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Could cancer be in itself a evolutionary process?
Could cancer be in itself a evolutionary process? Maybe in some way could it be a process of variation? Or would this idea be completely without support, if so, why?
I don't mean that each case would lead to evolution, but that within an entire group of organisms, it could lead to case of of individuals developing ways to resist what caused the cancer, maybe in cases of individuals beating the cancer or in cases of successive generations of off spring from individuals with cancer?
Could it be possible that in rare cases it could lead to the development of new organs or specialized cells?

Probably, I could imagine these rebel cells as Che Guevara comrades trying to destroy the Big Brother police state. Alex Jones except of the fact that he is a CIA tactician could be easily a virus ;)

Interesting question. I believe it definitely is an evolutionary process. unicellularity breaking away from a multicellular life.
There are two examples that I can think of, which can support this argument:

Hela cells: Hela cells have been classified as a different organism because they have the ability to grow outside the host indefinitely and their genome is different from Homo sapiens. Hela cells also have a new scientific name- Helacyton gartleri
Transmissible tumors: two tumors have been known to infect other hosts and therefore can be called obligate pathogenic lifeforms. One is Devil Facial Tumor Disease which infects Tasmanian devils and gets transmitted by biting. Another is Canine Transmissible Venereal Tumor which infects dogs and spreads via sexual route.

Could it be possible that in rare cases it could lead to the development of new organs or specialized cells?

Cancer as of now has a pathogenic identity. It is a simplistic process which in a thermodynamic point of view can be described as maximization of entropy(disorder) and thereby increasing the stability [like the way solutes diffuse]. If a cancer has to give rise to a new functional organ then it has to be supportive of the ordered lifestyle which it is trying to break away from in the first place. It may adopt a pathogenic lifestyle initially and then may redevelop order. I don't know of any such evolutionary event but it may nonetheless be possible.

This very interesting question has been explored in a paper, linked this Berkeley page : "Another perspective on cancer: Evolution within" (the paper is at the bottom of the page).
From the site:

If one of those mutations (or a series of mutations) allows its bearer to evade cell death and reproduce more prolifically than others, it will pass that mutation on to its daughter cells, and cells bearing that mutation will increase in frequency over time. Like organisms in an ecosystem, cell lineages within one's own body compete for resources. A cell lineage that gains an advantage in that competition, accumulating mutations that allow it to grab extra resources and escape the body's control mechanisms, will proliferate and may evolve into a cancerous tumor.

The researchers also state that looking at cancer through the 'lens' of cellular evolution could be a major reason why a 'cure' eludes us.
Further, in this article "Connection between cancer development and Darwinian evolution explored", the authors state that:

He believes that many of our genes are constructed such that they protect against cancer in the first part of our lives, but that they are programmed for destruction as we get older.

Essentially, the article asserts that as we get better at prolonging our lives, that cancer is a means to shut down the body over a period of time.  My understanding is (and I could be wrong) is that the increase in cancer incidents are an evolutionary way to put the brakes on the increasing human life span.

not exactly what i was asking, but i was already reading said paper. what it is talking about is the evolution of cancer in the body, about how cancer itself is evolution on the cellular level. what i am asking is in regards to whether it might also be connected to evolution in complex organisms as well

@John I added some more information with another article that link cancer to Darwinian evolution.


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Can a person be infected with HIV viruses without contacting them by person-related stuffs?
We know that a person can be infected with HIV viruses when he/she has sexual relationship with those having HIV viruses (and very, very, very rarely, urine/defecation-related transmission) - but I wonder if there are other sources of HIV transmission - so for example, let's say during sexual relationship, some cuts on body (for example, inside vagina) occurred. Then even if the partner did not have HIV viruses, and a person afterwards does not sex with partners with HIV viruses, is there a chance that he/she may get HIV viruses, still?

let's say during sexual relationship, some cuts on body (for example, inside vagina) occurred. Then even if the partner did not have HIV viruses, and a person afterwards does not sex with partners with HIV viruses, is there a chance that he/she may get HIV viruses, still?

No, because there is no virus present in any of the people involved to be transmitted in this scenario.  HIV doesn't spontaneously occur in people.  It should also be noted that HIV is also highly transmissible in the blood.

The virus must be present in one partner's body for transmission to occur.

Also, HIV can be transmitted through blood to blood contact.

There is currently a similar question/conversation that I have provided a link for here. It may provide some slightly more scientific answers than what I can:)
How does a person get AIDS?

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Do animals also dream?
By "dream", I mean:

Dreaming while sleeping.
Dreaming about their future life while being awake.

Thank you in advance.

I think this question is useful and clear even if it shows little research effort (+1). IMO dreaming is an interesting biological phenomenon. I wish that those who gave the two downvotes gave justifications.

There have been experiments with cats whose brains were leisioned to eliminate sleep paralysis. These cats exhibited behaviors like hunting I imaginary  prey, grooming, etc. this was interpreted as a cat dreaming

You might be interested by this post

Yes, they do!

According to this Psychology Today blogpost, it is quite likely that animals can dream.  Particularly mammals that according to the blogpost:

All mammals share the same neural structures that are important in sleeping and dreaming.

However, for your second question, I do not think it is at all possible to know what they are dreaming about (if they indeed do dream).

If I'm interpreting the Nature article linked to in that blogpost correctly, they not only claimed to know what the rats were dreaming about (sort of), but to be able to influence it!

Dreams are simulations created by the brain in order to train us to cope with challenging situations. Most of the dreams present situations where the individual is confronted with challenges or risks he/she might face during the life. Evolutionary concept of dream suggests that its a way by which brain try to notify some risks and train us to invade through it. The evolutionary acceptance of dreams is due to the "threat simulation" feature it possess. By which an individual can gain advantage of several situations he/she confronts in life.

Finnish psychologist Antti Revonsuo posits that dreams have evolved
  for "threat simulation" exclusively. According to the Threat
  Simulation Theory he proposes, during much of human evolution physical
  and interpersonal threats were serious, giving reproductive advantage
  to those who survived them. Therefore dreaming evolved to replicate
  these threats and continually practice dealing with them. In support
  of this theory, Revonsuo shows that contemporary dreams comprise much
  more threatening events than people meet in daily non-dream life, and
  the dreamer usually engages appropriately with them. It is suggested
  by this theory that dreams serve the purpose of allowing for the
  rehearsal of threatening scenarios in order to better prepare an
  individual for real-life threats.

Question 1

Yes they do. Studies suggests that animals can dream while sleeping, entire  human dreams occur during the REM sleep period. Most of the mammals do have the REM sleep period and it suggests that they do dream in this time of sleep.

Dreams occur during REM sleep. We typically have 3 to 5 periods of REM
  sleep per night. They occur at intervals of 1-2 hours and are quite
  variable in length. An episode of REM sleep may last 5 minutes or over
  an hour. About 20% of sleep is REM sleep. If you sleep 7-8 hours a
  night, perhaps an hour and half of that time, 90 minutes, is REM
  sleep.
REM sleep is characterized by a number of other features including
  rapid, low-voltage brain waves detectable on the
  electroencephalographic (EEG) recording, irregular breathing and heart
  rate and involuntary muscle jerks.
  Reference

This link provides much more examples.
According to the studies of MIT,

Wilson, associate professor of brain and cognitive sciences at MIT,
  and biology graduate student Kenway Louie trained rats to run along a
  circular track for a food reward.
They monitored the animals' brain activity during the task and while
  they were asleep. While the animal ran, its brain created a
  distinctive pattern of neurons firing in the hippocampus, a brain area
  known to be involved in memory.
Like us, rats go through multiple stages of sleep, from slow-wave
  sleep to REM sleep. In humans, it is during REM sleep that most
  dreaming occurs.
The researchers then examined more than 40 REM episodes recorded while
  the rats slept. About half repeated the unique signature of brain
  activity that was created as the animal ran. The correlation was so
  close that the researchers found that as the animal dreamed, they
  could reconstruct where it would be in the maze if it were awake and
  whether the animal was dreaming of running or standing still.
These memories were replayed at about the same speed that the animal
  had experienced them while awake.
  Reference

Question 2

Dreaming about their future life while being awake, good question. If they do so then it will be a contradiction to our long held view of animal thought process. Most of the animal thought process that we try to reveal is through the firing of particular areas in their brain with the association of certain hormones. By this process we can find that which all neural pathways are used while dreaming and which are not.
As we can find that animals also have dreams, then it is obvious that they could recollect it (some what vague) and can prepare mentally to face those particular situations. This doesn't mean that they do have plans about events coming for them in future, but researchers states that dreams are their only offline experience with those events. The memory of those dreams help them to ensure little advantage over those future events. While in the case of humans, we have a highly complex brain which is so good at simulating events by which we can plan our future, but other animals lack this complex structure(complex but not as much as ours), so they entirely rely on dreams for that purpose.

Why do animals dream about one experience and not another? "This work
  allows us to evaluate the content of dreams and create tests to see
  which awake patterns create patterns when the animal is asleep,"
  Wilson said. "If we are able to evaluate the content of the dreaming
  state, we may be able to find out why certain events get replayed and
  others don't."
This work also raises questions about long-held assumptions about
  animals' thought processes. Only a handful of species — among them
  chimps and dolphins — were thought to have any ability at all to
  recall and evaluate detailed sequences of events after they occurred.
  Wilson points out that "dreams are the ultimate off-line experience.
  This work demonstrates that animals are capable of re-evaluating their
  experiences when they are not in the midst of them."
  Reference

+1 you say that " rapid, low-voltage brain waves [are] detectable on the electroencephalographic (EEG) recording". Unfortunately your [Reference] link doesn't work, whether they give amplitudes (voltages) and frequencies of the brain waves there. Can you tell? Does this apply to humans or animals?

