 x (12/ 6.023 x 10^23 ) g = 1/ 6.023 x 10^23 g  which is g/mole
(1 MOLE = 6.023 x 10^23 )
=> 1 Da = 1g/mole


text:
If animals aren't getting tooth decay because they don't eat processed foods, could similar work for humans?
In previous question here on stackexchange biology I read that animals don't get dental caries because they aren't exposed to refined carbohydrates like sugars. My question is: in theory, could a human be completely dental caries-free if he followed the diet of not eating any processed food? :))
And also, are fruits like apple or orange 'safe' against dental caries? (since they're not 'processed' sugars?) Thank you kindly for answers.

What does "processed" sugar make bad? It comes in high concentrations and is ubiquitous, but else? It is purified (not more) from a natural source (either sugar cane or sugar beets). And natural products as pure apple juice can contain more sugar than a coke...

Chris, I'm not sure, but I in the previous question discussed here someone said that "plaque is colonised by acidogenic (acid producing) micro organisms cavities are produced in the presence of refined carbohydrates" and also "...besides wild animals are not exposed to refined carbohydrates like sugars.", hence "wild animals do not have these two diseases".
I don't really know much on this matter, that's why I'm looking for more answers.

Tooth enamel is almost entirely susceptible to acidity. So grass eating animals and fruit eaters have different issues.

I think your assumption is wrong : Our small mixed breed had to have all her teeth pulled in 2 operations a year apart. The caries were so bad it damaged her kidneys.  i have had other dogs with caries but not so severe .

There is something missing from this: what was/is the dog's diet?

Her diet was the same, i expect, as most dogs in US, dry prepared dog food. Our other dog has excellent white teeth ( same food).


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How necessary is human zygote cytoplasm for generating a human?
I'm primarily questioning the roles of genetics and cytoplasmic factors of zygote in generating a human being with a natural embryological process.
For instance, is there an experiment where we check if we get a human when we replace the DNA of a mice zygote with human DNA?

The zygote itself is necessary because in the early embryo there is almost no transcription of its own genome, instead it uses mRNA deposited in the egg cell by the mother (see also maternal to zygotic transition).
That being said, I don't think any ethics committee would allow an experiment like this in the first place.

Agree +1. It would be interesting though to know if such DNA swap has been successful among other vertebrates species and we could try to generalize it to humans.

mouse>pig here


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How exactly do mosquitoes navigate directly on target?
There is a question on mosquito orientation in darkness, however the answer does not address it very specifically and I'm more interested in mosquito ability to lock on target than general navigation.
I know that they use their antennae to detect CO2 and lactic acid. However smell alone doesn't seem good enough for precise landing.
They do have eyes, however they can operate in complete darkness which means the eyes are redundant system for the attack.
They can sense heat, but they do not seem to attack non-fire based heat sources.
So how exactly does a mosquito succeed to land on piece of uncovered skin? Does this tell us anything about interfering with their navigation system?

In my experience, they don't navigate directly to their target: they fly around for a long time making an annoying high-pitched whine that's worse than the actual bite, at least if you're trying to sleep.

Mosquitoes do not rely on a single cue to find its host. It is the combination of CO2, temperature and odor cues, that makes mosquito an efficient blood feeder.
 These two papers might help you in understanding how mosquitoes target their hosts.
Genetic analysis of mosquito detection of humans
Multimodal Integration of Carbon Dioxide and Other Sensory
Cues Drives Mosquito Attraction to Humans

+1 for an answer from Mosquito man about mosquitos


text:
Which extinction event killed the highest proportion of organisms?
The P-T extinction (a.k.a. the Great Dying) tends to be considered the worst - for example, Wikipedia states:

It is the Earth's most severe known extinction event, with up to 96% of all marine species and 70% of terrestrial vertebrate species becoming extinct. It is the only known mass extinction of insects. Some 57% of all families and 83% of all genera became extinct. Because so much biodiversity was lost, the recovery of life on Earth took significantly longer than after any other extinction event, possibly up to 10 million years.

