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Are Bovine serum albumin, Avidin, Ficoll-70 and Dextran-70 positively charged or negatively charged?
Bovine serum albumin, Avidin, Ficoll-70 and Dextran-70,are they
positively charged or negatively charged ? And which other solvents can be used as a substitute to water for preparing solutions in each case ?

What part is giving you difficulty. At least for the charges you can use Gooooooooooogle...

yes but mainly I require to know about the solvents.

Flagging because this is a bunch of unrelated questions. (each molecule should be its own question, solvents are also a separate question entirely) The question as is is unlikely to be useful for future users.

For charge, you could check this one by sequence level, for example for Bovine Albumin (Uniprot: P02769) you can get the theoretical pI of 5.82, as the mean of pKa aminoacid values, to do this can use protparm, so when the pH > pI, the protein has a net negative charge and when the pH < pI, the protein has a net positive charge.
And there are only two organic polar solvents I known to work proteins, DMSO (pKa = 35) and
Dimethylformamide (DMF, pKa=-0.01 (20ºC))


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Why don't teeth glow?
Hydroxyapatite is the main component of tooth enamel. It contains phosphorus in the form of phosphates, pyrophosphates etc. that are found to exhibit the the property of phosphorescence. But why don't the teeth glow in the dark ?

Why is this being downvoted? I think it is a good question. Anyway, if you downvote please give a reason.

I agree with nico. I think this is a good question. It offers another perspective about the subject which I have never thought before.

Just to add a little more on the interface between optics and dentistry:
Whilst teeth do not phosphoresce, they do in fact autofluoresce.
The differential auto fluorescence of healthy tooth and carious tooth has been used for the early diagnosis of caries. (Gugnani N, Pandit IK, Srivastava N, Gupta M, Gugnani S. Light induced fluorescence evaluation: A novel concept for caries diagnosis and excavation. J Conserv Dent 2011;14:418-22 and http://www.opticsinfobase.org/boe/abstract.cfm?uri=boe-2-1-149)
To see teeth glow, or rather, fluoresce, they should be illuminated with short wavelength light, like blue light (wavelength 450 nm) and the teeth will glow green, which will be visible if the the blue light is filtered out.
Also see http://www.inspektor.nl/dental/qlfmain.htm#QLF%99%20Basic%20Principle

I'm gonna test this and vote based on results.

Firstly, phosphorus does not exhibit phosphorescence on its own (don't let words mislead you, they often don't mean what they seem like): See http://en.wikipedia.org/wiki/Phosphorescence#Materials and http://en.wikipedia.org/wiki/Phosphor#Standard_phosphor_types
Even if phosphorus did do so on its own, it would not do so in the body because it is always (almost always?) present as phosphate (PO4-), and this again is most often incorporated in other compounds such as nucleotides.

Teeth are made up of 3 substances.  Enamel, dentin and cementum.  Inside is the pulp.  The best chosen answer is incomplete.  Enamel fluoresces and undergoes phosphorecense but dentin of teeth is three times more phosphorescent than enamel.  Phosphorescence is a specific type of photoluminescence related to fluorescence. Unlike fluorescence, a phosphorescent material does not immediately re-emit the light radiation it absorbs. The slower time scales of the re-emission are associated with "forbidden" energy state transitions in quantum mechanics. As these transitions occur very slowly in certain materials, absorbed radiation may be re-emitted at a lower intensity for up to several hours after the original excitation.  When exposed to light sources containing UV components are turned on teeth, the fluorescence of human teeth gives them the quality of vitality, and they exhibit a fluorescent emission with a peak of 440 nm observed peak light. (bright blue hue)  Because of dentin's atomic composition contains special collagen and mineral matrix phosphorescence allows it to collect light photons slowly to change tooth color.  In this way, natural tooth color can be used as a measure of oral health and health of the brainstem which innervates the dentition.  Dental OCT is now used in this way. Optical coherence tomography (OCT) is based on low-coherence interferometry, typically employing near-infrared light as its source because it deeply penetrates tissues with water. Water is the ideal chromophore for red light. The use of relatively long red wavelength light allows it to penetrate into the scattering medium of teeth and the pulp.  Using light this way, OCT can provide “optical biopsy” without the need for excision and processing of specimens as in conventional biopsy and histopathology. Application of OCT in dentistry has become very popular since 1990.  This is why in my Redox Rx blog I have used pulp testing as a modern redox variable for human health.  It is from the dentinal pulp where light is released from cells and collected into the atomic lattice of dentin to change its frequency and this changes its color we observe.  Tooth color can be used a health metric. So for these reasons the accepted answer is quite incomplete.  We have known about tooth phosphorescence since 1941 as published in pubmed.

