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Do oysters feel pain?
Do oysters feel pain when you bite into the inside, or when you crack open the shell? I tried google searching it to no avail. When you bite inside the oyster or when you break the shell to open the oyster, does it feel pain?
EDIT: (Since some people think that mine is a duplicate) I'm asking if the oysters feel pain when we eat the inside, or when we crack open their shell. To the least of my knowledge, ants and oysters have a different body so I don't know if they do feel pain.

Possible duplicate of Do ants feel pain?

This question is already answered by many of the "do X feel pain?" questions.

This is not duplicate of 'Ants feeling pain' since ants and oysters have different organisation and differ in terms of their sensory organs.

@VishalKumarSahu no, but a lot of those questions need to start with definition of pain. We can't measure "pain" of an organism, only observe reaction. So OP can google more about oysters and how they react to X

You should define what you mean by "pain". Do you mean "pain" simply as a reaction causing them to do something such as (try to) withdraw from the cause of the stimuli, and possibly ability to develop automatic reactions to similar situations so they try to avoid the experience of this pain in future? Or do you mean something deeper, "suffering" or "psychological trauma" or "fear of pain"?

I saw a text across the internet (antivegan joke) claiming even plants feel pain. Even when they are already cut. I'm just wondering what is your intention? To claim that oysters should not be ate? Any being tries to survive, whether it feels pain or not and you eating them already contradict their "goals".

I just wanted to know whether they feel pain so maybe I can eat them quicker and make their death quick. It does sound a little.. weird.. but I do like eating oysters.

I vote to transfer this question because it is about philosophy, not biology.

It is very unlikely that oysters feel pain however it's not clear what the question actually means
What does it mean to say something feels pain? The most reductive biological interpretation is to say that "feeling pain" is simply the capacity to sense damage, or the threat of damage, to the body and communicate that to the nervous system in a way that elicits a response. However, that's not really what we're usually talking about feeling pain, but rather the unpleasant sensation that accompanies these signals.
And that's more difficult, because we know that the two are not equivalent. For example, disabled athletes are able to improve performance by inflicting injuries they cannot directly feel, but their bodies still respond to. In this case the reductive biological pathways are active but the sensation of pain is absent.
Oysters have no brain, but simply an couple of enlarged ganglia that perform some rudimentary centralised functions, and so it seems very unlikely indeed that they are capable of experiencing any sensations and thus almost certainly do not experience pain in the sense we would usually use of "feeling pain". But they do have a nervous system which can respond to stimuli including damage, or threat of damage, to their tissues so they have what could be described as having a pain response.

@BenCrowell: No, it doesn't; it convinces me that snails have a pain avoidance response. I do not think that this is either equivalent to or implies that the snails feel a sensation of pain.

Referring to this research article on PubMed, oysters have their sensory system and organisation like humans. So any change or invasion in the system of Oyster is communicated through sensory organs. So Oysters do feel pain. It's like, pain is a result of something harmful or negative is going on.
Regarding break opening the shell, as it is a sort of insult to their protective system, they have the sense of removal of the covering, we can term it as 'pain'.

Articles listed on PubMed are not necessarily from NIH, any more than websites you find through a Google search are not from Alphabet. All the paper you mention demonstrates is that oysters have a nervous system, which is far from controversial and says nothing about the organization of their nervous system with respect to humans. From a neuroscientific perspective, pain and sensation are not the same; I suppose yes, you can term it 'pain', but I could also hold up an apple and term it 'pain': that doesn't mean it's valid or is how people in the field talk about pain.

"they have the sense of removal of the covering" I would be very interested in how we would prove/disprove such a statement.

@BryanKrause, but an apple is not a sensation. And this is not meaningless, how can you know other people feel pain and not just a sensation? Monkeys, fish, worms?

@rus9384 Other people, as well as monkeys, have the exact same neural organization of pain pathways. Fish have some similarities, though not identical; worms are much different. It is quite possible in humans to have reflexes without pain, and other types of sensation are carried separately from painful ones, so simply having sensation does not mean having pain, even in the context of aversive stimuli. That also doesn't prove that something like an oyster doesn't have pain, but if it does it is instantiated differently than ours. The answer says "oysters feel pain" without support.

Please add options for the questioner, about the education like if he is graduate or post graduate, if he has published paper or not, and the people who give answer should answer based on that. or always answer like they do publish a research paper.

Bioethicist Peter Singer argues that "organisms evolve a capacity to feel pain because it warns them of dangers from which they can then move away. As oysters don't move, there is no reason why they should be capable of feeling pain." Singer consequently does eat oysters though not meat.
Philosopher of science Peter Godfrey-Smith, cited in the accepted answer, has spoken directly to the question of pain in oysters:

"An oyster, in contrast [to shrimp], has a very small and decentralized nervous
system. Whereas recent evidence pushes quite hard in the direction of
recognizing crustacean pain, there is no such evidence I can find for
oysters. It’s difficult, though, to find any work in recent years on
oyster behavior. One reason is that even compared to other shellfish,
such as clams and scallops, there is not much that oysters can do.
Clams can dig and scallops can swim. Scallops and some clams have
genuine eyes. Oysters may have some light-sensitivity, despite lacking
eyes, and they have tiny ‘tentacles’ that are sensitive to various
things. But their behavioral responses, as adults in shells, are very
limited.† An oyster will not swim up towards you like a castanet, as a
scallop can. As far as I can work out, oysters can do little more than
open and close their shell, and make other adjustments to the flow of
water they bring in. Their reproductive behaviors are simple, too. It
is always possible to imagine a very simple system having rich
experiences like pain – and imagine any very complex organism lacking
them – but those acts of imagination are not evidence for much. There
seems no role for pain in an oyster’s life – in the way there is for
shrimp and crabs, as Elwood emphasizes ... Shrimp are pretty clearly in the category where it at least makes sense to consider their subjective well-being, and oysters most likely are not."

All animals feel pain. We know this in our souls as human beings. All animals feel pain when they are being ripped apart, eaten alive or physically harmed and all animals fight for life. Only in 2021 in the UK scientists finally substantiated that crabs feel pain. This is definitely not a new discovery, this is just finally telling people the truth . And oysters are actually in the crab family . Oysters have a nervous system and a heart, they are alive so it is merely common sense and basic biology to understand that they feel pain . Anything with a heart feels pain when it is murdered. Some people will even argue that cows and pigs don’t feel pain because they like the way that they taste. But if you ever see and hear a pig or a cow being slaughtered you will know instantly that they feel pain. Even pearls in oysters are a protective me mechanism to survive. Oysters create pearls only when a grain of sand or pebble invades its shell and to protect themselves they create this secretion called nacre to coat the irritant that had invaded its shell and protect the oyster and this is what we call pearls.And that’s just an irritant like a grain of sand, not being eaten alive by a human .


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Why are more children being hospitalized with Covid-19?
I see that more children are being hospitalized with Covid-19. If I recall correctly, throughout the pandemic, researchers have thought that children were more resistant to the virus because they are often exposed to other viral pathogens, and therefore often have a Type I IFN response activated (which I've taken it is very effective at preventing infection).
I'm curious to know why more children are being hospitalized now. Some possible reasons that come to mind are that the coronavirus has evolved to better subvert the Type I IFN response, or that it has evolved to be able to better infect cells that are mounting a Type I IFN response, or that children are being exposed to fewer pathogens now (than they were even recently), or that the number of children hospitalized is independent of the number of children infected.

Since Delta is so much more transmissible than earlier variants, it's likely that many more children are being infected than previously. More infected -> more hospitalized.

Children have the lowest vaccination grade. They're also a lot less likely to keep their distance from each other.

Right now, at least, it's not clear whether anything significant has changed biologically for children with respect to the Delta variant.
What is known for certain, however, is that Delta is very infectious, and that the vast majority of kids are still unvaccinated, either because they are under 12 and not eligible or because they are teenagers whose parents didn't feel a sense of urgency to vaccinate.
In the US, where COVID is surging and more than 70% of adults are vaccinated, just comparing vaccination rates for different age groups means that we should expect to see a far larger fraction of the infected being children than in the previous waves. There's a lot of infections going on right now, and thus as a baseline, even if the danger for any given child is the same as with the prior variants, we should expect a lot more sick kids than before.

Add to this the anti-mask crowd and the start of in person schooling and we will see many more sick before this thing is behind us.

Washington Post reported on August 3rd that 57% of US adults had at least one vaccine dose. Has the number changed that much in less than a month, or is there an inaccuracy in one of these figures?

@electronpusher You are getting the figures in the article confused.  Currently 59.9% of all people in the US (including children) have at least one dose. When you remove children under 18, it's currently 72.3% of adults.  Children in the 12-17 age bracket are currently at 44% with at least one dose. All of these numbers were just a few percent lower two weeks ago.

Is Delta more infectious than other variants though? Yes, it's very prevalent, but you probably wouldn't call this year's strain of influenza more infectious than last years, and the year before that and so on. So while your statement that it's very infectious is true (every SARS-CoV-2 variant is), it may mislead some people who may think that Delta is somehow worse than other variants, while it just has better fitness in the current population.

@JohnEye Although the exact r-value isn't certain, the data so far shows the Delta variant to be far more infectious than other strains. See, for example: https://context-cdn.washingtonpost.com/notes/prod/default/documents/8a726408-07bd-46bd-a945-3af0ae2f3c37/note/57c98604-3b54-44f0-8b44-b148d8f75165.#page=1

The document was criticized recently on This Week In Virology podcast for various reasons, the exaggerated and weakly-supported claims about infectivity among them, see for example here (link with timestamp): https://youtu.be/EmdBoM8g9m4?t=3700 The whole episode is quite interesting and the hosts go into considerable details about R0 estimates, how much of a slippery number this is since it changes with vaccinations, naivety of population, human behavior, seasons, policy, cultural factors etc, and they discuss how difficult it is to untangle these factors and produce anything useful.