@draks...: These low voltage brain waves are called "delta waves". Delta waves, like all brain waves, are detected by electroencephalography (EEG). Delta waves were originally defined as having a frequency between 1-4 Hz, although more recent classifications put the boundaries at between 0.5 and 2 Hz. Delta waves occur in all mammals, and potentially all animals as well.

From the ScientificAmerican

Yet, given the vast documentation of realistic aspects to human dreaming as well as indirect experimental evidence that other mammals such as cats also dream, evolutionary psychologists have theorized that dreaming really does serve a purpose.

Although the linked article doesn't look like they were talking about animals. But I wont purchase the article to check that...
As for your second question, I would say yes, when you would say, making a plan is equivalent to dream of the future. Crows are smarter than you think...

@fileunderwater OK I included it, but why do you think my edit is not an answer to the second question?

Mostly because it wasn't a full answer on its own, and only hinted at a possible answer. As a small addition to your first answer it might useful, but it would be much better if you expanded and explained what you actually mean. At the moment, the addition is only an empty proposition and a link.

@fileunderwater why protecting this question?

It has received 6 comment-like answers that are now deleted. The protection only serves to discourage comments/answers from users that are not familiar with the site (<10 rep), and it has no other effect.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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What determines whether I will have any dream or not?
Sometimes I have many consecutive "dreamfull" nights but sometimes there is no dream during week. Why? What determines whether I will have any dream or not?

According to the DreamResearch.net of UCSC, typically, we dream up to 10 times a night (sometimes more, sometimes less), and it is likely that on those nights when you feel that you have not dreamt, you may have forgotten the dream.
Dream amnesia is very common, where we forget most of the dreams (an any instances of sleep walking etc), this article Dreaming: A Neurocognitive Approach has more of the study.


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Can I control my dreams?
Is it possible to completely realize that I am only dreaming and to completely manage my dream?
Thank you.

According to Psychoanalysis101.org, it is quite rare to be able to control dreams, though apparently it can happen 9according to the article.  Lucid dreaming is the term to describe when the person is aware that they are dreaming, further research and scepticism of lucid dreaming are outlined in this section of the article.

I should also add, at the base of the Wikipedia article, there are dozens of links and resources about this.


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What is the difference between vegetable and fruit?
Is there any exact definition of vegetable and fruit? How can new plant be classified?

A true fruit is a ripened ovary that usually starts ripening when it is fertilized. And vegetable is any vegetative part of the plant which is edible and contains stored food probably in the form of starch.
These definitions are not exact as there are a lot of fruits which are fruits but do not strictly follow the given definition. See Syconus, Composite fruits, Sorosis.etc
Classification is based on several different criteria, for example the mode of reproduction, arrangement and design of flowering parts and flowers and also on the basis of habitat and habit.

From a culinary point of view, the difference between a vegetable and fruit is are they sweet or not.
Hence eggplant, tomatoes and bell peppers which are biologically fruits are considered vegetables.
Potatoes which are tubes, are considered vegetable. Kale which are leaves are considered vegetable. And cauliflower which are flowers are considered vegetables.
The question of fruit and vegetable would be might be tested if somebody made a very sweet and soft carrot, at which point I am not sure what the master chefs of the world might say. Could a soft and sugary sweet carrot be able to graduate into the word of fruits and leave the world of vegetables behind?

Please always make sure to include sources in your answers. See here for tips in writing good answers. This answer, which describes [biologically improper] culinary definitions, is inappropriate here (a biology site). Also, half your answer is proposing a new question -- which is further inappropriate within an answer. Please drastically improve this answer or it will likely be downvoted and/or deleted. Thanks.

I am answering the missing part of the question because somebody will then ask... but wait why is an eggplant called a vegetable? The phasing of the question vegetable or fruit... indicates this question. And really.. vegetable... that is not a biological category. A vegetable is a culinary category.

Then please provide that context and structure to your answer to make that clear. As written, your answer is off-topic. Regardless, you need to provide sources to back up all of your claims.


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Can breathing in helium (from balloons for example) cause damage to the throat in the long term?
Often an activity to do at a party, breath in helium and speak like one of the chipmunks. But, I am wondering, would infrequent inhalation of helium cause long term harm to the throat? in particular, the vocal cords?

When we speak, our vocal cords vibrate to the air. Helium makes them vibrate a lot faster (that's what makes the funny sound of your voice after inhaling helium), because its atoms are a lot lighter than nitrogen and oxygen atoms. Obviously, lighter atoms, can travel faster. This faster vibrations are unusual to the cords and they can cause sore throat or even strong throat ache. After you stop inhaling the gas, things should get back to normal, especially if the inhalation really is infrequent.
Breathing helium balloons at parties is a very dangerous fun activity, because it replaces the oxygen and this could lead to hypoxia - a condition when tissues can't get enough oxygen one reason or another. In some cases, this could even be fatal.
Even though inhaling of pure helium is dangerous, in submarines, divers breathe a mixture of nitrogen, oxygen and helium as helium is better under higher pressures. At these depths the low density of helium is found to considerably reduce the effort of breathing. Divers often have problems with dry throat and constant thirst due to the need of more oxygen. At least, inhaling helium, when it's mixed with oxygen, is far less harmful than breathing it directly from a balloon.

small addition: helium oxygem mixture is also used for medical purposes. Because of its lower density compared to air, it flows easily (reduced turbulence in flow) and effort of breathing is reduced.


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Why does ostrich meat look and taste more like beef than chicken?
Some time ago I tasted ostrich meat, and what was amazing to me was that the meat very much resembled beef, much more than it resembled chicken, turkey or duck meat. And even more than lamb and pork resemble beef.
The resemblance is both in look, both raw and grilled, and in taste (only tried grilled). I would have thought that the meat of related animals would have similar taste. Why is it that the meat of an ostrich, which is a bird, doesn't taste like that of other birds?
Warning, the following links are to pictures of meats!

A picture of beef
A picture of ostrich meat
A picture of chicken meat

There is a very plausible explanation here.
Basically, it explains that meat colour is due to the protein myoglobin (a haem-containing protein related to haemoglobin). There are two types of skeletal muscle: fast-twitch and slow-twitch (Wikipedia). Slow-twitch muscle is red muscle because it contains lots of myoglobin. Fast-twitch muscle is white muscle, containing less myoglobin. The Wikipedia link explains a little more about these muscle types and their functional differences. Evidently the lifestyle of the ostrich dictates that it have more fast-twitch muscle, and so it has red meat. It isn't unique in this: duck and goose are classified as red meat too.
Incidentally the role of myoglobin is to improve the rate of diffusion of oxygen from the haemoglobin in the capillaries through the cytoplasm of the myocytes to the mitochondria. It has also been suggested that it acts as an oxygen storage mechanism in diving mammals which have very high levels of myoglobin in their muscles, but this storage function is unlikely to be important in other mammals, despite what you may read in textbooks.

Great answer, and it also explains why tuna has red-meat-like qualities.

"Slow-twitch muscle is red muscle because it contains lots of myoglobin"
"Evidently the lifestyle of the ostrich dictates that it have more fast-twitch muscle, and so it has red meat"
Huh?


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Differences between right and left handed people
Are there any articles reporting any significant differences in behavior, attitudes, intelligence, appearance, etc., between right and left handed people?

According to this Psychology Today article: 3 Myths and 3 Facts about Left-Handers (with numerous links to many papers throughout the article), there are no particular difference between left and right handed people in terms of intelligence, personality, creativity or mortality.
There seems to be a noticeable difference in the number of people having the language centre being in the left hemisphere of the brain (95% for right handed people vs 70% for left handed people).


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What type of distribution should binding affinities fit?
I've been averaging Ki values from the PDSP Ki Database, and I can't help but to wonder: how I can determine p values for the binding affinities, so I can exclude anomalies in the data if need be?

What does your distribution of Ki look like? If it's reasonably normal, then convert to Z scores and pick an unacceptably low probability to discard (e.g., +/-3).

@kmm Ki values have to always be >0, yet normal distributions normally give a high probability for Ki values <0 and hence the normal distribution is something I'm wondering whether I should discard. It depends on the drug and receptor target too so I would like a nice and general answer if possible. I find that the kstest usually comes up for a p<0.1 that it fits a normal distribution so it might, but the negative values do concern me.

Can you add a histogram of your Ki values? Not all normal distributions have a mean of 0.

P-values reflect how well the data fits some background model. This background model should reflect some assumptions you make about the data. What assumptions do you think would be reasonable in this case? For example, do you assume high values are more likely to be incorrect?
Throwing away outliers like kmm suggested is probably not a good idea, because it means you will remove $K_i$ values which are very high or very low. It is not clear there is much biological justification for that, since we know some $K_i$s can be low and some can be high, but it doesn't tell us they are wrong.
The bottom line is that without making some assumption about what the values should look like, you can't identify what incorrect values look like.


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Can humans' ability to dive with only breathing modifications tell us anything about our evolution?
Can humans' ability to dive with only breathing modifications tell us anything about our evolution?
For example, it is possible to imagine a human anatomy that would be destroyed by the pressure of a few meters of water, and yet humans can, with scuba apparatus dive to several hundred meters.

This is not a complete answer to your question, but your question prompted me to research the Mammalian Diving Reflex, which is used, according to the article, as a survival mechanism rather than assisting us in day to day functioning.
Looking at the evolution of the diving reflex, and how it appears in varying degrees in all mammals, suggest that it has been around for a long time, this article suggests for over 125 million years.