http://www.ncbi.nlm.nih.gov/pubmed/17774027

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How did the first self replicating organism come into existence?
When people try to explain evolution, they tell me that evolution is a cumulative result of mutations & natural section of the more superior individuals of a particular species. I think I'm fairly convinced with this explanation.
But when I think about it, all of them assume that there was an organism, however simple, that was capable of self replication & occasionally mutate. How did such an organism come into existence? Can anyone explain this?
An answer I found on Reddit didn’t really convince me.

If you want a good start, I would suggest looking at the RNA World hypothesis.

Can we please leave out the entropy canard? It’s totally irrelevant. Earth isn’t a closed system. Period. Furthermore, this would be completely off topic on a biology site.

I remember reading this entire article a few years ago, it was pretty revealing. http://en.wikipedia.org/wiki/Abiogenesis

Entropy is not irrelevent for this question (how could it be in organic chemistry??). Earth is not a closed system,but in these considerations you have to consider the scale of the experiment.

However, I agree that entropy can be an enormous distraction.

If you actually run the calculations, the second law of thermodynamics does show you something related to evolution: the entire evolution of the current biosphere could not have happened in much less than a month (http://physics.gmu.edu/~roerter/EvolutionEntropy.htm).  As long as you take longer than a month (say 4 billion years), there's no problem at all.

@NoahSnyder Thanks for the article. This is why I love StackExchange :)

Evolution or (as Darwin called it) "descent with modification" is a theory which explains the origin of the species NOT the origin of life.  How the first life arose is completely irrelevant to the theory of evolution.  What evolution does explain is how and why we have such variety of life on earth all descending from the same organism.
What you're asking about is not a theory of "evolution" but rather a theory of "abiogenesis."  Although there are many interesting hypothesis for how abiogenesis happened (e.g. the RNA world, the "metabolism first" theory, etc.), the fact is we simply do not know yet how life first arose.  What we do know is that life first arose between 3.5 and 3.9 billion years ago.  That's a really long time ago compared to lots of other important events in natural history (even the Cambrian explosion where modern animal phyla evolved was only half a billion years ago), and so it shouldn't be surprising that it's a hard problem.

Yes, you are right. I am asking about a theory of "abiogenesis". But I do think that its related to Darwin's theory because it assumes that an organism with the required qualities existed. Isn't Darwin's theory based on an unproven assumption? Can you clarify?

We know that organisms with the required properties existed 3.4 billion years ago, by looking at fossils of bacteria.  There's no unproven assumption there.  Evolution describes the most recent 3.5-4 billion years of natural history.  To go beyond that you need another theory.  That's fine, that's how science works.  You wouldn't say that gravity relies on unproved assumptions because it doesn't explain electricity or radioactive decay; it's not supposed to, it's supposed to explain gravity.

Agreed. I have nothing against Darwin's theory. All I wanted was a convincing theory of abiogenesis.

@GreenNoob The theory of evolution (only creationists call it Darwin's theory, just FYI) deals with changes in populations.  It says that given a starting population, changes will occur because X,Y, and Z in a way that you seem reasonably convinced by.  That starting population is an objective fact; we can see it in the fossil record.  Further, the theory of evolution says nothing at all about where that population came from.  It could be abiogenesis, aliens, or a deity; it really doesn't matter.  Abiogenesis uses many of the same ideas as evolution, but it's a completely separate theory.

It doesn't really matter here how scientists subdivide and name topics. There is only one nature. The question is about reality, not about organization of scientific fields.

We don't know how self-replicating molecules first arose (and probably never will know exactly) but the Earth is large and had 500 million years (i.e. the prebiotic Earth timescale) or so to experiment in organic chemistry. The land-sea interface (such as tidal pools) are a good candidate site since these are areas where high concentrations of organic goodies can be found.
In this context, one focus that researchers have been looking at is self-replicating molecules.
For example, one lab in Cambridge,UK has come up with tC19Z.
tC19Z is the name of a RNA enzyme that acts like a self-replicating molecule. It can copy chunks of RNA almost 50% as long as itself. It can also make copies of other RNA enzymes. This molecule is not "alive" itself, but clearly demonstrates how greater complexity can arise.