@JohnEye Yes, evaluation of the situation is still in flux and there are caveats on any number. Current evidence still generally points toward "significantly more infectious", however, and arguing the point is splitting hairs with respect to the question at hand.

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CRISPR-Cas9 knockout
With CRISPR-Cas9 I have conducted a targeted knockout of a DNA region encoding a certain protein (working with leukocytes). My question is, how long does it take until this protein is not detectable any more (e.g. via surface staining + flow cytometry) after the DNA has been manipulated? Or in other terms: how often are transcription, translation etc. taking place?

What cell line are you working with? Different celltypes can have fast differences in turnover rates of (DNA/)RNA/proteins.

Thank you! Actually I am working with fresh human PBMCs (and thereof with CD4+ cells)

To answer your question multiple parameters which one should be taken into account.
There are two main sets of parameters: gene specific and cell line specific.
Parameters related to your specific gene of interest :

Do you know the half-life of the RNA of your gene of interest? Most of the time it is not known but there are several tools and resources which can predict it based on a lot of different features such lengths and stability of 3'UTR, 5'UTR, number of exons introns, etc.
Another indication is if there are already people who have either perform a genetic perturbation (siRNA, CRISPR, etc) or a degradation assay. In this case you might be able to guess what is the relative half-life of the RNA or the protein.
Which leads us to the half-life of the protein of interest. Proteins which are soluble tends generally to have a smaller half-life than membrane proteins (not necessary true there are exceptions). For example doing a complete functional knockout of a transcription factor might be easier than a GPCR receptor. If it is a membrane protein, to which organelle does it localize? Is the organelle recycling the membrane a lot or is the cell dividing? In this case you might have chances that the viable proteins present before the genetic perturbation get diluted. In these examples, you might get ride of a soluble protein in less than 24-48 hours, whereas a very stable membrane protein might take 7-10 days.
The number of RNA copies is important as well as the number bound to ribosomes (less important) and their localization in the cell (less important)
The abundance of the protein in general.

Parameters related to your cell line of interest:

The lineage of the cell line you selected: different cell lines have different global transcription and translation rates.
The rate of division of the cell line (extremely important parameter): the faster the cell line will divide the faster  the mRNA copies which were not perturbed (wild-type) and the proteins present before the genetic perturbation will be diluted between daughter cells.
Number of copies in the cell line: if there are multiple copies of your gene of interest, you would need to make sure that each copy of the gene has been perturbed to lead to a functional KO.
Genomic stability of the cell line: some cells lines like HeLa are quite known for genomic instability where a lot of the genome can be rearranged can perturbed copies can be fix using viable copies

Last but not least, it depends technically how you do the CRISPR-Cas9 genetic perturbation: transfection of the gRNA, electroporation of the Cas9 with the gRNA, lentiviral mediated delivery etc. The time I have provided are after all the components have been delivered and are present in large amount in the nucleus.
I hope that helps!

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What is the most difficult feature to explain evolutionarily?
I wonder what are examples of organs/structures/behaviours/cooperation that evolutionary biologists themselves find most difficult to explain -- to explain how they could appear evolutionarily -- within known mutation rates, generation frequency, and known time frames.
Excluding issue of appearance of life itself.
Knowing rates of mutation and generation cycle (and population size), it would be possible to estimate time needed for appearance of new feature.
Thus it would be possible to spot counter-examples, such examples that are probabilistically beyond possibility to appear in given evolutionary time. Are such examples known ?
I might be naive, but I think some rare behavioral trait can be a candidate, behavior that does not trigger even once in a lifetime of organism, on average, that triggers really rarely.

@J.M.: sure, but their point is absolutely unexistent...

This is a classic survey question that begs for arguments not based in fact, but on a gut "feeling" about the likelihood of the evolution of characteristics

@Tyler try suggesting a way to improve this question. It is always valid to question even if it is the paradigm.

@Tyler: According to Dawkins, speed of evolution of not gut feeling but is subject to numeric estimates and computer simulation. Rates of gene mutations are known, cycle of reproduction can be estimated, sizes of population can be estimated, hence pace of evolution can be estimated, even if with large estimation error, but still, simulated.

@Andrei: this question assumes the existence of a metric by which we can 1) quantify rate of evolution, and 2) find anomalous development under that metric. Maybe it's better to ask questions about this metric before speculating that it has been used and then asking for the ranking.

@Andrei, would it be possible to clarify your last paragraph? I can't make any sense of it.

I won't claim that these are the most difficult things to explain evolutionarily, but these two are hard:

Host-Pathogen dynamics. They start out easy enough, but the interaction between a pathogen and its host is intensely complex. You have the immune system, pathogen-pathogen interaction, the balance between weakening a host and killing a host, dozens of different transmission mechanisms, at least two levels of evolutionary pressure (inter-host and population), etc.
Social/Societal level traits. Evolutionary psychology has, for example, been criticized for not being able to get much past the level of "Just So Stories" in terms of its ability to explain human societal traits using evolutionary theory.

I agree with (2) simply because it’s very hard to find good evidence (as you mentioned with the “just so” stories). I disagree with (1) since this can be explained by quite easy models and is a classical example of evolutionary arms race.

@KonradRudolph I work on some of those models, and they're less than "quite easy", especially when multiple pathogens are pulled into the equation, or you start working on multiple scales.

Fair enough, point taken.

To answer your question directly, there are a number of examples which creationists like to bring up, such as woodpecker's tongue which is wrapped around its brain or the archer fish which shoots down insects with water and has to adjust it's aim for refractive difference between water and air. These features supposedly 'couldn't have evolved' but of course one's disbelief doesn't make anything true or untrue. This is what Dawkins calls 'argument from personal incredulity'.
Let me also point out a few evolutionary counter arguments to such reasoning.
The presence of selection radically changes what is 'likely' or 'possible' to happen. For example, you wouldn't argue that it's highly improbable that the stones on the beach are ordered by size, if you know that the action of waves orders them in a certain way. Dawkins' weasel (http://en.wikipedia.org/wiki/Weasel_program) also demonstrates this principle.
Another Dawkins' argument is that, contrary to what creationists claim, complex features such as eye don't have to be completely functional to be useful. In the early history of life, when no organism had eyes, any simple system which could distinguish light from darkness could provide a huge advantage to its owner. The simple system can then evolve to a more complex one to provide a competitive edge etc.
Finally, evolution happens over time scales we cannot grasp. We don't have a good feeling of what billions of years of small changes which are selected for can add up to.

I am avolutionist myself and I have read Dawking. You misunderstood my question. I did not ask what looks unbeleivable in eyes of creationists. That would be easy question.I am asking which examples looks difficult to evoluion biologists themselves. Dawkins gives impressive explanations about evolution of the eye etc. Again, are all feature that easy to explain to evolutioninsts ? Evolutionists not only beleive in evolution. They seek specific explanations. Are not sometimes explanations difficult to find ? What are examples ?

@andrei what role does belief play in science?

The Nautilus eye used to be (still is?)  a "problem" and became a poster boy for creationist arguments. It has a pin-hole camera eye, which is the highest resolution non-lens eye. However, I understand that several genera arose during the Cambrian and the existing species haven't changed much since. So, the Nautilus saw fit to develop a sophisticated but non-optimal eye several hundred million years ago (other cephalopods have much better vision), but not develop it further.
This may hard to explain in evolutionary terms, although I note that they probably hunt via olfaction not vision.

At which depth they live. Is there light at this depth at all.

I found myself skipping the Grasso "olfaction not vision" paper when seeing "marine vertebrates at every scale from small crustaceans to sperm whales" in the abstract.

@mgkrebbs Yes, I admit not the best start to a paper.

saw fit to develop? Please explain this in an evolutionary framework

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How do the lungs act as a sieve to trap blood clots?
Does anyone know? I'm curious to find out  as my human anatomy and physiology book doesn't go into much detail on how the lungs function as such

Just as an intro...
The heart pumps deoxygenated blood from the right ventricle, through the pulmonary arteries (pic) which then eventually split into small capillary networks that surround the alveoli. The alveoli are formed by the trachea eventually branching off. So when you breathe in, the alveoli become filled with higher levels of oxygen.
The blood then becomes oxygenated and returns to the heart via the pulmonary veins to be pumped to the rest of the body.
The deoxygenated blood becomes oxygenated because there is a difference in oxygen and carbon dioxide concentration between the capillary network (O2 low / CO2 high) and the alveoli (O2 high / CO2 low) and so gas diffuses across because of the difference in concentrations (pic).

Physiology textbooks explain these mechanisms but for blood clots in particular, you'll need to check out a pathophysiology book.
Blood clots
When a blood clot travels to the lungs, it's referred to as a pulmonary embolus or PE.
Most of the time (90%), pulmonary emboli are formed in deep veins of the lower leg. These then travel to the pulmonary circulation system.
Large emboli block larger vessels - the pulmonary arteries and their branches. The smaller ones travel further into the network.
Patients can sometimes be asymptomatic and the emboli can at times resolve on its own. The extent of the severity of a PE is determined by:

how much blood flow is obstructed;
how long the embolus has been there; and
presence other underlying lung or heart disease.

There are a number of things that a PE can cause physiologically.
Reduced Gas Exchange - alveolar dead space occurs when an alveolus is ventilated, but not perfused with blood. This, along with other factors, cause varying levels of hypoxemia (lack of oxygen).
Pulmonary Infarction - in a small amount of cases loss of blood flow to lung tissue can cause tissue death. This is fairly uncommon.
Right Ventricular Failure - if there is a large enough blockage (> 50 - 60%), the pressure in the pulmonary arteries increase. Subsequently, the load on the right ventricle is higher.
So in acute cases, the ventricle hasn't had time to adapt (hypertrophy) and so the right heart can fail.
At any rate, the haemodynamic balance can be disrupted when a PE is present.
In the elderly or people with underlying disease where their lung function is already decreased, PEs can have a significantly larger effect because they can't compensate. There are many more important points related to this but hopefully this is a useful (very) basic overview.