Actually, there was a very interesting Animal planet episode (http://www.youtube.com/watch?v=Cm3XdC-p8_I) on the recent news about the probable discovery of a mermaid body. In the show, scientists suggest that may be our evolution has had some roots under water. First, our body structure is far more plastic and ergonomic than the structure of a monkey. We are great swimmers in our movements and as you mentioned - our ability to hold our breaths under water for a very long time - the record is about 20 minutes! We can easily control our breathing which is something usually connected with marine mammals. In difference of other animals, we are almost hairless. Just like other marine mammals, we are born with insulating fat distributed throughout our bodies. This keeps us warm in water. All this takes place in the "Aquatic ape hypothesis". This view claims that our alleged ancestors went through a watery stage in our evolutionary development.
Of course, although all those facts connect very conveniently, the theory has not been proven yet by experiments and is so far just an idea that should be considered and investigated more.
In addition, some people still have marks from gills as an atavism.

The animal planet "documentary" is fake: http://oceanservice.noaa.gov/facts/mermaids.html.

@kmm: this post on Skepticblog also covers the fake documentary http://www.skepticblog.org/2013/06/05/mermaids-pullllease/


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Why can cats interpret things on a monitor/tv, but dogs cannot?
E.g. you can see a lot of videos where cats are smashing some mouse or spider on an ipad, but I have never seen it with a dog. I have a dog myself and I know that he sometimes responds to the sounds from the TV, but not to the images.
Why is that?

Cats and dogs can both view tv screens & monitors ... though their viewing experience is a little different to ours thanks to differences in cone structure leaving them color blind and giving low acuity.
Both species have lower levels of color vision than humans. Cats see slightly more color (in the blue green and yellow end of the spectrum) than dogs do so they may get more of an immersive experience from watching TV.
Further, cats and dogs need a higher frame rate than humans to make it appear as a smooth film, a phenomenon known as flicker fusion, in humans we require 15-20 frames per second, dogs require 70fps and cats about 100. Before the frame rate of televisions increased in recent years it would appeared to them to be flashing images, similar to when you point a digital camera at a screen which may explain why the dog is not interested in the TV, it'd be like staring at a strobe for hours on end. Here is a paper which discusses flicker rates and color vision in dogs.
To summarize there are several factors which influence the "enjoyment" an animal can take from watching a TV - their response to TV imagery will depend on the frames per second, colors, contrast, clarity, movement, subject matter, and (perhaps most importantly in my opinion) the temperament of the animal, for all of which there are difference between the species.
From sciencenordic.com:

"We humans need about 16 to 20 images a second to perceive what we see
  as continuous film, whereas dogs need about 70 images per second.
So a few years ago, Fido was probably confounded by his master's
  behaviour of sitting for hours staring at a flashing succession of
  images. With modern resolution and quicker imaging, dogs have become
  potential television viewers.
This has not gone unrecognised in the USA, for example, where hopeful
  TV producers have started special TV channels for dogs.
If you have other pets, however, you need to think twice before
  placing them in front of the TV.
Birds need at least 100 frames per second to see TV images as a moving
  picture. Having a bird in the same room as a TV with a lower frame
  rate than that will be very stressful for the creature."

@derfder I've added some more content for you to make more comparisons between dogs and cats.

Some dogs definitely react to TV, otherwise I don't see how people came up with channels specifically for dogs like this one: https://www.dogtv.com


text:
Is life expectancy linked to intelligence in animals?
For example, animals that live only a few days or a few years are often not very intelligent. In contrast, the most intelligent animals seem to live longer.
Is this true? Are there any studies to prove or disprove this statement?

I imagine that the first problem a study like this would run into is how to objectively measure intelligence in a wide variety of animals with vastly different modes of life. I do not have a clue on how to answer this, but "problem-solving" ability in their natural living environment could possibly be one criteria.
Have you done any background research (e.g. on life expectancy in different groups of animals)? The question is very vague and broad.

it would be nice if you can provide references to your argument.. there are several "unintelligent" animals which live long (such as some fishes and echinoderms)

@WYSIWYG I agree that there are exceptions. But on average animals like insects, fishes, small mammals, birds don't live very long. Again, on average. I have one explanation and that is that the heart(or lower forms of heart) is pumping slowly for bigger organisms, (and because each organism has preprogrammed the same ammount of heart-beats per life (as well as mitochondrial "replications"), on average, of course , therefore hummingbird (fast metabolism) lives shorter than a whale or a human. But I am curious if it correlate with the intelligence too and if there is some study.

One way to look at this question is to consider if for lower life expectancy potentially results in less experiences, hence less chance to learn.  But, I doubt that directly relates to what you are asking.

Could you at least list a couple of "intelligent" (longlived) and "non-intelligent" (short-lived) examples that you have as a starting point? Then others can contribute counterexamples or examples that support your claim. You cannot build an argument on anecdotal evidence based on a handful of species. You name fish, birds and insects, but there are quite a few species in these groups that are long lived (and unintelligent?). There could also be an assymetry, so that all "intelligent" species are relatively long lived, while "unintelligent" species can be both short and long-lived.

@Derfder: let me put this argument in this way.. it is wasteful for a shortlived organism to invest in a complex machinery like intelligence or cognitive ability.. it rather aims to fulfill the primary motive of reproduction

whales and elephants are more intelligent than we are?  not sure, but its hard to be smart when you live only a few days on the other hand.

not too big not too small ;)

Limiting the conversation to mammals, and taking relative brain size as a proxy for intelligence (which, of course is not necessarily "true", but at least is quantifiable), the answer is yes: body-size relative  brain size correlates with   body-size relative longevity in mammals.

using a global database of 493 species, we provide evidence showing that mammals with enlarged brains (relative to their body size) live longer and have a longer reproductive lifespan (González-Lagos et al.).

They present data by species in the paper, which is available free online, but so as to have something on SE, I've mocked up a chart based on the averages they give for each mammal order:

 González-Lagos C, Sol D, Reader SM. 2010. Large-brained mammals live longer. Journal of Evolutionary Biology 23: 1064–1074.

Nice graph. Did you make it (smells like ggplot2)? I cannot find it in the paper.

Thanks and yes! I used GraphClick to estimate the data, then made the graph in ggplot2 and added the custom symbols in Illustrator. This version is based on figure 1 in the paper. In fig 2 they display the variation within orders, but it's pretty crowded (there's a point for each of the 493 spp, and they use 18 different symbol/color combinations for the different families) so I thought I'd simplify it a bit (mostly because I didn't feel like GraphClicking 493 points!).

@Oreotrephes Absolutely gorgeous, and definitely above and beyond.  I'm an R n00b but am setting some time next week to try to pick it up; replicating this is my new target.

This is too long to be a comment. Life expectancy is apparently affected the size of an animal, and this is especially evident in mammals and supported by the heartbeat hypothesis. This hypothesis says that all mammals have a similar number of heartbeats, and that the larger an animal is, the less heart beats it has per minute. Therefore, the larger an animal, the longer it lives. A larger size is also associated with a larger brain (which is associated with higher intelligence, although this is not true in all cases since for example some dinosaurs were very large but had very tiny brains). All I'm saying is that any correlation between intelligence and life expectancy may not necessarily be brought about directly by intelligence, but by the size of the animal. Hope this helps.

I'd imagine it's more correlation than causation , just like you suggest, and can find no evidence of a causal relationship

Are you referring to a relatively larger brain with larger body size, or just a larger brain in absolute terms? To me, the first case should be most interesting for intelligence (see brain to body ratio), since, everything else equal, a bigger brain is required to control a larger body.

[cnd]: ... Therefore, the 'residual' brain size should be most interesting for higher cognitive functions. However, this seems to be an area of discussion (see e.g. Marino, 2006. Absolute brain size: Did we throw the baby out with the bathwater? PNAS 103(37).


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Do teeth have the capacity to heal?
Could a cavity in a human tooth "heal over" or possibly fill back in?

The answer is a simple no. Cavities in the teeth caused by dental decay cannot heal. Enamel which is affected by dental decay cannot heal as they are fully formed at the time of eruption and then on only deteriorates. The deeper part of the tooth which has dentin cannot heal the cavity formation, however it can produce a protective barrier between the advancing cavity front and the pulp inside. The cementum the third mineralised tissue of the tooth cannot heal a decay cavity. Its main function is to attach the tooth to the bony socket through the periodontal fibres.

I see you're an oral pathologist, so your answer has merit. However, can we improve the answer with some explanation or reason to believe the things you say are true, other than just your testimony? I'm not suggesting what you're saying is false, I just want to be 100% convinced. I do appreciate your answer and hope you're not offended by my request. How do we know enamel cannot heal because it was formed at the time of eruption? Why can't dentin heal cavity formation? How does dentin produce a protective barrier? Thank you!

Enamel is not formed at the time of eruption, it is formed before eruption. Enamel is secreted as an organic matrix which subsequently gets mineralised by cells called ameloblasts from inside out. Enamel formation is completed before tooth eruption. After enamel formation the ameloblasts regress and are completely lost after eruption. So no further enamel formation is possible if there are no ameloblasts. Hence once a cavity is formed in the enamel it cannot get filled up with enamel.

Where as dentin forming cells are retained live on the pulpal side. So reparative dentin can form on the pulpal side and not on the cavity side to fill it up. These are well established facts which can be found in any standard book on Oral and dental histology and Oral Pathology. Feel free to ask further clarification if required.

That makes sense. Thanks so much!  I've seen reports of decayed enamel before eruption. Is there truth to this?  If so, how does enamel decay before exposed to food acids?

Teeth completely embeded in tissue cannot undergo decay as they are not exposed to plaque. However they can undergo a process called resorption under some circumstances. Rosorption of teeth are by cells called odontoclasts. In xrays these partially resorbed teeth may appear as decayed in xrays. If you can link the reports you have seen I can look at them and comment on it.