We don't know how self-replicating molecules first arose (and probably never will know exactly) Ouch, that hurt. You mean the whole of Darwin's theory rests on an assumption that is unprovable?

No, I just mean that how are we really ever going to know what the exact sequence of events was? I suppose it depends whether you are a contingency or convergence type!

Although we don't know exactly, we do have lots of examples of ways it might have happened. Not knowing exactly which one it was is not a problem, the important thing is we can demonstrate that it could easily happen that way.

@GreenNoob: Darwins Theory of Evolution doesn't deal with this aspect of life at all, and it rests upon two very provable assumptions: Life exists; and life changes.

@WillihamTotland Can you elaborate?

@RichardSmith We can demonstrate that it could easily happen that way Can you give some examples?

@GreenNoob: See my answer.

They teach us in Physics that the entropy of an isolated system is always increasing or at least constant. Then how can an organism be born under these conditions?

The sun sends energy to the Earth, allowing for a decrease in entropy on Earth at the expense of the sun's entropy.

But when I think about it, all of them assume that there was an organism, however simple, that was capable of self replication & occasionally mutate. How did such an organism come into existence? Can anyone explain this?

That organism you're talking about is just a molecule that copies itself. Exactly how it has come about is not clear to me but it's not hard to imagine the possibility. A vast planet with molecules flying all over being bathed in ultraviolet light and if any molecule anywhere acquires the characteristic of copying itself, it will start growing exponentially and quickly spread all over the world.

If any molecule anywhere acquires the characteristic of copying itself, it will start growing exponentially and quickly spread all over the world Don't you think that's a big 'if' for a scientific theory?

Upvote for the "Sun sends energy to the Earth" part. Really cleared things up :)

No I think its a small if because its the only plausible explanation for the emergence of life I have ever encountered.

@GreenNoob It's not at all a big if - there are lots of molecules which demonstrate that property, some are biological like DNA or RNA, and some, like crystals, are mineral.

@RichardSmith Can you give examples other than DNA or RNA? I don't think that such complex molecules originally existed in the primitive earth's atmosphere.

@GreenNoob crystals are the simplest example, including ice and kaolinite. There are also lots of ways in which complex organic molecules could have arisen under conditions found on the early earth. See the wikipedia page for a round-up of them, or read Robert Hazen's book Genesis.

This is an extremely interesting and extremely fundamental question, indeed, and thus far, biologists have failed at coming up with a satisfying answer.
We know that all the parts are there, we just don't know how they were arranged, or which ones go where.
The question is, in essence, composed of three sub-questions:

How did the fundamental building blocks of life come about?
How did the first self-replicating molecules come about?
How did cell membranes come about?

The answer generally takes the form of "On primordial Earth, a small selection of the billions of organic compounds generated when UV-light hits a mess of carbon dioxide, nitrogen and water where captured in a tide pool where concentration and foam led to random chance producing self-replicating molecules in proto-cells."
This answer, while almost certainly true, is also incredibly dissatisfying, because all it tells us is what deductive logic has already taught us, almost intuitively.
Incidentally, the fact that all of this happens with a million to one odds isn't a problem: The Earth is big, and the time frame for this happening is along the lines of hundreds of millions of years: Anything that might happen once per year by a million to one shot would likely happen hundreds of times in that timeframe.
In any case, when it comes to evolution, or Darwin's Theory of Evolution, or any other theory of evolution, this is all irrelevant.
Evolution is something that happens in any sufficiently complex (open) system, assuming it has the capacity to change at all.
It is most easily observed in living organisms, because they are at the right scale, and incredibly diverse, but it happens on all scales of the universe.
In fact, the easiest way to explain how life first originated, is just to keep counting backwards when you reach the Last Common Ancestor (of All Life on Earth), and propose models for how this proto-bacterium could be even simpler, until you're left with CO₂, N₂ and H₂O, and other simple molecules.
At that end of the spectrum it is well-understood that e.g. H₂O "evolves" from H₂ and O₂, because H₂O has a quality that makes it more "fit" than either of its components, chemical stability.
Furthermore, H2 "evolves" from free hydrogen by a similar mechanism, and free hydrogen "evolves" from protons and electrons, because it has the property of being electrically neutral, which is also a desirable property.
Of course, at the level of protons and electrons, things get a little muddy, and evolution kind of breaks down as a method for explaining how things come about.
Edit: For reference: Current Models of Abiogenesis on Wikipedia.