The possible advantage of this is that if the embolism being trapped in the lungs is that it does not continue on through the left heart and into the systemic circulation, where it could cause a stroke, acute myocardial infarction (heart attack) or infarction of other vital organs.  Of course, if the pulmonary embolism affects a large portion of the the lung then this advantage is entirely negated.

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What is background binding?
I'm reading a journal article about mitochondrial protein import and it mentions that one of the mutant proteins tested showed background binding with another protein. What the heck is background binding?

Was an IP involved by any chance? http://en.wikipedia.org/wiki/Immunoprecipitation#Background

"Background binding" usually refers to aspecific binding between two proteins. The details depend on the test that was used.

can you post a link to the article?

Background binding in this case would be the extent to which two proteins associate together by chance.
A hypothetical example: you may have a mitochondrial protein import complex.  Usually cases there is a specific peptide sequence the import complex binds to , but proteins without an import peptide sequence will occasionally be bound to the import complex.  This is called the background binding for the protein complex.  The experimentalists might have measured this by cutting the import peptide sequence off a mitochondrial protein for instance.
Any candidate would have to bind to the complex more than the background case to be considered a target for mitochondrial import.


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Is there a term for tool use in animals?
Is there a technical/scientific term that scientists use to refer to tool making abilities found in certain types of animals?
Reference http://en.wikipedia.org/wiki/Animal_cognition#Tool_and_weapon_use

Note that you actually ask two different questions here - 'tool use' and 'tool making' are two different behaviours. Although, to the best of my knowledge, the correct terms for them (whatever the species) are 'tool use' and 'tool making' respectively.

Having read this article on tool use in Chimpanzees in full, I am inclined to say that if such a term existed then either the article itself or the titles of any of the 30 articles referenced would have included it.
Searching a couple of online biological dictionaries and ethology sites hasn't yielded anything either, therefore until someone else points out that I'm missing the obvious I'd say you're free to coin the term yourself!

Yeah, I've never seen anything more formal than just plain "tool use". For instance, see the article "The Ecological Significance of Tool Use in New Caledonian Crows"

Ok. Thanks for the answer. Appreciate it. Was hoping for a "scientific term" if such a thing exists. Thanks anyway!

I think "tool use" could serve as a good term on it's own, don't you think?

Yea... But I am looking for a phrase which confuses the layman. :-p haha.

:-) All these years I've wondered why an "ophthalmologist" couldn't just be called "eye doctor"... Let's please just call "tool use" as "tool use". No more Latin, Greek. Let's just stick to the current state of English.


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What does "nesting failure" mean?
According to the Wikipedia article on swans, swans are mostly monogamous but may sometimes separate, particularly after a "nesting failure". What "nesting failure" may mean is not entirely clear to me. Does it mean that they they have literally failed to build a physical nest? Or is it that they have failed to produce offspring? Or is it something else entirely?

Apparently it refers to the inability of nesting the eggs, because the nest was somehow destroyed, or environmental conditions were unfavourable.
I found a few examples pointing in this direction:
The Trumpeter Swan page on the Yellowstone National Park websites reports that:

Nest flooding is the primary cause of nest failure. Egg predation by coyotes, ravens, and otters does occur.

From the abstract of: Nesting Ecology of Bewick's Swans on Vaygach Island, Russia - Syroechkovsky et al., Waterbirds, 2002

Nest failure was mostly due to abandonment of nests in cold weather rather then to predation. Climatic conditions in spring are the main determinants of nesting success for swans on Vaygach Island.

From this article:
Reproductive Success of Exotic Mute Swans in Connecticut - Conover et al., The Auk, 1999 (PDF)

Egg survival was defined as the proportion of eggs in successful nests that hatched (Johnson et al. 1992). Successful nests were those from which at least one egg hatched. Egg survival is referred to by some authors as hatching rate (Willey and Halla 1972). Eggs left in the nest after incubation ceased were considered abandoned.

and

We determined the cause of failure for 33 nests: 46% were flooded, 27% were abandoned, 15% were disturbed by humans, 6% were lost to predators, and 6% failed after a parent died.

Actually, nesting failure means that nesting trial fail before offspring could even leave the nest. In case of precocial species (where chicks leave nest immediately after hatching, like swans) it means that eggs was destroyed or parents abandoned nest, as @nico point out. In case of altricial birds (offspring stay in nest) nesting failure may also mean that all nestlings died before leaving nest.
for example among House wrens (Belles-Isles & Picman 1986):

About 81%
  of nesting failures (n = 30) were due to predation (contents disappeared before the expected fledgingdate). Females abandoned seven nests, and starvation (presumably because
  of desertion by parents) accounted for one nesting failure.


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Were dinosaurs 'hot-blooded' or 'cold-blooded'?
Were dinosaurs hot-blooded or cold-blooded? NOTE: The popular term 'hot-blooded' means having an internally maintained average body temperature, which is generally more than that of the surroundings, despite the variation of the temperature outside.  And obviously 'cold-blooded' is the opposite of 'hot-blooded'.

This is a question I have often heard and there is no one certain answer to it. There are several scientific hypothesis about the methabolism of dinosaurs, but none of them has been ever proved or completely disproved.
Arts of methabolism
First of all, the term "cold-blooded" and "hot-blooded" are not scientific. In biology the organisms are classified according to how constant their body temperature is:

homeothermic (from greek "hom(e)o" = equal, same) -- organisms, who manage to maintain constant body temperature.
poikilothermic (from greek "poikilos" = changing, changeable) - ogranisms, whose body temperature fluctuates over time. It is implied here, that  the body temperature follows the fluctuation of the environment temperature, even though this is strictly not correct (see below)

There is another orthogonal classification, which takes into account the metabolic properties of the organisms:

endothermic organisms actively produce heat in their bodies, whereas
exotermic organisms mostly rely upon external heat sources.

What do we know about dinosaurs' methabolism?
Unfortunately there is no one living dinosaur, so we can only reason about their methabolism basing upon the fossils (and possible DNA from moskitos trapped into ambers).
One of the most cited works here is the "Dinosaur Fossils Predict Body Temperatures" (link to the free full text), where the authors write:

Perhaps the greatest mystery surrounding dinosaurs concerns whether
  they were endotherms, ectotherms, or some unique intermediate form.
  Here we present a model that yields estimates of dinosaur body
  temperature based on ontogenetic growth trajectories obtained from
  fossil bones. The model predicts that dinosaur body temperatures
  increased with body mass from approximately 25 °C at 12 kg to
  approximately 41 °C at 13,000 kg. The model also successfully predicts
  observed increases in body temperature with body mass for extant
  crocodiles. These results provide direct evidence that dinosaurs were
  reptiles that exhibited inertial homeothermy.

And exactly here we need the terminology I presented above to understand the findings:

Dinosarier were endothermic -- they were able to actively produce heat in their bodies.
The produced heat can only be taken away through their body surface. Due to the fact that the body surface increases quadratically (n2) with the size, whereas the weight grows cubically (n3), the bigger dinosaurs were the higher temperature their bodies reached. That could be one of the growth limiting factors and explains why especially big species preferred to live in water.
Even though the dinosaries were homeothermic, we don't know anything about their thermoregulation. Modern reptilia do not have the thermoregulation mechanisms that would keep the body temperature constant. Dinosariers, however, due to increased heat production might have less fluctuations in their body temperature, than smaller reptilia. This is termed as "inertial homeothermy" here.


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Do trees age on a microscopic level?
Most animals age via at least two mechinisms:

at a "macroscopic" level, basically wear and tear to the point where (on evolutionary time scales) it's more genetically advantageous to optimize for reproduction rather than longer lifespans.
at a microscopic level, e.g. shrinking of telomeres. This prevents cell division after a certain point (good to prevent cancer and other growths, bad for regeneration).

Do plants also age microscopically? If so, how are we able to clone (in the horticultural sense) plants?

Although I understand telomeres are fancy these days, I wouldn't really restrict aging at the microscopic level to their shrinkage. There are many more things going on, telomeres are surely one of the components of aging, but they are not the only one.

I don't mean to say telomeres are the only thing which causes aging on a cellular level, I just mean to say that something is happening. If you extract a single cell from an old animal, is should theoretically be distinguishable from a cell from a younger animal. Given that clones of plants are indistinguishable from plants grown from seeds, I'm wondering if such a distinction is possible in plants.

Hi. A quick google returned this review which implies that whilst plants have telomeres, their expression of telomerase is more wide-spread, and thus they have a greater regenerative potential. On a separate note, when cloning cells in the lab the biological clock needs resetting so that the 'old' donor cell loses its hallmarks of aging. This is done naturally for every germ cell created, and mostly involves epigenetic re-programming. Read this review, it's really interesting!

@Luke this smells like an answer to me...

@Shep I was only speculating about the plants really, and supplying additional (non-answer) info of interest. As has been pointed out, telomeres are only one aspect of cellular aging, and I am no expert on plant biology.

I’m not convinced by the distinction. Macroscopic aging doesn’t really make sense – do I age when I injure myself? Clearly not, since the body can repair itself. The loss of these repair functions is what constitutes aging. But that is once again at the microscopic level.

@Luke do you have a ref.  for the second review you mention? The Cell website is down.