I am unable to find the text I had read before, which was making the claim that diets deficient in calcium resulted in children's teeth decaying before eruption. All I can find on the matter is this http://cyberdentist.blogspot.com/2006/11/can-tooth-get-cavity-before-it-erupts.html which backs what you've already said. I am curious how calcium in our diets affects how resistant our teeth are to decay. And how phosphoric acid in soft drinks may remove calcium from the body and promote decay.

Yes, it can be done to a certain degree.
Cementum is capable of repairing itself to a limited degree and is not resorbed under normal conditions. Some root resorption of the apical portion of the root may occur, however, if orthodontic pressures are excessive and movement is too fast. Some experts also agree on a third type of cementum, afibrillar cementum, which sometimes extends onto the enamel of the tooth.
Cementum is produced by cells called cementoblasts.
more here:
http://en.wikipedia.org/wiki/Cementum

The answer is not relevant as the question is on healing of a cavity. Root caries affect the cementum first which is only few microns thick and does not heal by itself since the cells capable of formation is no longer in relation to the caries cavity. The reference quouted does not substantiate the healing of a cavity involving cementum. Healing of a resorption site of cementum is totally diffierent and is not applicable here.


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How do PLINK files and HapMap Phased files differ?
I know that PLINK and HapMap files show the same information, but can you give a thorough explanation of how exactly they differ.

Better ask this question in biostars :-)
http://www.biostars.org/

According to http://pngu.mgh.harvard.edu/~purcell/plink/data.shtml#ped:

The PED file is a white-space (space or tab) delimited file: the first six columns are mandatory:
 Family ID
 Individual ID
 Paternal ID
 Maternal ID
 Sex (1=male; 2=female; other=unknown)
 Phenotype

[...]
Genotypes (column 7 onwards) should also be white-space delimited; they can be any character (e.g. 1,2,3,4 or A,C,G,T or anything else) except 0 which is, by default, the missing genotype character. All markers should be biallelic. All SNPs (whether haploid or not) must have two alleles specified. Either Both alleles should be missing (i.e. 0) or neither. No header row should be given. For example, here are two individuals typed for 3 SNPs (one row = one person):
 FAM001  1  0 0  1  2  A A  G G  A C
 FAM001  2  0 0  1  2  A A  A G  0 0
 ...

And here is what I find in the begining of a HapMap .ped file I got a few years ago (hapmap3_r2_b36_fwd.YRI.qc.poly.ped):

 Y001    NA18488 0       0       2       -9      C C     T T     ...
 Y014    NA18519 0       0       1       -9      C C     T T     ...
 ...

So far, it seems to me than this is plain .ped format: the number of "header" columns is the same, and seems to conform to the specifications given in the above-mentioned web page.
Now let's have a look at the .map files.

By default, each line of the MAP file describes a single marker and must contain exactly 4 columns:
 chromosome (1-22, X, Y or 0 if unplaced)
 rs# or snp identifier
 Genetic distance (morgans)
 Base-pair position (bp units)

[...]
Note: Most analyses do not require a genetic map to be specified in any case; specifying a genetic (cM) map is most crucial for a set of analyses that look for shared segments between individuals. For basic association testing, the genetic distance column can be set at 0.
[...]
The autosomes should be coded 1 through 22. The following other codes can be used to specify other chromosome types:
 X    X chromosome                    -> 23
 Y    Y chromosome                    -> 24
 XY   Pseudo-autosomal region of X    -> 25
 MT   Mitochondrial                   -> 26

The numbers on the right represent PLINK's internal numeric coding of these chromosomes: these will appear in all output rather than the original chromosome codes.

Here we have something that may be different.
The end of the .map file corresponding to the HapMap .ped file looks like this:

 26      rs28357376      0       15825
 26      rs2853510       0       15925
 26      rs2854125       0       16149

The HapMap .map file uses "plink's internal numeric coding" for the chromosome instead of the letter code (MT).
Otherwise, it looks a pretty standard .map file, with no genetic distance indicated.

I should have specified, I meant the HapMap phased/legend/sample files as compared to map/ped files


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Distribution of nutrients throuought a drink made of plants?
In an attempts to eat my veggies for the day in one shot, I blended together a bag of salad with some water. The mixture separated by density, a thick top layer containing the bits of leaves, and a bottom layer of just juice. My question is: how many vitamins and nutrients are actually found in the top layer compared to the bottom, and how efficiently would the body process them?

I removed the sentence about you throwing up in case this appears to be a personal medical question to some people. I don't think it really is myself.

@dd3 that's ok I still got a good answer.

If we assume the drink was very well blended most of the water-soluble vitamis (B and C) as well sugars could dissolve in the juice. Fiber would mostly remain in the plant debris. Oils and fat-soluble vitamins (A, D, E, K) would form their own oily layer or be found in an emulsion with the fruit juice.


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How compatible are mammal wombs?
I had read about science working towards the creation of artificial wombs however I wonder how compatible are mammal wombs and connected systems to develop fetuses. What species are so compatible that they would be able to surrogate the embryos and fetuses of another species?

it is not just the womb.. immune reactions can also cause incompatibility.. even in case of same species... see erythroblastosis foetalis

@WYSIWYG thanks i edited and added connected systems to include immune resactions

In short: Not completely, but more than you would expect.
The project to clone a mammoth considered using an adult female elephant as a surrogate mother, so in theory closely related species can do this.


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How do individual plants adapt to changes in temperature?
If you grow a plant from seed in your nice warm house, then plant it out in your temperate garden, it will stop growing for a while, possibly die, and if not, subsequently resume growth. Standard gardening practice is to 'harden off' plants, moving them to an area of intermediate temperature for a while before planting them out.
Why does this happen? What is the difference between a plant adapted to a warm environment and one adapted to a cold environment?
Expression of cold-tolerance genes? Levels of some secondary metabolite? Thickness of cell walls? Density of root hairs?
An unidentified author on the Royal Horticultural Society website states that
"The effect of hardening off is to thicken and alter the plant's leaf structure and increase leaf waxiness", which is not quite detailed enough to satisfy.

Cf. Why are some plants frost tender

As far as I know, the main challenges the plants have to face in cold environment are metabolism reduction and membrane fluidity. If the temperature is even lower, they may face freezing.
Increasing the metabolism is quite hard, because plants usually are unable to increase their temperature by its own. Plant may produce more pigments in order to absorb more sunlight; grow trichomes and other structures that may generate an air layer which acts as an insulator or simply reduce its metabolism by, for instance, hibernation. The amount of stomata is also related to temperature, and a plant growing in low temperature needs less stomata.
In bacteria sometimes there exist isoforms of many enzymes that are expressed during different conditions, and since plants usually have large genomes with tons of duplications, it's reasonable that some plants may express different genes for the same processes in high and in low temperature. One group of genes that are certainly expressed in cold exposition are membrane desaturases, which introduce unsaturation in the lipids, increasing the fluidity of the membranes. Some plants also protect themselves of freezing by accumulation of some substances, such as glycerol or proline, avoiding the formation of ice inside the cells.

Miguel Angel Naranjo Oritz Excellent answer. Could you provide a source for your information that plants hibernate ?

In botany the term hibernation, or winter dormancy (as opposite of estivation, wich is the same for summer months) describes the reduction of metabolism during winter. The most obvious example are trees that lose their leaves during the fall. Maybe I used a term a bit confusing.


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Do fake wasp nests actually fool wasps?
I have seen fake wasp nests sold as a deterrent against wasps and similar insects. Do they really work? Is there some scientific evidence for it?
A related link: http://www.scienceworld.ca/do-fake-wasp-nests-fool-wasps

I once heard someone who researches on wasps and he said that if you move the nest then the wasps get fooled and remain in the new location. I don't know about the fake wasp nests though.

Wasps are extremely territorial creatures. They also have great sight. Wasp colonies will send out foragers and scouts to look for uninhabited areas with food in which they can build a nest. Because wasps are so fiercely territorial, a scout wasp will generally stay away from an area with another colony already in it.
Because of this fact fake wasps nest works!!

Source: http://www.environmentalsociety.ca/main/wp-content/uploads/2011/05/Fact-Sheet-Wasps.pdf

It appears your picture has gone down.


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How animals maintain their body shape after development to maturity?
I've recently read a book on evolutionary-developmental biology for laymen, and it described how a fetus is progressively divided into more refined zones of genetic activity. These zones, kinda like GPS coordinates define which genes will be activated at which time and at which location.
What interests me is - after development to maturity, what defines how animals maintain their body shape? Is it the same "GPS" system that defines boundaries of an organism? Or is it something else within the specialized cells that tells them to grow in certain directions and avoid others?
To clarify the question with an example - lets take blood vessels - what prevents blood vessel lining from growing forever in all directions, taking up all available internal cavity space?

after development, the cells and tissues generally retain their transcriptional "memory" through epigenetic mechanisms. All they need to do is to maintain this state by replacing worn out cells etc..

Reference for the book? & possible to quote it?

@GriffinEvo.. i think any standard book on developmental biology has this topic (for e.g. Scott F Gilbert's).. It is known that developing embryo is divided into zones (governed by Hox proteins).. This is particularly well explained in case of drosophila

The laymen book is "endless forms most beautiful" by Sean b. Carroll

Normally, cells do not proliferate without a "command". The "zones of genetic activity" you mentioned are defined by gradients of morphogenic molecules (and cell interactions). In the adult organism the original "map" of concentrations of these molecules is already realized and the pattern they defined before is no longer present.
Another closely linked idea is that most cells in mature tissues are not able to proliferate, because they have already undergone the process of differentiation. In contrast, stem cells maintain their ability to reproduce. [There are still some ways to de-differentiate some types of cells, i.e. to obtain induced stem cells in vitro.] Thus, embrya are composed of embryonic stem cells, while adult organisms have several restricted pools of stem cells (for example, in haematopoetic organs, where new blood cells are produced.)