Your odds are a little off.  A million to one isn't even close.  More like a billion, trillion, trillion, trillion, trillion to one it happened in the time period described.  It is the mathematical definition of impossible.

While many point to RNA, or a variant of it, as being the first molecule of "life" very few people know where it came from. Some suggest that it came from outer space because it's uncertain how the material for sugar-phosphate backbones could have developed on earth and that the perhaps these materials found their way here via meteorites. There are several hypotheses as to how an early earth environment may have promoted the properties of these molecules, but it's difficult to ascertain what exactly happened.
Somewhere within that abiogenesis wikipedia article is the mention of the role of deep-sea vents. The deep-sea vents and the currents that surround them basically facilitated a PCR reaction. Some of the early emerging DNA, maybe with some RNA and free nucleotides floating around, could have leveraged such an environment for replication and by sheer number (and some chance) entered into symbiotic relationship with other molecules to form the first cellular structures.

If you are interested in this question, I highly recommend you look at the work of Jack Szostak -  Nobel Prize winner at Harvard who is currently doing some of the best work in this area. His work is grounded in good experiments that point to how abiogenesis could
 have happened.

I think that it started like this:
First stage:
Chemicals like Na, Cl, O₂, O₃, CO₂, CO, HCN,  and H₂SO₄ react to form small molecules.
Second Stage:
Next those small molecules react to form macromolecules.
Third Stage:
DNA, being the most stable was first to replicate. A membrane eventually enveloped this and formed the nucleus
Fourth Stage:
Via Endosymbiosis it envelops mitochondria in an outer membrane
Fifth Stage:
Cell starts forming membrane and protein for all of its organelles. It is now a eukaryotic cell.
This is the DNA world Hypothesis.
Because DNA can be single, double, triple, or quadruple stranded in organisms(That would be ssDNA, dsDNA, tsDNA, and qsDNA respectively) it can do much more than just code for proteins or rRNA or tRNA.
In the single stranded state it can act like an enzyme forming deoxyribozymes.
In the triple and quadruple stranded states it can act inhibitory without needing another protein or methyl group.

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Can my dog really understand me?
Are dogs capable to understands human language ( for example after order sit it sit because he know that word) Or can sence our order by body language and intonation if so why this type of communication developed only at dogs?

What do you mean by recognize human language? Do you mean "able to tell which language is being spoken" or do you mean "understand words in a specific language?"

I mean if he is actually capable to recognize my orders only in my mother language or he is used to my intonation and the sight for the specific order.  I thought the understanding of single word is came in hand with this question.

Your dog understand you facial and body expression and gestures along the tune of your voice and the actual word being said. If you change the word and keep the rest, your dog might still understand the rest. In fact, many dogs tend to have an easier time to learn gesture than vocal commands. My dog will sit, lie down, give the paw, go to his bed and twirle much more easily if I make the gesture than if I say the command.

I think tyou are right. But i remember experiment, where researcher tried to learn dog by giving him a reward. He lerned him to bring specific item by his order (i saw it in documentary but dont know name). Fact what i tried to explain that he said bring for example doll and the dog bring it to him (but with hard drill).

@Remi.b: WRT tone and body language, how does this really differ from humans?

It does not. Both humans and dogs use somewhat similar cues to interpret someone else attempt to communicate. Why?

@Remi.b: Because your comment seems to be saying that dogs respond much more to tone & body language than to actual words.

(https://www.petmd.com/dog/behavior/dog-brain-facts-understanding-canine-cognition) according to this remi.b you should be right, but i am not stil sitysfied with the communication part. Its kind of strenge things about that the dog evolve the abillity to communicate with us because we gave them food, and our love. But if dometication can do this with dog, why not with others ??