@Poshpaws certainly: Rando, T. A., & Chang, H. Y. (2012). Aging, rejuvenation, and epigenetic reprogramming: resetting the aging clock. Cell, 148(1-2), 46-57. doi:10.1016/j.cell.2012.01.003

I've been doing some reading, and have come up with the following interesting information.
Telomeres
During cell division the DNA is replicated, but the mechanism is imperfect and in each round of cell division a small section is lost from the end of each chromosome. To compensate and protect the genetic information there are caps – regions of excess nucleotides – at the ends called telomeres (Silvestre, 2012).
Mammalian cells do not replenish their telomeres after cell division, giving them a replicative lifespan;  a maximum number of cell divisions before the telomeres run out. The cells then either enter a state of senescence and no longer divide, or initiate programmed cell death. However each cell has the genetic information for telomerase – the enzyme that can replenish the telomeres – but cannot use it. Only embryos and stem cells are able to express telomerase in mammalian cells - this protects against the build up of damage to DNA causing uncontrolled cell cycle progression. Activated telomerase is a core feature of many cancers (Campbell, 2012).
Plant Telomeres
You mention telomeres in your question, and it is an interesting question I had never considered. Plants have no germline preserved, so their progeny must bear all the defects of their particular parent cell, and that plant cells must therefore all have the capacity to regenerate their telomeres. I found a paper by Fajkus and colleagues that finds telomerase activity in plant cuttings grown in culture (Fajkus, 1998). Their hypothetical Plant Telomere-Length Regulating (PTLR) protein must arise in the early stages of the culture and last only a few cycles. Interestingly it seems that the efficiency of this process varies between different plant species. The authors note that their plant of choice – tobacco – is particularly proliferative and that other plants such as barley were harder to grow from cuttings, which may be down to a different way of regulating the telomerase (for instance it could only be activated occasionally at low amounts).
Do Plants Get Cancer?
It seems to me the next obvious question. One of the first papers I came across (published in 1916 by the Journal of Cancer Research!) talks of Crown Gall in plants and its relation to human cancer (Smith, 1916). Many websites cite galls as being the equivalent to cancer in plants, but it appears that the outgrowths (galls) that appear very tumour-like are in fact caused by bacteria encouraging their surrounding cells to proliferate. (See this question for more detail on galls).
I later found an abstract (I cannot access the full paper) from a paper published in Nature in 2010 called “Walls around tumours — why plants do not develop cancer” (Doonan, 2010). It appears that Plants can and do develop tumours, but they are less frequent and less lethal due to fundamental differences in development between plant and animal cells. Singh and colleagues found that in 2 plant species (Arabidopsis and rice) there were DNA damage repair pathways well conserved but with variation; there were several gene duplications in different DNA repair pathways (Singh, 2010).
Plants Do Not “Age” As We Do
Although I could find no conclusive evidence, it seems to me likely that plants may also have enhanced maintenance against other cellular stresses than DNA damage, such as build-ups of aberrant proteins. It therefore appears that in a protected environment some plants could live indefinitely. I say some, because others deliberately end their lives after reproduction. Traits such as longevity are inherently hard to be selected for, as the advantages come long after reproductive maturity and are therefore under much less selective pressure.
We see plants wither and die, but this is because they are constantly subject to environmental insult. Animals and insects may eat them, there may not be enough food or water, or sunlight, or the plant may become infected. All of which are at the macroscopic level. Due to completely different evolutionary constraints and pressures plants are highly resilient to cellar stresses, possibly due to differences in metabolic rate, and apparently have indefinite replicative potential.
Edit:
Although the more I think about it, the more it seems that most plant must have an ultimate lifespan, in that as they forever grow and expand their tissues would gradually harden and become less functional (I am mostly imagining bark plants here). Although as the layers of bark are pushed out the layers below take the place. In this way a tree could possibly live indefinitely by continuously remodelling it's layers.

Nice answer. See this question for more detail on galls. Also the Singh paper looked at Arabidosis (not a grass) and rice (a grass) :)

@RichardSmith - thanks for the correction and info - have updated my answer.

Even if outgrowth are caused by bacteria, that doesn’t make them less cancerous (plenty of human cancers are caused by viruses, but some also by bacteria). The criterion here is more likely lack of malignancy.

Very interesting answer Luke!


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Do somatic cells alter their own nucleotide sequence?
I seem to remember reading that embryonic cells will frequently replicate the section of their genome containing rDNA by splicing in duplicate genes. The cells use this to produce ribosomes at a rate which would be impossible with the DNA present in cells from full-grown organisms. Is this real? Are there other examples of cells altering their their own nucleotide sequence?

Would you consider transposons as a cell altering 'its own DNA'?

@Armatus: that would be a good example I would say. An answer explaining Barbara McClintock experiments would be great for instance!

@Armatus How often does this happen though? Transposons are usually silenced. In fact, it’s a problem if they aren’t.

@Konrad Rudolph: happens quite often in maize...

Cells have many tandem repeats of the rDNA genes (in part to produce many transcripts simultaneously), but I believe the number of copies is generally set by inheritance, although because they are tandem repeats they are subject to copy number variation that occasionally occurs in such an arrangement.

One case where human cells alter their DNA occurs in the immune system.  In the early stages of the continuing production of B-cells and T-cells, the developing cell recombines (shuffles) genes in a particular DNA region which codes for what are called Variable, Diverse, and Joining gene segments.  This shuffling is called somatic recombination or V(D)J recombination.  This rearrangement gives the cell a genetic template for a random instance out of a enormous set of possible antigen-recognition proteins used by the immune system to recognize foreign molecules (in order to fight infection).

yes that's an important one!

I'm assuming you mean, physically changing the DNA polymer.
The answer is yes.  And how they do this depends upon which cells they are and what they are supposed to do.   A partial list:
In multicellular animals, cells DNA 'ages' where the telomeres, sequences at the ends of the chromosomes, will be degrade and shorten.  This relates to how many times the cells have divided and acts as a sort of clock for development and probably also ageing.  Telomere degradation does not happen in all cells - the germline cells are not modified of course.  This is one of the probable reasons that cloning animals sometimes doesn't make perfect copies.
Cells will also add Methyl groups to the DNA nucleotides.  Methylation is triggered when environmental or developmental conditions.  The textbook example for methylation is the markers on the DNA of children whose parents have experienced starvation conditions.  Methylation can disappear in subsequent generations.  It also happens to cells in the brain which mark different stages in their brain development.
Meiosis, When sexual mating happens, the cells that make the sperm and eggs shuffle the pairs of chromosomes, editing so that about half of the resulting single set of chromosomes contain half of each parent's chromosomes.
Then, there is DNA repair. When radiation or chemicals breaks the chromosome, there are enzymes that repair them. Usually they read the opposite strand of the DNA to see how the repair happens. Sometimes the DNA is not reparable from the strand, and the result is not the same as the DNA the cell started with.
Short repeat DNA seem to show up in chromosomes - segments of short repeats can change length (AGGAGGAGGAGGAGT -> AGGAGGAGGAGGAGGAGGAGTAGGAGG etc). I'm not sure how this happens, but its different between identical twins.  It also probably happens to cells in different parts of your body.
What else have I forgotten everyone?
There are also enzymes that coil the DNA up onto nucleosomes, but don't really make any changes, but we won't count that.

He's referring to some sort of selective multiplication of rDNA - have you heard of anything like that? Apart from viruses (and DNA fragments what probably originally were viruses) I haven't heard of such gene-specific replication.

there are segmental duplications too.  I know of no bias to rDNA, but that isn't my forte. There are many more copies of LINEs and SINEs and viruses in the human genome than rDNA.

This answer has shown that my question wasn't precise enough. I've fixed it now. I'm asking about cells altering their own nucleotide sequence, not so much turning on / off genes. Telomeres are a good example of this, though.

There aren't too many examples of this happening.  By nature cells tend to avoid editing their DNA.  Germline editing is almost never done. Meiosis is the largest DNA edit imaginable.  two sets of chromosomes go in, only one comes out.


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Why do men have nipples?
I'd be tempted to call nipples in men vestigial, but that suggests they have no modern function. They do have a function, of course, but only in women. So why do men (and all male mammals) have them?

I concur with one of the answers in that it is evolutionary not very important to remove features that are not used, specially in the case of female/male traits. Another more dramatic example is that of fish that live at the bottom of the ocean, that have developed new sensory organs to adapt to life without light, but they still have eyes from when they where living in shallower waters where light was present.

This is a typical case of if a trait is not advantageous, why does it exist.

Human male nipples are sexual markings, just like eyebrows, they are used to communicate. Also DNA has to be compact, so to program a complex body part like a chest, the same gene is used in both sexes. The same gene is used for hands and feet, also, which is why they are so similar with same number of toes in all animals except for bats and birds. Hooved animals get the same 4 limbs, exactly, because the same genes code for all limbs to be compact. I don't think that males can keep a newborn alive, but the nipples stay a bit big in males because they are visual markers like eyebrows.

In case you haven't noticed, male nipples function as an erogenous zone.  In humans, anyway.

@com.prehensible do you have a source for nipplesbeing used in communication, because this is the first I have ever heard of it.

Figuratively speaking. When I am walking along and I have my phone in my shirt pocket, it has happened that my nipple writes a text message and sends it to someone in my contacts list.

The two key concepts here are:

sex-specific selection, and the fact that
males and females share the majority of genes

1) sex-specific selection
Obviously, any population where females lacked nipples would be in trouble. Men, on the other hand, have no evolutionary need for them, but they don't pay much either - there is no strong selection against men with nipples. So at first sight, it seems that nipples are positively selected in females while seem to be quite neutral in males.
2) Males and females share the majority of genes
If you consider two separate species where the two species undergo different selection pressures, you will just see one species evolve toward one optimum while the other one will independently evolve toward the other optima.
However, males and females are not independent entities. The vast majority of our genes can be found in one sex as well as in the other sex. In other words, most male phenotypes do not evolve independently of female phenotypes. As a result of this interdependence, you can end up with the trait that is selected in one sex present in the other sex.
Evolutionary equilibrium
This is all much more rigorously defined in terms of selection coefficients and evolutionary pressure. Without going into the math, the questions of who has the highest selection coefficient and How differential is gene expression for this trait are important questions to predict the equilibrium trait value in both sexes.
Lack of a strong selection pressure
Finally, any trait that is seemingly not-useful has to have a significant disadvantage on the fitness of the organism to be selected out (Why do some bad traits evolve, and good ones don't?). Even if a trait is useless for both males and females it may persist. The case of females needing the trait just makes its elimination in males even more difficult, as explained above. However, in some mammalian species, the males do lack the nipples (Evolutionarily, why do male rats and horses lack nipples?).