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What are the biological and nutritional benefits of having numerous smaller meals a day?
I have heard here and there that instead of consuming 3 largish meals (the traditional 3 meals a day), that consuming several smaller meals throughout the day is beneficial for health (and weight loss).
How true is this statement?  What are the biological advantages, if any, of such a diet?

One rationale is that smaller meals will cause less insulin secretion compared to a larger meal. With less circulating insulin over the time, insulin will be under the threshold required to activate the adipogenic program in the white adipose tissue. So, you will burn ingested carbohydrates instead of converting them in fat despite the same caloric intake. See for instance Munster and Saris, Plos One 2012.

From a practical point of view many patients miss the feeling of being full. They don't eat because they are hungry but to feel the satisfaction. So many patients end up eating more, then with 3 meals a day. Also there is still a argument if a steady insulin level is beneficial for non-diabetics. So good for weight loss - yes, but good for health - don't know.


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Organism identification, what is this?
Im trying to find out what this is, see image below.
Im thinking these are either some insect eggs or some sort of mosslike plant.
The substance is stuck to a steel pillar, outside, about 5 feet above the ground.
The substance is found in the Netherlands in a wet meadow area.
The substance has multiple tiny cells or eggs, seems to be only 1 layer thick and has a soft/smooth feel to it.

Excuse me for the bad picture, my camera would not focus better because of the reflective surface of the pillar.

I think this will be really tricky to answer, and it can probably be several different things. Insects can certainly produce egg clutches that are similar to this and usually in single/few layers. However, they are generally quite specific about their substrates (placing eggs on suitable substrates for larvae) and a steel pillar doesn't fit very well. However, e.g. moths (which often have spherical eggs in neat patterns) sometimes place eggs close to light sources they are drawn to, for instance windows.

I'm not sure this could be answered with much confidence, perhaps the Family or Genus are possible.

@fileunderwater, This was also my first tought exactly, I started googleling all sorts of dragonfly, moth and butterfly eggs. Yet all those eggs seem to be individual eggs clustered together. In the case of our unknown substance they look more like plant cells, with no space between the cells.

What we have here appears to be clustered insect eggs, and examples such as this tend to have some type of moth or butterfly as the culprit. It appears similar to moth eggs that I have observed on surfaces. See this page with information and this page with an example that look vaguely similar to your photograph. You would need an expert to identify a specific species though, if it's possible.

As I commented earlier, they dont seem to be butterfly or moth eggs since all of those are quite clearly individual eggs. This substance is more like a whole. If indeed these are eggs of some sort they seem to be covered in some protective layer.

This is more likely snails eggs.  If it is in a wet or very humid area, and the eggs seem to be immersed in a matrix of a clear substance, that help retain water.  Insects do not lay their eggs in substances like that, since there are more resistant to desiccation.

Hi Julio. Welcome to the site. It would be nice if you post some referenced pictures to support your answer.

If you get a higher resolution and closer image, it would be a little easier, but from what I can make out, I have two suggestions. To me, it appears to be tiny yellow eggs grouped together which leads me to believe it could be milkweed bug or a lady bug.
The eggs of the milkweed bug look like:

The eggs of a lady bug look like:

Since these pictures are of a much higher quality, it easy to tell the eggs apart and they have height. If I stumble across any more viable options, I will post them.


text:
How can pasteurized milk last 7 days?
In Estonia, the product bought from the shop lasts about 2-3 days, in Finland 3-5 days and In Oslo Norway 7 days.
The better infrastructure of transportation explains some for Finland and Norway.
But how on earth so big difference between Norway and Finland?
I heard today that some countries are fluoridating milk.
Ii is not in Finland and Norway.
However, it may be the case that some minerals are existing naturally more in Norway than in Finland. Also, more rain dissolves more minerals in Norway than in Finland.
How can pasteurized milk last 7 days?

Is it not more likely to be a difference in food safety regulations/company policy than a biological difference?

In the UK pasteurized milk lasts around  7 days. I'd assume 7 days was pretty typical.

I'd go with @RoryM there but I can't find any regulations on-line to suggest so - can't think of any other reason... perhaps processing techniques, have you looked at different brands within nations which might have different processing techniques?

I would rather think about regulatory differences instead of biological ones. (Edit, as also Rory M highlighted in a comment)
Extended shelf life can be obtained through microbial ultrafiltration. However in Europe, ultrafiltration labelling is not mandatory, so it is difficult to distinguish if a milk product was simply pasteurized or also ultrafiltrated. The converse case, biologically speaking, two milk products could be generally the same but one country could be more stricter than the other on shelf-life legislation. (The shelf-life relates more to the unsuitability for sale rather than for consumption).

Evidently the shelf-life of pasteurised milk is very dependent upon post-pasteurisation temperature of storage. Here is a paper in which the effect of temperature on shelf-life has been analysed. A sentence from the abstract says:

The microbiological stability for pasteurized milk packaged in HDPE bottle and stored at 2, 4, 9, 14, and 16 degrees C was estimated at 43, 36, 8, 5, and 3 d, respectively.

I think that you would need to know exactly how the milk had been handled from pasteurisation plant to retail outlet before you could make any valid comparisons. Any period out of cold storage could clearly have a big impact.


text:
Bacterial division and mutation rate
When a bacteria A divides it produces two cells A', A''. Each of them receives a copy of the chromosome/plasmids. Now, DNA replication occurs way before division in a semiconservative manner. That is, each new chromosome has an 'old' strand and a 'new' strand. Since the polymerase is error prone, my belief is that both genomes can potentially have mutations. Now when people refer to the mutation rate/genome/replication, e.g. 3x10-4 , Does this mean that:

Only one of the resulting genomes have this mutation rate? (according to me not likely).
The mutation rate takes into account the total number of mutations in both new genomes.
Each of the genomes can potentially have independently as many mutations as the mutation rate specifies.

i'm referring to replication erros, and not the two strands in a single genome, but to the two new strands in each of the two genomes.

edit of previous comment: I believe it would be option 2 or 3 depending on what sort of error has occurred and when - i.e. if there is damage to the old strand it could affect a strand of dna in both cells, if it is a transcription error in the new strand it may only affect a strand dna in one cell (A') and the A'' cell may be identical to the parent... (just a quick estimate at an answer)

Your question comes down to the definition of the units you state in your question - mutations genome-1 generation-1. In my opinion the answer is your choice (2).
How are mutation frequencies measured? Usually it is a case of scoring the appearance of a mutant phenotype as an indicator of underlying mutational events (see Drake,JW (1991)A constant rate of spontaneous mutation in DNA-based microbes. Proc. Natl. Acad. Sci. USA 88:7160-7164 for a detailed explanation.) Since, as you say, DNA replication is semi-conservative, the two daughter cells of a bacterial cell division each inherit one old DNA strand and one new DNA strand and so have the same probability of sustaining a given mutation. The overall mutational frequency has to be an aggregate of what has happened in both of them (and in all other cells in the population) since there is no way of distinguishing between them. In terms of your question the answer is (2) and this is why the mutation rate is normalised per genome.
In practice this figure is arrived at as follows. Suppose that you study a 1 kb gene, gene X, and measure the rate of spontaneous mutation in that gene (by some convenient assay) as 1 mutation per 107 cell divisions (again see the Drake reference for details). Assume also that the bacteria have a genome size of 2 x 106 bp.  Since each cell division equates to the creation of one new genome we get:
mutations per gene X per generation = 1 x 10-7
mutations per bp per generation  = 1 x 10-7/1000 (because it is a 1000 bp gene)
mutations per genome per generation = 1 x 10-7 * 2 x 106/1000
mutations per genome per generation = 0.0002
Now this is an underestimate because not all mutations will create a detectable change in phenotype. Drake uses a correction factor of 3.12 for this.
true mutations per genome per generation = 0.0002 * 3.12 = 0.0006 or 6 x 10-4
These were made-up numbers. See review in Drake JW et al.(1998) Rates of spontaneous mutation. Genetics 148: 1667-1686 for real examples.

Sorry for being so dense i think i understand why the rate is normalized by genome, but then can i say that daughter A' has N mutations and daughter A'' M mutations, then can i say that both N and M are distributed as a poisson variable with the mutation rate as the lambda?


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Which kind of tick is this and what is that thing around its back?
I was recently bitten by a tick. After having removed it from my body, I put it in a glass. By now, it has stopped moving, so I put it under a microscope and looked at it. I was surprised about being unable to get a sharp image of its body (upper part in the images) – what could that be? And can someone help me identify it?
I found a picture of a tick with a somewhat transparent thing around its back here – maybe that's what made it hard for me to get a clear focus on the back? And maybe it's related to this one?

It was found in Oldenburg, Lower Saxony, Germany. Its length is between 1.2mm and 1.4mm (I don't have anything that's very usable for precise measurement of such small lengths).
If clearer focus on a particular part of that thing is needed for identification, please tell me.

Where geographically was it found, and how large is it?

@kmm: edited to address your questions

As your link suggests, it looks like a female tick of the genus Ixodus. It is likely female because the scutum or shield only covers part of the dorsal surface. E.g.,

which comes from Bristol University Tick ID. The translucent posterior portion may just be from light passing through.
If you are able to zoom in closer on different parts, you can key out what species it is.