Some researchers say that dogs have the intelligence of a two-year old.
Many dogs can understand more than 150 words and intentionally deceive other dogs and people to get treats, according to psychologist and leading canine researcher Stanley Coren, PhD, of the University of British Columbia.
He is a reasonable and serious scientist who is biased towards overstating dog intelligence. he sais:
The average dog can learn 165 words, including signals, and the “super dogs” (those in the top 20 percent of dog intelligence) can learn 250 words, Coren says. “The upper limit of dogs’ ability to learn language is partly based on a study of a border collie named Rico who showed knowledge of 200 spoken words and demonstrated ’fast-track learning,’ which scientists believed to be found only in humans and language learning apes,”
Dogs can also count up to four or five,
http://www.apa.org/news/press/releases/2009/08/dogs-think.aspx


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Can a person become addicted to tea?
Can one become addicted to tea like coffee addicts or smokers? I heard there are some common substances in tea and coffee, do they cause addiction?

Note that there's physiological/psychological addiction. Two very different things.

Yes, both tea (black tea at least, English speakers usually mean black tea when they say tea anyway) and coffee have caffeine which is addictive.
Apparently, being able to correctly reply to this question involves defining the word "addiction". My guess is that the negative connotation of the word "addiction" will cause some pressure to not use it.
Here's a recent review on caffeine addiction that says that caffeine is not addictive. I do not agree with their arguments but I'll leave it to the reader to judge.

Here's a decent link affirming different articles I've read before: http://www.medicinenet.com/caffeine/page2.htm     Basically, carandraug is correct. Caffeine is addictive, though not to the entire population, and the withdrawal symptoms (which are basically lack of energy and headaches) rarely last more than a few days. It is NOT a narcotic that acts as a neurotransmitter (like nicotine), thus its addictive capacity and withdrawal symptoms aren't comparable.

Doesn't green tea have caffeine, too?

@rwst yes, green tea does have caffeine as well (I said black tea at least, other teas may have caffeine. But I'm sure this days, one can buy even green tea without caffeine)

@rwst: green tea and black tea are the same plant (the tea plant, Camelia sinensis). carandraug: I will gladly upvote this answer if you link to some study or review showing that caffeine is addictive (should not be difficult to find).

@nico I did the opposite. I added a review that says it's not addictive and invite the reader to be critic of what they read.

I think I've heard that green tea (and white tea) have less caffeine than black.


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Why are some viruses not communicable person-to-person?
Below are two quotes from the CDC about Hantavirus:

"Researchers believe that people may be able to get the virus if they
  touch something that has been contaminated with rodent urine,
  droppings, or saliva, and then touch their nose or mouth."

and:

"You cannot get the virus from touching or kissing a person who has HPS."

This is hard to believe.  So, since human saliva is not a problem, can you be contaminated
by human urine or human droppings?  The only way for me to interpret this logically is to
say that this virus lives at the end of the digestive tract (for both rodents and humans)
and people can be kissed because they have much better hygiene than rodents.  Is there a
better interpretation?
Also, is there a simple reason why Hantavirus leaves the mouth (moving to the end of the
digestive tract) of an infected animal, but influenza does not?

I think (after research) that we don't know enough. As to a possible explanation of the different behaviour in rodents vs influenza, rodents don't get ill from Hanta, so the immune system isn't involved.

Viruses can have many different conditions necessary for transmission.  Viruses which have membrane surface coats (like HIV ) need to be in water all the time to survive.  Cold and flu viruses are more resilient and can survive on a surface such as a doorknob with a halflife of 18 hours(!).  Fortunately we are also have a reasonable intrinsic resistance to cold and flu and I think most infections do not result in symptoms.
Viruses often only infect some parts of the body.  Venerial diseases are a classic example of this where only contact of genitalia might cause transmission. Its probable that Hantavirus is not excreted through the sweat glands or in saliva.  If it did it would certainly be a more devastating disease.   It may also only be serious when the virus is introduced into the lungs, which may make transmission difficult.
For Hantavirus human to human transmission looks possible as observed by these folks. Even so, transmission is still so rare that there is no accounting for it in public health policy.  (they might also have been mistaken!).   Its possible that the virus requires transmission from a mouse to be virulent in humans. Its possible that the human transmission mechanism is so improbable (ingestion of faeces of infected human for instance) that you just dont' see it happening with the few cases of Hantavirus infection we have on the books.

Thanks.  I understand much is not known, but in your expert opinion/guess, do you think the probability of catching Hantavirus from kissing an infected rodent is significantly higher than that from kissing an infected human?  If so, is it just because of the hygiene point in my question (i.e., the probability would be the same if the rodent's mouth only touched clean food after it got infected)?  I'm struggling with understanding why rodents are so different from humans; rwst's point about rodents not getting sick could be a factor here.