I believe it is for this reason: the female body plan is the default one. Males are a variation upon that, in humans at least. Nipples are part of the basic body plan. For a man to not have them, he would need to actively evolve something that would prevent nipples from developing. There is no selective pressure for the development of such a thing, so it hasn't happened. Keep in mind that the code for the general body plan is shared between males and females. The Y chromosome modifies the development of that body plan so the person becomes male.

I think your answer makes sense from the 4th sentence on. As for the first three sentences: why would you define the female body plan as the "default" when half the population is male? Consider the opposite stance: given that the Y chromosome has fewer genes, it seems just as reasonable to say male is "default", female a modification. The point isn't that either is default, only that referring to either as default is subjective at best.

Female is default because organs first develop as female in the embryo and fetus, then transform into male. Also bear in mind that both sexes have X but onlymale have Y.

@Shep: Preece and Armatus are right, 'default' refers to sex determination. At the beginning of development, the cells have bipotential state. Then, the Sex-determining Region of the Y chromosome (SRY gene) express a transcription factor that initiates male development. In absence of Y chromosome, the human embryo develops as 'default' into a female.

@leonardo I was explaining why he would call it 'default', which is really just a word definable however we wish, like all other words. More importantly though, I kept it short because it's extremely annoying to type on SE on a phone.

Consider this. If a boy is born without the receptors for androgens, they will develop physically as a female. Check it out: http://en.wikipedia.org/wiki/Androgen_insensitivity_syndrome

Yes, I read it: "The gonads are testes regardless of phenotype due to the influence of the Y-chromosome. A 46,XY female thus does not have ovaries or a uterus, and can neither contribute an egg towards conception nor gestate a child." This means that if you have XY chromosomes, you will never be a normal woman, even if you insensitive to androgens.

That the female form is the default, and that there's no selection for removing some default trait, isn't enough to explain male nipples without  more information about the developmental sequence.  If nipples developed late in the process after sex determination, then the default status of female traits would be irrelevant to male nipples.  So the hypothesis should include the suggestion that nipples arise early in development.  Another possibility is that, regardless of what sex is the default, nipples are generatively entrenched.

No one has mentioned the Neutral Theory of Evolution, which explains mutations that are not necessarily motivated by increased "fitness".
Similarly, (and more to the point for this question) there is no selective pressure with regards to men's nipples.
Men have nipples because they find a purpose on women, but for men, there is no reason to not have them. From an evolutionary standpoint, it is simpler for men to have them. The more complex situation (women have nipples but men do not) would most likely only occur if there was some selective pressure for men to not have nipples.

@Shep And yet it misses the most crucial piece of information, while simply restating other things that have been said. In fact, his second point is almost an exact restatement of something I said. The female body plan is the default one, and that fact is the heart of a real answer.

No Preece, it is not saying the female body plan is the default one.  It is saying that if a trait is necessary for one gender, it is simpler to have it for both genders as well, unless it hinders the gender that doesnt' require it.

I agree that males probably have nipples just because there is positive selection in females for having nipples while it is neutral in males (there is gender specific selection coefficient for having nipples). However, this is not exactly what the Neutral Theory of Evolution states! This is probably why no one mentioned the Neutral Theory of Evolution. Therefore, the answer seems a bit misleading.

Also, the sentence mutations that are not necessarily motivated by increased "fitness" should better be replaced by the existence of alleles present at high frequency even though they don't confer a selective advantage (that is, they don't confer higher fitness to the carrier).

I'm astonished that this answer has 20 upvotes and was accepted. The correct answer to this question has nothing to do with the neutral theory of evolution (which, as Remy notes, is not the same as observing that some traits are neutral) and everything to do evolutionary constraint (in this case, with the timing of sex determination in the developing embryo).

This answer is wrong. The most active users of Biology.SE are considering the problem here.

Sorry to spoil the fun here, but male nipples are not completely useless. With stimulation and hormones, they can be used to make milk. I don't have a great peer reviewed source for this, because it is sort of common knowledge. I heard about it at a Le Leche Leage meeting when my son was small.
Here's another article

This is interesting: are there any documented instances of males (in any mammalian species) actually providing nutrition to their young this way?
Don't get me wrong; I certainly don't want to oppress men by suggesting that they shouldn't breastfeed if they want to, I've just never heard of them doing it. Maybe a question for SE.Parenting?

I remember seeing a male breast feeding in a discovery documentary long time ago. Though I was very small then and don't remember the name of the program.

It seems like it is more common in people and domesticated animals, but here is An Article about a bat that regularly suckles its offsrping, Here is a recent general article about this topic


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What is an operon?
What is an operon in a eukaryotic cell, and how does it regulate the expression of genes? I've already read Wikipedia, but it is not enough clear to me. Unfortunately my knowledge in genetics are very poor!

You could check out the Encyclopedia Britannica.

There are some naturally occurring polycistronic mRNAs in flies and worms. You can also make artificial polycistronic DNA using IRES sites or self-cleaving 2A peptide sequences (which were isolated from viruses). Which one are you asking?

Is an operon just several genes with the same regulation, so they are transcribed at the same time? In prokaryotes the genes in an operon are often placed next to each other so they can be transcribed as one mRNA and take advantage of their ability to translate polycistronic mRNA, but in eukaryotes where polycistronic mRNAs are less common, they might not need to be near each other in the genome.

@Superbest: I'm asking about naturally occurring polycistronic mRNAs

Operons were once thought to appear only in prokaryotes (and viruses of prokaryotes), but there are now known to be a number examples in eukaryotic organisms. These are mostly seen in nematodes and insects.
Generally an operon is a functional DNA unit which contains a cluster of genes which are regulated by one promoter/repressor element and which are transcribed together. These are genes which functionally work together in a close context. A good example for this is the lac operon in bacteria.
In prokaryotes the expression of the operon leads to polycistronic (multiple open reading frames on the same transcript) mRNA, which is then translated into proteins.
Operons in eukaryotes are also gene clusters (often of functional closely related proteins), which are regulated by one regulatory unit (promoter). See figure 1 from reference 1:

There are different ways of mRNA arising from this phenomenon. First the mRNA can be dicistronic and most likely has internal ribosome entry sites (IRES) which allows the initiation (or re-initiation) of the translation of the second gene. Another possibility is the cleavage of the primary mRNA strand into two (or more) monocistronic mRNAs. And finally it is also possible that the dicistronic transcript is alternatively spliced to get different (monocistronic) mRNAs.
If you are interested in the details of eukaryotic operons, I strongly recommend reading at least the first reference (and probably also following up some of the related citations (on the right on the NIH website)).
References:

Blumenthal, T. (2004). Operons in eukaryotes. Briefings in Functional Genomics, 3(3), 199-211.
Pi, H., Lee, L. W., & Lo, S. J. (2009). New insights into polycistronic transcripts in eukaryotes. Chang Gung Med. J, 32, 494-498.

One of the best examples for eukaryotic operonic RNAs can be miRNAs produced from clusters. They arise from same primary transcript.

Since the OP specifically asks about eukaryotic operons, and appears to be understand prokaryotic ones, is it possible to at least also include a diagram of a eukaryotic one? The fly Adh/Adhr paper has a simple figure, but I haven't had time to read it very thoroughly.

+1 for using c elegans and drosophila examples in your answer


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Can methylisothiazolinone/methylchloroisothiazolinone (MI/MCI) behave as bacteriostatic in low concentrations?
Wikipedia mentions this as a biocide. It also mentions that low concentrations of certain bacteriocides is bacteriostatic. (I am assuming that biocide and bacteriocide play the same role, here.)
Hence, the question. (The only information I can find about MI is with regards to allergies.)

Yes, MI/MCI can behave as a bacteriostatic at low concentrations.
Check out table 1 in this paper: The Mechanism of Action of Isothiazolone Biocides. For a bunch of different isothiazolones (including the two you're interested in, though they call them MIT/CMIT instead of MI/MCI) it gives the Minimum Inhibitory Concentration (the concentration at which the isothiazolone acts as a microbiostatic) and the Minimum Biocidal Concentration (the concentration at which the isothiazolone acts as a biocide)*.
It's my understanding that basically everything that can act as a bacteriocide can also act as a bacteriostatic at a lower concentration. At low concentrations bacteriocides will kill some cells while leaving others alive in a stochastic (ie random) fashion. At some concentration this stochastic killing will balance out with the natural growth rate of the bacteria, and so thus act as a bacteriostatic.
*It should be noted that the paper lists these values for isothiazolone activity against yeasts, but the results would likely follow the same trends for isothiazolone activity against bacteria, since "CMIT/MIT has broad spectrum efficacy versus bacteria, algae, and fungi" (from the above cited paper).

Is my understanding right that "this sort of bacteriostaticity is different from the one caused due to bacteriostatic drugs such as tetracarbon/tetracycline"? And should we be worried about MI/MCI, present in Dettol Liquid handwash and some cosmetics, going down in water drains, where bacteria may develop resistance for it, due to its low concentration present there? Also, can we discard the risk that MI/MCI can lead to bacterial-resistance against other bactericides? (This risk was present with tetracycline & other bacteriostats, which FDA banned.) [Sorry for the late reply; not-my-field.]

There are plenty of antibiotics that can only be administered to human patients at bacteriostatic concentrations, but any bacteriostatic will become a bacteriocide at some concentration.

@Shubham1999 The answer to your question about resistance is that yes, of course it can develop, and low concentrations are usually where it occurs. There's been a lot of good research work recently about how populations of bacteria will "pioneer" niches with successively higher concentrations of some antibiotic.

@Shubham1999 While multidrug resistance is a real thing (which probably hasn't received enough study to date), it's not necessarily something you have to worry about. In fact, there's good evidence that in many cases a bacteria that becomes resistant to one drug will become more vulnerable to one or more others. Essentially, a bacterium will always pay a price (in terms of its overall fitness) for any given resistance.