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Single Nucleotide Polymorphisms and diseases
I am writing a report on how Single Nucleotide Polymorphisms occurring in each of these regions:

Transcription factor (TF) binding sites
Epigentic signals
Splicing variants
MicroRNA binding sites
Coding regions

can cause diseases.   Related literature suggestion from you or just informations that you know would be grateful

SNPs in all these regions will modify the DNA sequence. Effects will depend on where exactly the SNP is. I'll summarize the conditions in which effects can be maximum

Transcription Factors (TFs) binding sites: SNP in the nucleotide positions that bind to the recognition amino acids in the TF
Epigentic signals: C->X [x: A,G,T] SNPs can disrupt DNA methylation hotspots
Splicing variants: SNPs at splice donor/acceptor sites can cause intron retention
microRNA binding sites: SNP in seed region can abolish miRNA targeting
Coding regions: certain SNPs can create premature stop codons for e.g. CAG (Gln) -> UAG (stop)

there is a lot of work on SNPs. If you search in pubmed for all these categories, you'll get many research articles as well as reviews.

SNP in the nucleotide positions that bind to the recognition amino acids in the TF.. What consequence does it have? H can it cause disease?

I meant what is the mechanism by which regulatory region SNPs causes diseases?

@Zizo here is an actual example where a SNP in a regulatory region leads to disease: http://www.ncbi.nlm.nih.gov/pubmed/16728641

Thanks @Bitwise, if you could kindly also give me examples for Epigenetic singlas, Splicing variants, MicroRNA binding sites and Coding regions or just some of them it would be awesome

@Zizo Google it - it is easy to find.


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What is the name of the appendage that mantis shrimp use to rub their eyes?
In this short clip, you can see the mantis shrimp using some sort of feathery arm/claw to rub its eyes. Looking at a diagram here, it appears possibly that it's using maxillipeds. Someone with knowledge of crustaceans (the behavior is probably not unique to mantis shrimp) would be appreciated.

Mantis shrimp use their first maxillipeds for grooming (maxilliped=modified appendage), which is specialized for this purpose. Details and a picture of the organ can be found in the link. The second maxilliped is their famous specialized organ for striking or spearing prey with enormous force. More about their raptoral appendage, with links to further references. Mantis shrimp also have very complex eyes, described as "...the most complicated visual system of any animal on Earth". Their eyes can see a range from ultraviolet to infra-red and has specialized regions for observing motion, form, depth, and color. More on Mantis shrimp eyes can be found in Marshall & Oberwinkler (1999).


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Can someone explain the color-changing unit (CCU) to me?
I've been physically carrying out serial  tenfold dilutions on samples of Ureaplasma to work out the color-changing units (CCU).
As a definition, the CCU is the highest dilution at which there is a color change.
If the highest dilution is 10^3, apparently that means that there are 10^3 cells per ml in the original sample. But this is what I do not understand. How are we sure of this?
I feel like there is a lot that I am missing.
Any help would be greatly appreciated.


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How different are tissue-specific fibroblasts from each other?
I am planning to utilize a new system in our lab, in which I will co-culture cancer cells from different tissues with fibroblasts.
I have the option to receive skin-derived primary fibroblasts. I have been told the normal fibroblasts are very similar all over the body. Is this really true? I assume that fibroblasts secrete factors, for example, that are tissue specific. The question is, how quickly do they adapt to a new environment? For example if I take these skin-derived fibroblasts and co-culture them with breast cancer cells, how long will it take the fibroblasts, if any, to become more like fibroblasts derived from the breast?

I have been told the normal fibroblasts are very similar all over the body. Is this really true?

No.

Strong evidence indicates that fibroblasts in different parts of the body are intrinsically different, and there may be differences between them even in a single region [3].

They have morphological similarities, but they act differently (at least in cultures):

Examination of skin and lung fibroblasts derived from the same human fetuses revealed significant in vitro differences. Fetal lung cultures had faster cell replication rates, greater [$^3H$]thymidine incorporation into DNA, higher cell numbers at confluency, smaller cell volumes, decreased cellular RNA and protein contents and lengthened in vitro life spans when compared with fetal skin cultures. In addition, these cell cultures had different responses to the addition of hydrocortisone to culture media [1].

They hardly adapt to a different serum (in vitro) [2]. Yet they have a great capacity to differentiate (in vivo):

[...] fibroblasts also seem to be the most versatile of connective-tissue cells, displaying a remarkable capacity to differentiate into other members of the family. [...] “Mature” fibroblasts with a lesser capacity for transformation may, for example, exist side by side with “immature” fibroblasts (often called mesenchymal cells) that can develop into a variety of mature cell types [3].

References:

E.L. Schneider, Y. Mitsui, K.S. Au, S. Stuart Shorr. Tissue-specific differences in cultured human diploid fibroblasts. Experimental Cell Research. Volume 108, Issue 1, August 1977, Pages 1–6. DOI 10.1016/S0014-4827(77)80002-5
Zamansky, GLEN B., et al. "Adaptation of human diploid fibroblasts in vitro to serum from different sources." Journal of cell science 61.1 (1983): 289-297.
Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Fibroblasts and Their Transformations: The Connective-Tissue Cell Family. Available from: http://www.ncbi.nlm.nih.gov/books/NBK26889/


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Possibility and feasibility of producing designed antibodies with bacteria
As stated here it is possible to produce fragments of antibodies in bacteria and harvest them (from the medium, I guess, but I don't have access to the full article).
As it is possible to design antibodies, would it be possible and feasible to produce important antibodies large scale through bacteria like it is done for example with insulin?

Today, I fail at reading.

I'll preface this by saying that I'm talking about antibodies of mammalian/human origin, consisting of two identical heavy and two identical light chains disulfide-bonded into the classic antibody structure:

It is possible to produce antibody-like molecules known as single-chain antibodies, including single-chain variable fragments (scFv) in bacteria and viruses, where it is also known as phage display. These hosts can also produce a modified Fab fragment that is engineered as a single polypeptide chain, and multiple other single-chain antibody-like molecules as shown below. In the past, this has primarily been done in E. coli, as they are a common tool used in protein expression, and have many advantages as an experimental system in general. However, single-chain antibody production in E. coli is hampered by the fact that these exogenous proteins tend to form inclusion bodies instead of being secreted into the medium, where they can be collected and purified much more easily, without the need for lysing the host cells. The paper you linked to describes a method for producing scFvs in the Gram-positive bacterium Bacillus megaterium, which is becoming more common for the production of recombinant proteins.

So, it is possible to produce antibody-like molecules in bacteria. However, unlike insulin, full-length antibodies are made up of multiple polypeptide chains, and are both glycosylated and disulfide-bonded. While there is evidence that bacteria can accomplish both of these biochemical tasks, the processes seem to require additional chaperone, trafficking, and regulatory proteins that bacteria do not possess, and as far as I know scientists have so far not been successful in producing full "proper" antibody molecules in prokaryotes.
However, there are many mammalian/human expression systems for producing fully functional recombinant antibodies in very high yield, and a number of FDA-approved monoclonal antibody drugs are now on the market, with many more in various stages of development and clinical trials.

Great answer, but I'm not aware of evidence that bacteria can carry out mammalian-style glycosylation. Insulin is of course two polypeptides linked by disulphide bonds, but I believe that the A and B chains are produced in separate fermenters followed by assembly in vivo. Linking two Ig heavy and two Ig light chains in the same way just sounds like a step too far in view of all of the possible wrong pathways.

@AlanBoyd check out PubMed. I'm reading through this review now, and there is also evidence for N-linked glycosylation as well.

Thank you for the detailed answer, it really helped a lot!

@MattDMo hit the highlights, but I wanted to comment on the creation of libraries of anbitodies for screening in bacatera.  But there has been interest in nanobodies - the antibodies of camelids  (llamas and camels) have only one chain, which makes the idea of heterologous expression in bacteria even simpler.

.. on the other hand its easier to make a monoclonal antibody from a mouse than a llama!


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Could humans and chimpanzees hybridize?
In some cases two species can hybridize. For example, Tigers and lions can hybridize to produce "Ligers".
Would it also be possible for humans and chimpanzees (or any other species) to hybridize ?
If not, what would be the likely cause of failure?
Why do some hybridization matings produce offspring, like the Liger, and some not? What mechanisms prevent hybridizations?

I've rewritten your question because I saw it getting downvoted after just a few minutes online - the basic principle of the question is interesting so I wanted it to survive

Related (but not a duplicate): Interbreedability between current humans and his ancestors

The concept of a human/chimp hybrid is called a humanzee. No humanzees have ever been recorded despite the fact that sexual intercourse between humans and chimps have been recorded on several occasions. This suggests that male-human/female-chimpanzee is not capable of producing viable offspring, at the very least.
As to why, several reasons will contribute: humans and chimps have a different number of chromosomes, making cross-fertility unlikely (although animals with different chromosome numbers can and do breed so this isn't absolute). Humans and chimps are anisomorphically quite different (i.e. the ratios of limbs are different and so on) so it's quite plausible that the growth patterns are not compatible. I'm not aware of any exhaustive studies into reasons why cross-breeding is impossible but it's also quite plausible that there are changes in the chemistry of fertilisation, etc. that will limit cross-breeding.
I'd note, finally, that there's evidence from the X chromosome that the human line continued to have some level of interbreeding with chimps for some million years after the initial split (Patterson et al, 2005†).

† I see that there are some later publications that have disputed the claims made in that paper. So I'll leave you to judge the merits of the arguments.

Goats and sheeps can mate, even though it is rare, and produce a live offspring, https://en.wikipedia.org/wiki/Sheep%E2%80%93goat_hybrid. Are they more closely related to each other than humans and chimps? Or is it just a numbers game, goats and sheeps try more often than humans and chimps?

@d-b There does not seem to be any good rule of thumb on exactly which species can interbreed based on relatedness. Your example is surprising given the difference in chromosome count, but sheep and goats are similar animals in body shape and size which may help.

But so are humans and chimps (or bonobos). However, goats and sheeps are frequently herded together and no one really cares if they try to mate so there has probably been a large number of attempts to produce a few results. The opposite is true for humans and chimps, very few attempts/opportunities and people in general are probably very concerned about any attempts.