Probably somewhat higher, but the virus seems to come from the other end of the rodent.  It might not be a respiratory virus in mice at all.

This paper is referred to in the Wikipedia entry for hantavirus as an example of human-human transmission. It may discuss the reasons why transmission is not normally via this route.

Martinez VP et al. (2005) Person-to-person transmission of Andes virus. Emerg Infect Dis. 11:1848-53
Despite the fact that rodents are considered to be the infectious source of hantavirus for humans, another route of transmission was demonstrated. Andes virus (ANDV) has been responsible for most of the cases recorded in Argentina. Person-to-person transmission of ANDV Sout lineage was described during an outbreak of hantavirus pulmonary syndrome in southwest Argentina. In this study, we analyzed 4 clusters that occurred in 2 disease-endemic areas for different ANDV lineages. We found new evidence of interhuman transmission for ANDV Sout lineage and described the first event in which another lineage, ANDV Cent BsAs, was implicated in this mechanism of transmission. On the basis of epidemiologic and genetic data, we concluded that person-to-person spread of the virus likely took place during the prodromal phase or shortly after it ended, since close and prolonged contact occurred in the events analyzed here, and the incubation period was 15-24 days.

Wow, maybe you could've translated that to normal-human-understandable language :)

That paper doesn't help answer my two specific questions,and makes me worry that any Hantavirus might be person-to-person transmittable (maybe only in the prodromal phase).  I wonder what the CDC's confidence level needs to be to print something...


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Is vision a vestigial sense for deep ocean species?
Sunlight doesn't penetrate beyond a couple of hundred feet from the surface of the ocean. Species that exist at greater depth probably live in a state of perpetual night; yet from a quick google image search (i agree it isn't a very authoritative source) for deep ocean species I see that plenty of these have eyes.
So ...

Are the sight organs in deep oceans species merely a remnant from an earlier era?
If they are a remnant, has evolution/mutation modified these organs over time?
Regardless of whether the organs of sight are vestigial organs for deep ocean species, how do the eyeballs withstand the extreme pressure of water in the deeps?

I can't answer your third, but I can answer your first two. With one word, in fact:
Bioluminescence
http://brightnepenthe.blogspot.com/2010/08/palate-cleanser-90.html

That's the deep ocean at night for ya. Unlike underground environments and caves, it's not pitch black pretty much anywhere in the ocean. There are things to see everywhere, and they play an important role in predator/prey relationships and/or mating. The absence of natural light does make things harder to see, but that's why you see the enormous eyes on species which live far down. So, nope! The eyes on deep ocean critters are not vestigial. They're very functional (and, if anything, probably increased in sensitivity).
The basics are summed up here: http://www.lifesci.ucsb.edu/~biolum/functions.html

The answer provided by @MCM contains an important chunk of information (Bioluminescence!) but it does not answer the question entirely. First, let's correct a misunderstanding in the question.
Sunlight does penetrate beyond 200m in the ocean. The intensity is not enough for photosynthesis to occur (and thus no phytoplankton below 200m) but depths between 200-1000m can receive enough sunlight for vision.
The region between 200-1000m is called the mesopelagic. Because there is enough light for vision, many mesopelagic species have eyes to see. Because light is extremely dim (humans would not be able to see), mesopelagic species tend to have very large eyes to gather as much light as possible. Vision is very important to mesopelagic species.
Below 1000m, we reach the bathypelagic (and, continuing deeper, the abyssopelagic and hadopelagic). Here, light penetration is insufficient for vision. Below 1000m is pitch black. In the bathypelagic (and deeper), you tend to see a reduction of eye size and sometimes a complete loss of eyes. Bioluminescence is still present (although much more common in mesopelagic fishes) but much less important. The physiological cost of producing and maintaining eyes is energetically expensive, so most species that live below 1000m have very weak eyes, if they have them at all.
Because the eyes of bathypelagic (and deeper) species still serve their original function, I would say the eyes of deep-sea organisms are not vestigial, in the sense of having completely lost their original function or serving a new function.