This paper is something - tetracycline as a bactericide! So, all-in-all, would it be right to avoid using bactericide/bacteriostat (antibiotic) in places where soap-water does the job to the required quality, and get done away with antibiotic containing products if their efficacy is to be maintained as long as possible? (Is this question more suitable for Sustainable-Living-Stackexchange?)

@Shubham1999 What you say about biocidal soap makes sense, and I think overall it's correct (here's another question with a a lot of really interesting details: Is there an advantage to antibacterial soap?). In reality though, there's still a lot we don't understand about how resistance occurs, how it spreads though a population, and how different resistances interact. Also, as it mentions in that question I linked to, some biocides just don't cause resistance at all.


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Primary function of the enzyme lipoprotein lipase
I read here and here that the function of lipoprotein lipase is to facilitate fat uptake and storage in adipose tissue. Could anyone provide a slightly more expanded explanation, without going into too much detail, and without the use of too much jargon (I am not a biologist). I have read the wikipedia page, but sadly I didn't understand it....Thanks !
Edit: One of the things that is confusing me is what "fat uptake" means in this context.

Haven't read yet Stahl et al.,  Identification of the Major Intestinal Fatty Acid Transport Protein. To facilitate may mean no more than break down of triglycerides, as uptake mechanism is not known yet.

Fat uptake means cells eating fat.
I'll try to keep it simple, so forget the many approximations. You need first to consider that most fat circulates in the blood under the form of triglycerides (TG). TG are not soluble in water, so how do they circulate? They are hidden inside cargo vehicles called lipoproteins. When a circulating lipoprotein touches a cell, if the cell expresses lipoprotein lipase (LPL), first LPL would trap the lipoprotein cargo, and then will start to catabolize the TG.
Importantly, there are no efficient TG cargoes inside the cell, so the function of lipoprotein lipase is to make fat easy to move inside the cell. TG are a chemical assembly of one glycerol and three fatty acids. Of note, there are good fatty acid cargoes inside the cell, so LPL will break TG into glycerol and fatty acids so that they can be further metabolized depending on the cell type.
Heart and muscle cells will bring fatty acids to mitochondria where they will be oxidized to produce energy. With reference to your question, adipocyte cells will bring fatty acids to other cellular compartments where they will be converted back to triglycerides and stored as fat. That's why you read that LPL facilitates fat uptake and storage in adipose tissue.

Great answer. Thank you ! I would upvote, but I don't have sufficient rep myself (yet). Just a further query: when I read: "facilitate fat uptake and storage" would I be right in saying the /primary/ function is fat uptake, which then results in fat storage (in adipocytes).

No. All cells need fats, primarily to build membranes and to store in vesicles for later conversion to energy. Storage is not restricted to adipocytes.

@Larry_Parnell Sorry, by writing "(adipocytes)" I meant to query whether the /primary/ function of LPL in adipose tissue is fat storage ? I took home from the answer is that LPL performs fat uptake and thereby facilitates fat storage.

Haven't read much - it might be that the mechanism of uptake of  free fatty acids (produced by lipoprotein lipase, outside the cell) is yet unknown. Thus, LPL should not perform uptake at all. Free fatty acids might even freely diffuse through membrane.

Adipocytes are fat cells. On their outer surface are enzymes called lipoprotein lipase abbreviated as 'LPL' . the major function of LPL is to break down triglycerides into soluble fats and facilitate their transportation into adipocytes. So as more triglycerides are broken down, the fat cells increase in number by almost thousands times and in by 20 times. This means the more the energy intake, the higher the rate at which at which fat cells get enlarged thereby making an individual to be extensively obese

Maybe you can add some references to your answer to attract more upvotes.


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Hoechst or DAPI for nuclear staining?
When is it best to use Hoechst vs. DAPI for nuclear staining? They seem to be very similar on paper. Are there situations where one is clearly preferable?

The Hoechst 33342 dye is similar to DAPI in that both are UV-excited, minor groove-binding, and emit signals proportional to total DNA content. Both are maximally excited around 355 nm and emit around 460 nm.  A UV light source is required, which may harm the cell. However, this is only a risk with Hoechst, as DAPI requires the cells to be fixed and/or permeabilized, which is incompatible with life. DAPI is more stable, but Hoechst is brighter. Both are subject to photo-bleaching after long exposure.
There is another newer DNA dye called DRAQ5 that makes up for all of the issues I mentioned earlier - it is bright, quite photo-stable, can be used in live cell imaging, and its excitation and emission wavelengths are in the far red end of the spectrum, meaning that no UV is needed. I found a good comparison chart at http://www.biostatus.com/product/draq5/live_cell_comparison_chart/ if you're interested. I have no connection to them, by the way, I've just used DRAQ5 a lot in the past.

Sorry, but this answer is wrong: Most microscopes have a dedicated DAPI channel and both DAPI and Hoechst can very well be used together with FITC-like dyes. Also, you are missing the main point here: Hoechst can stain live cells, while DAPI can't. This is the main reason why people choose one over another. -1 not for that, but for the advertisement. I don't think this belongs here.

-1: DAPI is absolutely compatible with GFP, FITC and Alexa 488.\

my bad, edited to reflect reality.

Use dapi for fixed cells, it's very bright, very specific, will let you know if you have mycoplasma contamination in your culture, has a good shelf life and is generally pretty inexpensive. If you have to do live cell imaging use hoechst and like @user1850479 stated there are multiple types, they are all generally less toxic. If you can't use a blue nuclear staine Draq works good, it's a little dim I've found but it is in far red range, it's relatively non/toxic, does not have as good a shelf life as the other I mentioned here, also it's really  expensive $$$$$$$!!!!

DAPI and Hoechst 33342 (there are different Hoechst dyes, 33342 is one of the most commonly used) have very similar spectral characteristics. The only point is that DAPI is much better excited at 405 nm than Hoechst. Some microscopes and flow cytometers nowadays have 405 nm lasers or LEDs instead of UV sources, so this can become relevant.
The main difference and the main reason to choose either is that Hoechst can be used to stain living cells as it can pass the cell membrane, whereas DAPI can't. DAPI requires fixed and permeabilized cells.

Does this imply that Hoechst stains are more hazardous to the researcher or the environment? If DAPI can't enter living cells but Hoechst can, are there concerns about mutagenicity (similar to e.g. ethidium bromide)?

Yes, indeed. But we treat Hoechst and DAPI the same way in our lab.

I realize this is an older topic, but I'd like to clarify some misconceptions:
1)  DAPI is usually referred to as a semi membrane-permanent dye because its penetration through viable cell membranes is concentration dependant.  At lower concentrations it is mostly excluded from viable cells, while at higher concentrations it stains live and dead cells about equally.
2)  Hoechst comes in both membrane permanent and impermanent varieties.  Make sure you order the correct one for your application!
3)  It is not necessarily true that Hoechst is preferred for viable cells.  Hoechst has very slow diffusion through thick tissue for instance, so for in vivo imaging applications (or in tissue sections), DAPI often stains viable cells much better than the (much heavier) 33342 because it is better able to diffuse through tissue.  For isolated cells however, Hoechst 33342 can much more rapidly stain viable nuclei (seconds vs. minutes for DAPI).


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What is the state of automated quantitative analysis?
Quantitative analysis of microscope images is essential for many types of studies, but the techniques used most often are very labor-intensive. I have been able to find some literature about using computers to perform the analysis, but do not have a good picture of the state of the art.

Is there a good literature review on the topic?
Is there much use in practice which I have not yet seen?

Nature Methods seems to publish quite a few methods that facilitate this kind of analysis. E.g.
http://www.nature.com/nmeth/journal/v8/n3/full/nmeth.1558.html
And an editorial from them:
http://www.nature.com/nmeth/journal/v9/n7/full/nmeth.2102.html
As part of a special issue on BioImage Informatics with some nice examples.
http://www.nature.com/nmeth/journal/v9/n7/index.html

The word to look for is 'Image segmentation'. But also here, it very much depends on what you're looking at. Segmentation and quantification of simple fluorescence images is relatively easy and widely used. It can get very complex depending on how complex the structure is you're looking at. There are machine-learning approaches which are able to distinguish complicated structures from each other, such as different mitosis states.
Segmenting Hematoxylin-Eosin (HE) stained specimens is subject of intensive bioinformatical research. One goal is to assist pathologists in grading tissue lesions, such as in prostate cancer, but this is as far as I know not used clinically yet. Whole-slide scans of histological specimens are becoming more widely used clinically. These images are very huge (1 GB per specimen), so a research focus is also to provide a large-scale analysis of these whole-slide scans.
Also, take a look at CellProfiler (http://www.cellprofiler.org), this free open-source software saved my PhD project.
Literature I found:
Tabesh, A., M. Teverovskiy, et al. (2007). "Multifeature prostate cancer diagnosis and Gleason grading of histological images." IEEE Trans Med Imaging 26(10): 1366-1378.
Petushi, S., F. U. Garcia, et al. (2006). "Large-scale computations on histology images reveal grade-differentiating parameters for breast cancer." BMC Med Imaging 6: 14. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1634843/
I cannot provide you with a recent review, though...


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Can one assess muscle strength through imaging (e.g., MRI)? If so, though which type of imaging and how accurate is it?
Can one assess muscle strength through imaging (e.g., MRI)? If so, though which type of imaging and how accurate is it?
On How does muscle size relate to strength?, I read this answer from  Moses (mirror):

Strength training will increase the size and quantity of myofibrils, and subsequently increase the size of the respective muscle fibers; this process is called hypertrophy, and it results in larger and stronger muscles.

As a result, I assume that a medical imaging processing the physical strength of a muscle should assess both the size and quantity of myofibrils. That being said, it can be easier to assess the size as an approximation of strength, and if so, I wonder about 1) the quality of such an approximation 2) how to measure the size of a muscle that what cannot directly easily measured with a tape ( e.g., gluteus minimus or piriformis).