Presumably the "96% of all marine species" (which references two books, neither of which I have) is in terms of multicellular marine species or some similar subcategory that's easier to observe in the fossil record (I could be wrong).
My question is this: Would the Great Oxygenation Event not have killed a higher proportion of organisms (taking into account all organisms)?
I know that we don't have any records that can tell us how many died in the GOE and hence this question is necessarily speculative, but surely nearly all organisms pre-GOE would have been obligate anaerobes (and therefore found oxygen to be toxic)?
What I'm unsure about is how single-celled organisms fared in more recent (Phanerozoic) extinctions, as most discussion seems to be in terms of opisthokonts (i.e. animals + fungi) and archaeplastidans (i.e. plants + algae).

Would the GOE have actually killed organisms?  Seems to me that it was slow enough so that oxygen-favoring organisms just reproduced better.

I guess the nuclear war that happened in 2077 doesn't count?

@2077: No, because that just killed off a lot of humans, allowing the biosphere to recover from the Anthropocene Extinction Event.

Do you actually mean "proportion of organisms", or "proportion of species including single-celled organisms"? Your title says the former but your text suggests you mean the latter.

I'm voting to close this question as off-topic because this is SE Biology, not The Guiness Book of Records.

This is a great question. I decided to research it and here is what I found. For some reason the GOE is not on lists of the "big 5" mass extinctions. The question is why?
I think it's due to the pace of the event. The event is described as happening 2.45–2.32 billion years ago.

This is a timescale in billions of years. So it isn't really a proper mass extinction. Little is known about the time scale of the evolution of cyanobacterial lineages.

The GOE is not in the Big Five because the Big Five were recognized based on Sepkoski's work on marine invertebrates from the Phanerozoic (i. e. the last half billion years). The "Big Five" refers only to the main five extinctions of the Phanerozoic.


text:
Which organism has undergone the least evolutionary change?
A favorite documentary of mine is Encounters at the End of the World, in where, "Film-maker Werner Herzog travels to the McMurdo Station in Antarctica, looking to capture the continent's beauty and investigate the characters living there."
During his time there, he films under-ice divers who risk their lives to explore the depths of antartica's ocean waters to study organisms that are believed to have not evolved for millions (if not billions) of years.

I noticed that the divers, in their routine, were not speaking at all. To me,
  they were like priests preparing for mass. Under the ice, the divers find themselves in a separate reality, where space and time acquire a strange new dimension.

One of the foremost scholars in the world in his field, Dr. Pawlowski, studies the DNA sequences of foraminifera. What looks esoteric is in fact one of the fundamental questions about life on Earth. In the same way that cosmologists search for the origins of the universe, the scientists here are tracing back the evolution of life to its earliest stages.

While watching this part of the documentary, it always makes me wonder: Which form of live (lineage of organism) has undergone the least evolutionary change? And how exactly is this quantified - just differences in DNA/RNA?

Since when? Since LUCA? I doubt we know nearly enough about LUCA (and about the origins of viruses) to be conclusive. I very much doubt that genetic pairwise differences would help as I doubt any extant species would align with LUCA (even if we were to know LUCA's genome). If we use phenotypes, then it is likely going to be quite arbitrary as to what trait we decide to put attention into (and again, we don't know much about LUCA's phenotype).

Yes, I suppose since LUCA, or some evolutionary period around then. And yeah, I'm sure we don't have nearly as much data as we'd like to have.. however, is there a "front runner" as of now - an organism that currently holds the title? I did come across this, but I'm not sure if there are others.

Here is the original article. Looks like worth having a look. I don't know how they can make statement that these species went through such a long stasis.

@Remi.b Right.. I'm not too versed in this field. Do you (or anyone) know exactly how these evolutionary comparisons are made in a quantitative way?

No, I don't. But I suspect many users will be able to read this paper and eventually come up with an answer to your question. I might do it later if I find the time.

@Remi.b "For extant prokaryotes, phylogenetic relations and physiological characteristics can be determined by molecular biology backed by growth experiments. For fossil communities, however, the biomolecules required (DNA, rRNA, enzymes, etc.) have been lost during preservation. Thus, analyses of fossil communities such as those described here must rely on evidence provided by proxies—the morphometrics of the preserved fossils backed by studies of their regional and local geological setting and their paleoecology and community fabric." -- is this kind of analysis reliable enough?

Indeed. It will still give food for thoughts and may provide interesting insights to your question.