@d-b Humans and chimps are not similar in shape. We're bipedal, they are knuckle walkers; our brains are several times larger; our jaws are different shapes and sizes, etc.

I need to sendong d-b's point.  We know that it's not easy to hybridize with chimps.  However, given that many species, even species with different # of chromosomes, have been proven capable of occasional hybridization we can't rule out the possibility that rare hybrids with either chimp or bonobo's are possible but haven't been documented.  I'd say it's  improbable that humans can reproduce with chips or bonobo's, but I'm not confident enough to say it's 100% impossible.  Most would consider it unethical to test such a hypothesis though.


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Why must a planet be in a star's "habitable zone" to have life?
I have seen many articles that talk about a star's "habitable zone" as the ring around it which is just the right temperature for planets to have liquid water, which is necessary for life. My question is, why does a planet need to have liquid water in order to sustain life? Who says that extraterrestrial life can't live off of some other kind of sustenance?

Nice question, I guess this could get really philosophical and head towards asking "what is life?" - it's just what we define it as yet you are right, extraterrestrial objects might exist that under other definitions could be called life!

@GriffinEvo Really? The current definition of "life" involves surviving using water?

@GriffinEvo What are you asking? I don't understand the word "life" to require the use of water to survive.

This is really just a side point because I started thinking about it a bit... I think finding life that survives well outside of the conditions we define as being necessary for life would force us to reconsider what defines life. Part of our definition of life (google "define life") is the ability to respire (a process within "metabolism"), this requires oxygen, but what if we find something that doesn't respire in a way we recognize? i.e. not using oxygen. Can we call that a living thing? (I think we would have to call it life)

Your question is not complete. I would suggest to slightly change the title to something like:
"Why must a planet be in a star's “habitable zone” to have life as we know it from our experience?"
You are right, when you are assuming that there could be another than carbon based life as we know it from our planet Earth.
There are many hypotheses that life could be based on Si or other elements.
But carbon is still the easiest element to create bounds with other
elements and carbon too. Why? Here is the answer from wikipedia Carbon-based life:

There are not many
  other elements which even appear to be promising candidates for
  supporting life - for example, processes such as metabolism - but the
  most frequently suggested alternative is silicon.3 This is in the
  same group in the Periodic Table of elements and therefore also has
  four valence bonds. It also bonds to itself, but generally in the form
  of crystal lattices rather than long chains. Silicon compounds are
  generally stable but do not support the ability readily to re-combine
  in different permutations in a manner that would plausibly support
  lifelike processes.

There is a great documentary from a physicist Brian Cox published by BBC this year called Wonders Of Life which deals with the basic questions how carbon based creatures were "born" on this planet ;) + other interesting things about life.
Brian talks there why the first organisms were created probably in water and how it could be.
Why water?
http://www.pbs.org/wgbh/nova/evolution/liquid-of-life.html

And why is water the best liquid to do the job? For one thing, it
  dissolves just about anything. "Water is probably the best solvent in
  the universe," says Jeffrey Bada, a planetary scientist at the Scripps
  Institution of Oceanography in La Jolla, Calif. "Everything is soluble
  in water to some degree." Even gold is somewhat soluble in seawater.
  (Before you get any ideas about extracting gold from the oceans, I
  should add that, according to Bada, the value of dissolved gold in a
  metric ton of seawater comes to about $0.0000004).

If you take a route that there could be a different form of life outside of habitable zone, then many things are possible. E.g. life on asteroids, ouside of solar systems, life in other dimensions, life based on silicon or some other elements, energy based life? Or even dark matter and dark energy based life or gods/God-like creatures and all kinds of sci-fi ideas ;).

It should also be noted that other heat and energy sources are plausible replacements for stellar radiation. E.g., tidal warming of a Jovian moon and vulcanism.

Why does the fact that water is a good solvent make it necessary for life?

@Daniel It is necessary for the life as we know it on our planet. If you want to speculate then many other things are possible. But the scientists take in count the fact how the elements are spread through the Cosmos. And they came to the conclusion that hydrogen and oxygen are pretty common. E.g. you have ice on Mercury, Earth, Mars and on Jupiter's and Saturn's moons, asteroids, comets and probably many other objects ad planets in space. More about the importance of water is e.g. in the 1st or 2nd episode od Wonder of Life, when Brain talks about the "cell = batteries" and "waterfalls";)

@Daniel here is a summary of what the water is capable of and why it is so important for life (as we know it) and why astrophysicists are looking mostly for planets with water as a possible life candidate http://www.youtube.com/watch?v=7sA_JJ9gj2E Btw. the thing with God is exagerating, but everything else is a nice summary of some articles. So, if you want to watch a 10 min talk about how the water is good for life, watch that video.


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When a Lysosome's bonding sites all get bonded to, what is the most resource and energy efficient way to handle the used Lysosome?
Let's say a Lysosome that bonds to a hazardous material to neutralize it has all bonding sites used up. would it be more safe / efficient to excrete the entire Lysosome / hazardous material molecule or to bring it to a certain organelle / organ to unbind the material and send it for excretion and then have the Lysosome available for use again? In which way do Lysosomes in nature commonly handle this problem?

Enzymes are catalysts, i.e. by definition they don't get used up. More info on "cellular garbage disposal" can be found here: http://en.wikipedia.org/wiki/Lysosome

Are you sure that you are referring to enzymes? Sounds more like you are talking about things like hemoglobin (not an enzyme), which binds to the waste product CO2 and carries it to the lungs for excretion.

okay yeah, see, I learned something I didn't even  realize I was going to. updating question to fit Lysosomes. Does it make more sense now what I was asking?


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Can life subsist on anything else but water?
Inspired by an answer to a previous question.
It's hypothesized that extraterrestrial life could be based on silicon rather than carbon as its main structural element.
Are there similar theories about an alternative "life solvent" rather than water?

Ha, I was just about to ask the very same thing having read the same question!

Some scientists are indeed working toward inorganic life see here, bottom part. Not that they succeeded yet, but it's an active research field.

This is not a definitive answer.
The solvent closest to water in its properties such as dielectric constant, melting/boiling points, etc are formamide and sulphuric acid.
                        F       S       W
Melting point (⁰C)      2       10      0
Boiling point (⁰C)      210     337     100
Dielectric Const        109     84–100  80
Specific gravity        1.133   1.94    1

But water is the simplest i.e made up of only two types of atoms (Which are decently abundant).
Regarding silicon: even though silicon can undergo some level of catenation (silanes) it is not comparable to carbon. Silicon can form polymers like silicone (poly-siloxanes). But I think carbon seems to be more versatile. It is also more abundant (check this out. A nice representation of abundance of different elements in the universe)
Also check this out: it is about exoplanet habitability.
Since certain elements are more abundant than others, the likelihood of them giving rise to life is higher. Therefore water seemingly emerges as the life solvent.
[still most times we see everything in an earth point of view]

This may not completely answer your question, but provide some information.
Looking at this Wikipedia outline Non water solvents, other possible candidates are ammonia, hydrocarbons even hydrogen fluoride.
Digging a little deeper, this abstract of the article: "Many chemistries could be used to build living systems." (Abstract only) describes the possibilities of ammonia and liquid nitrogen as being potential suitable solvents.  Page 678 onwards of the article: "Is there a common chemical model for life in the universe?" also describes other solvents such as ammonia (I should say that there quite a lot of Star Trek references in that paper).
I hope this goes part of the way to help.


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What causes the colors we see in eyes?
Genetics aside, what are the biochemical reasons for the different colours of human irises?
Also, related, how does eye colour change, particularly in childhood?  (example:  my eyes used to be blue, but are now greenish-hazel).

Do you mean what are the molecules/reactions that generate eye color? Your question is a little unclear.

Does this answer your question? http://biology.stackexchange.com/questions/728/how-is-eye-color-in-humans-inherited Or are you more interested in how eye color changes throughout one's life?

I'll clarify the question - but yes, I am looking at the molecules/reactions and changes over time

A large part of eye colour is determined by how light is scattered in the stroma. Are you interested in how this works as well, or only the underlying molecules? I can imagine that parts of changes with aging has to do with changes in e.g. the density of the stroma which would affect scatter.

@fileunderwater yes, I am definitely interested in that aspect as well.

Some relevant info here: http://biology.stackexchange.com/questions/7046/why-do-most-humans-cats-have-blue-bluish-eyes-at-birth/7049#7049 . Changes with age would be explained by changes in melanisation.

as @fileunderwater said the blue color is not because of any pigment but because of light scattering. In humans there is only one kind of pigment i.e melanin. The eye shades are because of varying levels of melanin combined with effects of light scattering.

The colour of human eyes is determined by the pigmentation present and the scattering of light. Variance in the colour and density of the pigments affects how light is absorbed and reflected causing the different iris colours we see. Wiki has a fairly comprehensive coverage on the topic so,I'll use a few of the wikipedia examples to explain how the pigmentation and scattering of light interact to give colours:
Blue eye colour is the result of pigment in low concentration and Rayleigh scattering (or Tyndall effect) of the short light wavelengths (blue is short, red is long).

"There is no blue pigmentation either in the iris or in the ocular
  fluid. Dissection reveals that the iris pigment epithelium is brownish
  black due to the presence of melanin. Unlike brown eyes, blue eyes
  have low concentrations of melanin in the stroma of the iris, which
  lies in front of the dark epithelium. Longer wavelengths of light tend
  to be absorbed by the dark underlying epithelium, while shorter
  wavelengths are reflected and undergo Rayleigh scattering in the
  turbid medium of the stroma. This is the same frequency-dependence
  of scattering that accounts for the blue appearance of the sky.
  The result is a "Tyndall blue" structural color that varies with
  external lighting conditions.