Direct measurement of muscle strength something isn't possible or advised, e.g. if the tendon is injured. Also, some muscles are difficult to isolate when testing. In the case of a tendon injury, assessing the muscle strength would be useful to find a good balance between muscle strengthening and tendon recovery.

Can you please add some details on what parameters would you consider for "strength"? Different imaging techniques can measure different parameters.

@WYSIWYG Thanks, I am interested in any parameter that has an effect on the muscle's physical strength.

To the close voters: this isn't a homework, and please let me know if the edit I made satisfy the "attempt at an answer" requirement.

@FranckDernoncourt The answer linked from Fitness.SE as well as the second answer on that question both make clear that there is a correlation but not a particularly strong one between muscle size and strength. It's unclear to me why this question is even relevant when there exist both simpler and by definition more accurate ways to measure muscle strength directly that don't require expensive medical scanner time (which is also valuable for diagnosing disease and injury).

@BryanKrause Direct measurement of muscle strength something isn't possible or advised, e.g. if the tendon is injured. Also, some muscles are difficult to isolate when testing.

@FranckDernoncourt Why would you be interested in muscle strength when a tendon is injured? What is the point of assessing the strength of some particular muscle independent of some real physical output (like the amount of weight lifted, the velocity of a thrown ball, etc)?

@BryanKrause E.g. to find a good balance between muscle strengthening and tendon recovery, in the case of a tendon injury.

One of the criteria for good SE questions is "You should only ask practical, answerable questions based on actual problems that you face." - I think your question would be better received if you situate it in the context of injury recovery in which case the measure of interest is probably not 'strength' per se but some measure of health, if that is what you are interested in. It would also be beneficial for you to do some further research on your own to properly scope the question.

@BryanKrause Thanks, sounds good I edited the question to mention the use case. The measure of interest is strength though, as the muscle itself is healthy, and muscle strength is often regarded as an important factor during tendon recovery.


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Does a full tear of the gluteus minimus tendon result in a long-lasting inflammatory response?
Does a full tear of the gluteus minimus tendon result in a long-lasting inflammatory response?
This answer mentions:

An isolated gluteus minimus tear still causes functional problems because of the associated inflammatory response

But I read on {1}:

“signs of either acute or chronic inflammation have not been found in any surgical pathologic specimens in patients with clinically diagnosed lateral tennis elbow syndrome,”

Note that tendon tears are present in a tennis elbow (a.k.a. lateral epicondylopathy). From {2}:

Review of MRI findings from 24 patients with epicondylitis reported increased intratendon signal on both T1 and T2 pulse sequences58 with occasional bone marrow edema pattern in the epicondyle. Other studies have shown thickening, edema, and tears of the common extensor tendon.

References:

{1} Bass, Evelyn. "Tendinopathy: why the difference between tendinitis and tendinosis matters." International journal of therapeutic massage & bodywork 5, no. 1 (2012): 14. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3312643/
{2} Taylor, Samuel A., and Jo A. Hannafin. "Evaluation and management of elbow tendinopathy." Sports Health 4, no. 5 (2012): 384-393.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3435941/

Why are you comparing a non-tear injury (tennis elbow) to a full tear of a tendon (gluteus minimus)?

@CharlesE.Grant tennis elbow is micro tear

Micro-tear seems very different then a full tear.

@CharlesE.Grant I don't know whether the difference impact the inflammatory response

The article you linked is interesting, but as @Charles E. Grant mentioned in the comments, it’s not particularly reasonable to compare a non-tear repetitive stress injury (like epicondylitis) to a full muscle tear. Non-tear repetitive stress injuries persist because the offending frequent motion doesn’t stop. A muscle tear, however, will recruit an inflammatory response that will eventually be resolved by anti-inflammatory factors (Th2 cells directing the cellular microenvironment towards healing / scarring).
This healing process might not result in an optimal resolution of the initial injury, and it’s not unique to any particular body system. Rather, pretty much anything in your body that can be injured will first respond with a period of innate inflammation followed by fibrosis and resolution (whether or not that restores function / alleviates pain depends on a number of factors including injury severity, therapeutic management, and healing conditions e.g. if there were repeated injuries during the healing process).
With regard to gluteus minimus tears — it depends on the injury. If a patient persistently aggravates an already-torn muscle, they will have more inflammatory cells recruited to the injury. If they do a good job allowing the injury to heal (not re-aggravating the injury, receiving surgery if structural correction is required), the inflammatory process will resolve relatively quickly.

Thanks. As mentioned in my comment in reply to @Charles E. Grant, tendon tears are present in an epicondylopathy (and more generally, any tendinopathy resulting from  repetitive stress). I have added one reference supporting this statement in the question. I believe there is a consensus from the medical community on this.

I think your second reference essentially corroborates what I’ve written above: “Four stages of lateral epicondylitis have been described, beginning with the early inflammatory reaction, followed by angiofibroblastic degeneration, structural failure, and ultimately, fibrosis or calcification.”

That's correct, I agree with the rest of your answer. I'll add another follow-up question tomorrow.

Follow-up question: Can an individual further aggravate a full tear of the gluteus minimus tendon (trochanter insertion)? Your insights are welcome!


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Does a full tear of the gluteus minimus tendon has any functional implications?
From what I read on Wikipedia, all functions of the gluteus minimus are mirrored by the gluteus medius. Additionally, the gluteus medius is larger than the gluteus minimus (see comparative images here), which leads me to believe that the gluteus medius is stronger than the gluteus minimus.
Subsequently, I would tend to guess that a full tear of the gluteus minimus tendon does not have any functional implications. I.e., a human might have a full tear of the gluteus minimus tendon without any limitation of their movements. Is my guess correct?

You’re correct that the gluteus minimus is redundant in function with the gluteus medius, but an isolated gluteus minimus tear still causes functional problems because of the associated inflammatory response and subsequent pain deemed “greater trochanteric pain syndrome,” as the greater trochanter is the insertion site for hip abductor muscles like the gluteus minimus and medius:

MRI Web Clinic — May 2004,
  Gluteus Minimus Tear & Trochanteric Bursitis,
  Michael E. Stadnick, M.D. (mirror)

Clinical History: 70 year-old female with chronic left hip pain...What is your diagnosis?
Diagnosis: Gluteus minimus tear of the left hip with associated trochanteric bursitis.
Discussion: Lateral hip pain is frequently a challenging diagnostic and therapeutic problem. In the past, the presentation of chronic lateral hip pain with tenderness over the greater trochanter was attributed to trochanteric bursitis. This symptom complex, called greater trochanteric pain syndrome (GTPS), can mimic other serious causes of hip pain...Abductor tendon (gluteus minimus and gluteus medius) tears are becoming increasingly recognized as a frequent cause of pain at the hip. In fact, tears of the abductor tendons, instead of trochanteric bursitis, are likely the most common cause of GTPS.
In a large majority of patients, trochanteric bursitis or distension will accompany an abductor tendon tear. The frequent coexistence of trochanteric bursitis and abductor tendinopathy has led some authors to suggest that bursitis may in fact be a result of the underlying tendinopathy.
Early descriptions of abductor tendon tears at the hip emphasized involvement of the gluteus medius tendon as being most common. However, subsequent papers have revealed a roughly equal frequency of involvement of the gluteus minimus and medius tendons.

Thanks! Follow-up question: Does a full tear of the gluteus minimus tendon result in a long-lasting inflammatory response?


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Why does Penicillin only affect bacterial cell walls
I was quite fascinated by the feature Should Science Pull the Trigger on Antiviral Drugs—That Can Blast the Common Cold? in this month's Wired magazine.
They explain that Penicillin is effective at killing bacteria because it interferes with the growth of bacterial cell walls.
How does Penicillin do that exactly? And why does it not dissolve human cells as well?

The simple answer is that human cells don't have cell walls.

The reason why penicillin affects only bacteria and not Eukaryota cells has already been explain. It is true that Penicillin can also kill Gram-negative bacteria. One study I conducted, several Gram-negative bacteria have been removed from my cultures using Penicillin G Sodium Salt. I presume it is because the outer-membrane that protects Gram-negative bacteria is weak or thin. But maybe GWW can provide some references as I don't have them.

Bacteria have a mesh-like structure surrounding their plasma membrane called a cell wall.  The cell wall is made up of peptidoglycan polymers that form a rigid crystalline structure that helps protect the osmotic pressure of the bacterial cytoplasm.
Penicillin and other β-lactams work by inhibiting the final step of peptidoglycan synthesis, which prevents transpeptidation (crosslinking) of the peptidoglycan molecules. This leads to the death of the bacterium by osmotic pressure due to the loss of the cell wall.
This drug doesn't affect human cells because they lack a cell wall surrounding their plasma membrane.

n.b. penicillin only affects gram positive bacteria.

@RoryM: That is not totally correct, penicillin does affect some gram negative bacteria but it is not very effective.  There are other ß-lactams that do affect gram-negative bacteria such as Carbenicillin.

I don't think that this is necessarily correct. The beta-lactams doesn't inhibit the synthesis but rather the reorganization of the peptidoglycans. The rigidity of the now static wall then prevents cell division.

@bobthejoe:  I updated my answer to better explain it. Thanks.


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Number of beneficial mutations cataloged?
I can see from Wikipedia that there are possibly thousands of harmful mutations that have been cataloged and linked to disease. There are also unnumbered neutral mutations. But, does anyone know how many "beneficial" mutations have been cataloged in scientific literature?

A "beneficial mutation" is often hard to point out: it would likely be very slight and context-dependent. For example, a "superhero" gene is obviously out of the question, and a very small phenotypic difference would probably either be insignificant or beneficial in one particular environment but not in another.

@LanceLafontaine: you mean this (and related article)?

The problem is that "beneficial" is entirely dependent on the environment and how it changes. E.g. for fish living in dark caves, mutations that lead to loss of the eyes are beneficial.