You are asking the question, so it's your job to define what you mean, not to ask others "how it is quantitate". And do you really mean "live"? More effort on that and less on eye-candy might have led to a better question.

@David As I previously mentioned, I'm not familiar with measurements and standards that are practiced in this field, so I'm not sure what to even define, and is the reason for me asking :)

@David Well, I do have the ability the edit the question, so.. :) And I'm not sure I know what you're referring to when you reference "live".. some more specificity would be appreciated. Also, I wanted to share my enjoyment for the documentary..theres nothing wrong with a couple pictures, I'm sure most would agree..

Has mixed reviews, but there's a lay book Survivors by Richard Fortey that looks at some examples of organisms that have undergone the minimal evolutionary change over time.


text:
Is a one ventricle heart feasible?
So this is derived from a lesson at Khan Academy.
The mind activity assumes that the one ventricle heart pumps blood to the lungs for oxygenation then rest of the body. However, the problem is that there is too much pressure at the lungs leading to bleeding.
This problem, however, can be solved if the lungs come before the one ventricle heart. This way, most of the pressure is used going through the body and pressure would not become a problem.
Thus, is a one ventricle heart that connects to body tissues first then lung feasible? If so, why have organisms not developed this way?

I removed the "evolution" tag because if this question could be tagged 'evolution', then really any question on this site could be tagged 'evolution'.

Alternative Heart Morphologies
Amphibians and some reptiles have a three-chambered heart, with 2 atria and a single ventricle. There are still separate circulatory pathways for the lungs and the rest of the body, but the oxygenated and oxygen-depleted blood mix in the ventricle, and are pushed at the same time to the lungs and body.
The disadvantage of this system is that it is less efficient at providing oxygen to the body than a four-chambered system, because the blood pumped to the body is a mixture of blood that has recently been to the lungs and blood that has not.
You seem to be suggesting another system, where there is just one serial pathway from heart to lungs to body, or from lungs to heart to body. This is more like the two-chambered heart of a fish: blood is pumped from the heart through the gills, and then to the body.
Lungs and body in series, and fluid dynamics
So why wouldn't this work for a mammal? It could, but gills and lungs are very different. The vasculature of the lungs requires a lot of pressure to get through, which is generated by the right ventricle.
Pressure is required to push fluids through a constriction (note that even a straight pipe is a constriction). After a fluid passes a constriction, there is always a pressure drop. That pressure drop is a function of the rate of flow and size of the constriction. If you give less pressure at the start, there is less pressure to "drop", and so you get a lower flow rate (note that this is nearly a perfect analogy with electricity, where flow is current, pressure is voltage, and the size of the tube is the conductance).
If you want to pass through a second constriction, you have to use pressure that is "left over" after the first drop: you can't use the pressure you started with because that was lost getting you through the first constriction. In reality, in a closed system, the total flow rate will be determined by the summed series resistance, so adding a second constriction slows the flow rate for the whole system, and you get a partial pressure drop after each.
If you put the lungs and body in series with each other, no matter which comes first, you need to have enough pressure left over when you pass one to get you through the next one, otherwise the flow will slow down. Blood in a human aorta has a mean pressure around 100mmHg, whereas back in the vena cava it is close to 10mmHg. That suggests you need about 90mmHg to get enough flow through the body's circulation. The lungs use a little less, but you still have a pressure drop of around 50-60mmHg. Therefore, you would have to increase the blood pressure by 50%-75% to get circulation through both lungs and body.
Higher pressures lead to more turbulent flow and take more effort to achieve. The four-chambered heart, with 2 ventricles, is simply more efficient.

@GerardoFurtado I'll edit to say some; only birds and crocodilians have a true fourth chamber, the other reptiles do not, though there is some separation compared to amphibians.

crocodiles actually have something bordering on a five chambered heart, it allows them to divert oxygenated blood away from non-essential organs during dives.

@John I agree that crocodiles have a more complex heart than mammals, although I think it's a stretch to call it five-chambered; I looked around and every source I can find describes it as a four-chambered heart and they note the second aorta that allows for diversion of blood away from the lungs.

there is this extended valve called the cog tooth valve that allows a one way diversion, it is just that that valve is right against the heart and is muscular, and it creates a one way communication between the aorta. hence why some call it five-chambered.