Brown eyes are the result of higher melanin concentrations which absorbs more of the light, reducing the amount of light being reflected.

"In humans, brown eyes result from a relatively high concentration of
  melanin in the stroma of the iris, which causes light of both shorter
  and longer wavelengths to be absorbed."

Green eyes appear to be mid-ground between blue and brown, they have more pigment than blue but less than brown.

"As in the case of blue eyes, the color of green eyes does not result
  simply from the pigmentation of the iris. Rather, its appearance is
  caused by the combination of an amber or light brown pigmentation of
  the stroma, given by a low or moderate concentration of melanin, with
  the blue tone imparted by the Rayleigh scattering of the reflected
  light."

More can be read on this in these two studies: study 1 & study 2
What is Rayleigh scattering / the Tyndall effect and why do they turn eyes blue?
I shall refer to this as the Tyndall effect but in the literature both Rayleigh and Tyndall are used because they are apparently very similar though Tyndall occurs with much larger particles. The Tyndall effect is caused by the variable scattering of light by particles depending on the wavelength of the light and relative size of the particles. Shorter wavelength lights are scattered more than the longer ones (so more red light is absorb than blue) which means more blue light is reflected. When more melanin is present in the iris it will better absorb the short wavelength light than when there is little melanin, therefore, people with low melanin levels appear to have blue eyes.

"An analogy to this wavelength dependency is that longwave electromagnetic waves such as radio waves are able to pass through the walls of buildings, while shortwave electromagnetic waves such as light waves are stopped and reflected by the walls."

Why do eye colours change?
Again, wikipedia has a fairly thorough section on this and I will just summarise and directly quote it. Eye colour can change because the melanocytes responsible for the pigments have to continually produce pigment and, just like those causing colour in hair, they can become less productive (which is why we have grey hair) and this happens more with age. Infants often have blue eyes that turn dark, just like yours did, because the melanin is gradually accumulated - it just takes time for enough pigment to build up and allow the eye colour to match it's genetic determinants:

"Most babies who have European ancestry have light-colored eyes before the age of one. As the child develops, melanocytes (cells found within the iris of human eyes, as well as skin and hair follicles) slowly begin to produce melanin. Because melanocyte cells continually produce pigment, in theory eye color can be changed. Most eye changes happen when the infant is around one year old, although it can happen up to three years of age. Observing the iris of an infant from the side using only transmitted light with no reflection from the back of the iris, it is possible to detect the presence or absence of low levels of melanin. An iris that appears blue under this method of observation is more likely to remain blue as the infant ages. An iris that appears golden contains some melanin even at this early age and is likely to turn green or brown as the infant ages.
  Changes (lightening or darkening) of eye colors during puberty, early childhood, pregnancy, and sometimes after serious trauma (like heterochromia) do represent cause for plausible argument to state that some eyes can or do change, based on chemical reactions and hormonal changes within the body.
  ... eye color over time can be subject to change, and major demelanization of the iris may also be genetically determined."

In this study 10-15% of those studied had changes in eye colour beyond childhood so, al though colour is generally stable past childhood, it is not uncommon for eyes to change, and this is likely due to changes in melanin composition. This study is an example of clour change in birds too.
A side note: Animals with other colours
It is common for animals to have other eye colours, for example Blackbirds (Turdus merula) have an Orange eye, which is caused by Carotenoid pigments, rather than melanin as in humans. The reason they have this could be as an indicator of quality in courtship - carotenoids are hard to get, males with bright orange eyes therefore have access to good food resources, and female blackbirds find that attractive. (This section is all from my memory after a talk with a tutor on my undergrad field course in the Isles of Scilly).


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Chromatin shearing: what is it and what are the effects of high-sensitivity?
I am reading a paper  which discusses a complex (MSL-DCC) involved in dosage compensation of the drosophila X-chromosome. Descriptions of the complex's structure and function are given in the papers introduction.
To start with, could someone explain what is chromatin shearing? what is happening during the process?
Secondly, the authors then say:

"Our data suggest that the complex is particularly sensitive to shear
  forces on transcribed chromatin so that only the direct interactions
  on MSL-3 with nucleosomes are retained" - discussion section (subheading: interaction of the MSL-DCC with target gene bodies)

Could someone explain what is meant by 'particularly sensitive to shear forces'? In comparison to what? And what are the consequences of it being more sensitive?

Shear forces are experienced by all molecules, and molecular complexes when they are treated roughly. So, for example, if you have a solution of high molecular weight DNA it will be very viscous, but if you treat it roughly by pipetting up and down through a narrow aperture the DNA strands will suffer shear forces strong enough to break covalent bonds and the solution will become less viscous. Another example of the use of shear forces in biology is lysis of yeast cells using small glass beads. As the slurry of beads and cells is vortexes the cells experience intense shearing forces (forces tending to pull different parts of the cell in different directions) and they break open. They are not being physically ground by the beads.
In the specific case that you quote, you apparently have a multimolecular complex (MSL-DCC) held together by weak (non-covalent) interactions and interacting with the nucleosomes through a component called MSL-3. Without looking at the paper, it seems that this complex is prone to falling apart (during isolation?) as a result of shear forces strong enough to overcome the non-covalent binding interactions. Think of a helicopter with a man hanging on to the undercarriage with both hands. Then imagine a second man hanging on to the first man's boot lace with his thumb and finger. Who will fall off first due to the shearing forces experienced as they are buffeted by the wind?
The helicopter is the nucleosome, the first man is MSL-3 and the second man is the rest of the complex.
added later in response to MattDMo
looks from this that I was wrong - it's actually a French press and other homogenizers that generate shear forces. I don't think I made the glass bead story up, but I can't remember who told me. The BeadBeater people also refer to "cell cracking" not shear. Apologies everyone, I think the rest of the post still holds up, and thanks to MattDMo for the challenge.

Fantastic analogy with the helicopter, I used that in the Journal Club today - turns out I wasn't the only one not familiar with the term. Helpful answer thanks.

Glad it was useful - after posting I was a little nervous about how it would be received.

I didn't know that cells were disrupted by shearing forces and not by the beads themselves. Do you have any reference for that? (not that I don't believe you, I'd just like to learn about it...)


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Why don't individuals with sickle cell trait suffer from sickle cell anemia?
Ostensibly, in people with sickle cell trait, half of the hemoglobin in their body would be defective.
Is it actually the case that sickle cell hemoglobin is produced in equal amounts?
If not, how is that regulated? If so, how does that still not cause anemia?

This could be a very long answer, but I'll try to keep it brief.
The first thing to understand is what causes the anaemia. I'm going to refer to defective haemoglobin found in a sickle cell patient as HbS and normal haemoglobin as HbA. Under certain circumstances (low O2 concentrations) the HbS protein is prone to aggregating into long filaments. Here is an image of a lysed erythrocyte releasing some of these filaments.

The presence of these filaments in the erythrocytes causes them to become misshapen (sickle-shaped) and this in turn causes them to get filtered out for destruction in the spleen which is continuously monitoring for defective erythrocytes (which could cause blockages in the circulation). This causes the anaemia (specifically a haemolytic anaemia, due to erythrocyte destruction, and nothing to do with a lack of iron).
The appearance of the ability to form filaments is due to a single Glu>Val mutation in the two β subunits of the haemoglobin tetramer. The new amino acid can fit into a pre-existing hydrophobic pocket on the surface of another subunit and so the molecules can daisy-chain to form the filaments.
The normal HbA can also bind on to a growing filament (it has the binding pocket) but that terminates the filament (because HbA doesn't have the Val residue). In this way people with sickle cell trait are protected from the anaemia by their normal haemoglobin.


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What is a pA(2) value?
I saw this article http://www.ncbi.nlm.nih.gov/pubmed/16710314 and it mentioned pA(2) values and I had no idea what they were. What are they? What do they mean?
If possible it'd be just dandy if you could cite some journal articles/books/other reliable sources for me to dig up.

I don't know enough about this to write a good answer, but you can find an explanation here. A p(A2) value describes the affinity of an antagonist for its receptor.

Digging around a bit, I found a few resources:
Design and models for estimating antagonist potency (pA2, Kd and IC50) following the detection of antagonism observed in the presence of intrinsic activity.
and PHARMACODINAMIC on page 30, describes pA2 as:

indicates affinity of antagonist for receptors

(as Alan Boyd just commented on)

Below are responses generated using the isolated guinea-pig ileum preparation to determine a pA2 value for a sample of the cholinergic antagonist homatropine.
Responses are expressed in millimetres +/- SDM (n =4). Plot the data and then determine by Schild analysis the pA2 value and Schild slope. What conclusions can you draw; does the experiment/data fulfil the criteria for a valid Schild analysis?
Acetylcholine      ACH Alone    ACH +Homotropine       ACH +Homotropine   ACH +Homotrop
Concentration                     3x10^-9 M              1x10^8M            3x10^-8M
[Molar]
3 x 10^-9            3+/-1
6 x 10^-9            8+/-3            Not Response
3 x 10^-8            28+/-6             10+/-4             No response
6 x 10^-8            38+/-8             21+/-9           5+/-2                                                    No response
3 x 10^-7            55+/-5             43+/-7                27+/-9             10+/-4
6 x 10^-7            56+/-5             52+/-3              38+/-7             20+/-7
3 x 10^-6              -                55+/-4              53+/-6             43+/-6
6 x 10^-6              -                   -                56+/-2             54+/-5

This is a well-written answer; however, it does not answer the question being asked. If you could state what exactly it is as opposed to how it behaves when tested on a guinea pig that would be helpful. Also, it is advisable that you put in references. Aside from this, you did well for a first answer and I welcome you to Biology S.E.! If you have additional questions, please visit The Help Center.