That would be hard to say because really beneficial mutations become well distributed through the genome.  Basically the differences between us and chimpanzees are a catalog of all the beneficial (or completely neutral) mutations since the ~4.7 M years since we diverged from each other.
Separating them from changes which have no special effect would be difficult too, but more to the spirit of your question, its difficult to explain what many mutations do, unless they cause significant changes in something we can observe in the individual (like height, weight, big nasty claws, etc).
For some more specific examples you can look at Online Mendelian Inheritance in Man.  Some mutations which are useful sometimes might be related to skin color for instance (really helps when there is a lot of sun about) or lactose tolerance (a variation which is popular amongst europeans who have been drinking dairy milk for thousands of years).

I was specifically asking about the number of beneficial mutations cataloged, not necessarily examples. Thank you though.

I guess i'm saying that you will never get a number for that, or if you do it will be nearly meaningless.  Wasn't expecting to get a checkmark for this one.

Just continue scrolling down wikipedia: there are also listed two examples of beneficial mutations: the one conferring HIV resistance, and the one conferring malaria resistance.
Note that 'beneficial' is relative. The mutation associated to malaria resistance is actually causing sickle cell disease.

I was specifically asking about the number of beneficial mutations cataloged.

Others have posted that the term beneficial in genetics is contextual - single mutations may be harmless, unless another mutation is co-inherited; this is called epistasis (where more than a single mutation/genotype/allele is required for the phenotype).
I have not studied the list comprehensively, but there is a 'catalog' of all robust genome-wide association study results here. Depending on your outlook, all mutations associated with a disease are therefore also 'beneficial' if you have the protective allele and not the risk allele. Using this logic there have been many SNPs identified that are protective, rather than beneficial per se, and these are listed in the GWAS-catalog I linked to. As of 05/11/12, the catalog includes 1258 publications and 6400 SNPs.


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Modern Whales with Vestigial legs Myth?
Is it a myth that modern whales have been found with hind legs sticking out of their sides and full formed tibias, fibias, and toe bones? I keep finding assertions, but no citations. For example, the wikipedia page has no citation for it.
http://en.wikipedia.org/wiki/Whales#Appendages

This might be better suited on Skeptics. @Rory, what do you think?

I posted this here because I was looking for a statement of fact. A simple "do we observe this" or not, whole vestigial limbs "legs" on modern whales that is. Whether the small bones in the pelvic area of modern / fossil whales are part of their skeletal anatomy or vestigial is another question.

@KonradRudolph I'm never 100% on what's suited to skeptics, I've only really lurked and read some of the higher voted questions.  Sure Mad Sci. will come across this later anyway xD

The link you give doesn't mention limbs sticking out of the body wall, but only vestigial hind limb elements. Many whales do retain pelves and femora, as this page at the Bergen Museum shows. Given the variation in limb development across vertebrates, it would not be surprising to find more distal elements (but I would be very surprised if they extended past the body wall).

So the stories I've heard of fishermen pulling whales out of the sea with legs sticking out their sides are myths/exaggerations? I just want to make sure I have my facts straight, that's all.

probably... lol.  Natural science was historically more of a circus business than institutional science as we know it.  People would garner fame, attention and wealth by bringing in animal stories and artifacts that confirmed ancient myths or fantastic ideas.  Examples are the market for narwhal horns which were sold as unicorn horns and mermaid exhibitions (http://en.wikipedia.org/wiki/Mermaid#Hoaxes).

Whales? I think not. However a dolphin has been seen with four flippers. (https://www.google.com/search?q=dolphin+with+hind+flippers&source=lnms&tbm=isch&sa=X&ved=0ahUKEwjbmK3N287TAhXF4iYKHb6LA4AQ_AUICigB&biw=1138&bih=515)

@JayCkat Dolphins basically are whales. Or rather the informal term "whales" randomly seems to exclude in its everyday use those dolphins who aren't already well-established whales (e.g. Orcas). So your evidence seems pretty rock solid in relation to OP's question!

Yes there are several published sources (with photos) of whales born with protruding vestigial legs.
http://digitallibrary.amnh.org/dspace/bitstream/handle/2246/4849/N0009.pdf;jsessionid=55D6453968F5461B1B6BFF8D53C81F16?sequence=1
Modern Right Whales have rudimentary legs--completely inside their bodies.
"approaching the inquiry with the most skeptical determination, one cannot help being convinced, as the dissection goes on, that these rudiments [in the Right Whale] really are femur and tibia. The synovial capsule representing the knee-joint was too evident to be overlooked. An acetabular cartilage, synovial cavity, and head of femur, together represent the hip-joint. Attached to this femur is an apparatus of constant and strong ligaments, permitting and restraining movements in certain directions; and muscles are present, some passing to the femur from distant parts, some proceeding immediately from the pelvic bone to the femur, by which movements of the thigh-bone are performed; and these ligaments and muscles present abundant instances of exact and interesting adaptation. "
http://etb-whales.blogspot.com/2012/03/hind-limb-rudiments-on-modern-whales_1221.html


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Can humans shorten their sleeping patterns?
Can sleeping patterns be trained, or are they genetic? I read that a human needs to sleep at least 4 hours. Can sleeping time be reduced without having a negative impact?

not really an answer, but this article about the myth of the 8-hour sleep was quite interesting! http://www.bbc.co.uk/news/magazine-16964783

a related question: http://biology.stackexchange.com/questions/2025/is-it-possible-to-live-without-health-problems-sleeping-one-day-and-not-the-othe

Polyphasic sleep can allow people to sleep at multiple regular intervals throughout the day and allows people to get by with less total sleep. I don't know of any training that can help people reduce the amount of monophasic sleep they need without a negative impact.


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What are common causes of unexpected ligation products?
I digested two plasmids, one with EcoRI and AgeI and the other with EcoRI and XmaI. Digests looked as expected, so I purified the respective fragments and set up the T4 DNA ligation (AgeI and XmaI sites are compatible).
After E.coli transformation, culture and miniprep from 12 of the resulting cultures, I digested the isolate from the minipreps with BclI to confirm I had the correct product (because there was one BclI site in the insert and another one in 1.4kb away in the backbone). The results of this digest clearly show that there are two different ligation products: four lanes share one banding pattern and the other eight share a pattern which is different from it.
I checked both plasmids for other restriction sites of the enzymes used which I overlooked before, but found none. Because EcoRI and XmaI/AgeI sites are radically different (AATT vs. CCGG), I would exclude the possibility of the insert being ligated in reverse orientation.
Are there any common causes of unexpected ligation variants besides unnoticed restriction sites and reverse ligation?

A second investigation has suggested that the ligation product in question was indeed the vector, without ligated insert!
The vector also contained a BamHI site close to the XmaI site, so in a subsequent digest with EcoRI and BamHI, I was expecting to see the same band sizes that I ligated together in the first place.
All colonies contained plasmids that produced the long (vector) band, and the same eight as before produced the shorter (insert) band as well. However, those four which were aberrant in the previous experiment were this time lacking the shorter band.
This means the eight colonies with two bands contained the desired ligation product, while the other four contained a plasmid which was restricted at a single site (undigested it would have produced three bands like the control).
As the BamHI site was in the vector and untouched throughout the whole process, I conclude that those four were missing the EcoRI site, which should have been regenerated during the ligation, and hence indeed the EcoRI site and the XmaI site must have been ligated without insert somehow.
Long story short
This means that either

An exonuclease digested the sticky ends of the vector away, or
The sticky ends simply degraded by chance

resulting in a blunt-ended re-ligation of the vector without insert and consequently loss of the EcoRI site.
I believe these to be quite important things to consider in cloning - in subsequent experiments I have had several colonies growing on negative control plates (i.e. colonies transformed with a control ligation that contained no insert), all of which were probably due to loss of sticky ends and blunt ligations, resulting in functional plasmids that conferred ampicillin resistance despite containing an undesired plasmid.

Could be insert polymerization.  If you have your stretch of DNA like this:
 (5')-AATTagctagcatcgtgatcgacg-(3')
          ||||||||||||||||||||
     (3')-tcgatcgtagcactagcagcGGCC-(5')

And you take that, flip it around, it will ligate onto itself, like this:
 (5')-AATTagctagcatcgtgatcgacg-(3')(5')-CCGGcgacgatcacgatgctagct-(3')
          ||||||||||||||||||||              ||||||||||||||||||||
     (3')-tcgatcgtagcactagcagcGGCC-(5')(3')-gctgctagtgctacgatcgaTTAA-(5')

This is easy enough to check for.  Just calculate the size fragments you'd expect from a vector with two inserts (there'd be an extra BcII cutsite now, and the extra fragment would probably be the size of the insert).  If this is just out of curiosity, and one of your things is the correct size, I'd ignore the ones that didn't work and go ahead with your ones that did.
If you do have a problem with it, or you are getting all your clones polymerizing, you can treat your insert with an alkaline phosphatase.  This will eat off the (5') phosphate that the ligase needs to stick the on to the (3') hydroxyl.  The result is that an insert cant bind to another insert, but once it finds a vector it will be able to ligate:
 insert to insert:    AATTagctagcatcgtgatcgacg-(3') :( CCGGcgacgatcacgatgctagct-(3')
                         ||||||||||||||||||||              ||||||||||||||||||||
                    (3')-tcgatcgtagcactagcagcGGCC  :( (3')-gctgctagtgctacgatcgaTTAA

 insert to vector:    ....ctagct-(3')     AATTagctagcatcgtgatcgacg-(3')(5')-CCGGcgacg....
                      ||||||||||              ||||||||||||||||||||              |||||||||
                      ....gatcgaTTAA-(5')(3')-tcgatcgtagcactagcagcGGCC     (3')-gctgc....

There will be nicks on the top left, and bottom right, but the bug you put it into should clean those up for you.  You can get alkaline phosphatase for fairly cheap from lots of places, NEB is always a safe bet.