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Gene & Protein nomenclature: N-Myc, c-Myc, et. al
Can someone explain (or point me to an explanation of) exactly what is meant by all the different symbols I see used for writing genes and proteins?
I think I know that for genes, we use an italic font and for proteins, we use a regular font.
I think I've also learned that for human, all letters are in uppercase (eg. SHH) whereas for mouse, only the first letter is in uppercase and the remaining letters are in lowercase (Shh). (From http://en.wikipedia.org/wiki/Gene_nomenclature)
But I'm stumped with all the other "tags" (in quotes because that's how they seem to be used and I don't know how else to think of them) that I see floating around gene and protein symbols.
For example, Myc (MYC?).
I see these three articles in uniprot.org:
http://www.uniprot.org/uniprot/Q99417 for C-Myc
http://www.uniprot.org/uniprot/P04198 for N-myc
http://www.uniprot.org/uniprot/P12524 for L-Myc
These proteins are all in human, and yet their recommended names are not all caps; what's up with that? But even more confusing to me are the "C-", "N-", and "L-" letters prefixed to them. What in the world are those supposed to be indicating?
Are these all fundamentally different proteins (coded by different genes), but maybe related somehow to each other (thus the common three letters, 'myc' even if they are not all the same case and not all upper case as I thought was supposed to be the case in human), and they are just given these "C-", "N-", and "L-" tags to distinguish one from the other? Does one tag indicate an oncogene or a proto-oncogene? Why do I sometimes see "c-Myc" and other times, "C-Myc"? Does the case of the "C-" mean something? Is there some kind of key or legend I can look at to get answers to all these questions? I've found some explanations in Scott Gilbert's Developmental Biology textbook, but it still doesn't give me all the answers I seek here
I just want to understand how these tags and symbols are being used because it seems to me that when I read research papers (of which I've read many), they are used by different authors in different papers in ways that are not consistent with each other. Either that, or else I'm missing something very basic, which is why I'm asking here.
Thanks in advance for any help.

There is a useful set of links to nomenclature guidelines for all of the main genetic systems at this Wikipedia page. Personally, I think that the Saccharomyces cerevisiae system works best: it manages to cover dominant and recessive alleles of a gene, the name of the protein, how to refer to a related phenotype, and the use of a parallel convention for the designation of ORFs.
Unfortunately there is now no going back - there are many different systems and there is no hope of unifying them. When this plethora of naming conventions is combined with the reluctance of so many scientists to stick to the guidelines, we have a recipe for near anarchy.
Edit - On the specific topic of MYC nomenclature:
The v- and c- prefixes come from the early days of oncogene research. Viral oncogenes such as myc and src were found to be related to (derived from?) similar genes in normal cells. Thus v- means viral and c- means cellular.
This can be seen if you peruse the HUGO entries for the four MYC family members encoded in the human genome (extracts below). They all have an approved name which relates them back to a viral oncogene found in the genome of avian myelocyomatosis virus. This was the founder member of this gene family. Thus c-myc was the first myc-related gene found in the human genome, and is the one that is responsible for Burkitt's lymphoma. It is true, as @Leonardo says, that in tumours the expression of this this myc gene in lymphatic tissue changes due to chromosomal rearrangements, but this is not the origin of the designation c-myc.

MYC
  Approved Symbol:      MYC
  Approved Name:   v-myc myelocytomatosis viral oncogene homolog (avian)
  Previous Symbols & Names:   "v-myc avian myelocytomatosis viral oncogene homolog"
  Synonyms:   bHLHe39, c-Myc
  Chromosomal Location: 8q24
MYCL1
  Approved Symbol:      MYCL1
  Approved Name:   v-myc myelocytomatosis viral oncogene homolog 1, lung carcinoma derived (avian)
  Previous Symbols & Names:   MYCL, "v-myc avian myelocytomatosis viral oncogene homolog 1, lung carcinoma derived"
  Synonyms:   bHLHe38, "l-myc protein", LMYC, "myc-related gene from lung cancer", "oncogene lmyc"
  Chromosomal Location: 1p34.3

MYCL2
  Approved Symbol:      MYCL2
  Approved Name:   v-myc myelocytomatosis viral oncogene homolog 2 (avian)
  Previous Symbols & Names:   "v-myc avian myelocytomatosis viral oncogene homolog 2"
  Synonyms:   bHLHe38
  Chromosomal Location: Xq22-q28
MYCN
  Approved Symbol:      MYCN
  Approved Name:   v-myc myelocytomatosis viral related oncogene, neuroblastoma derived (avian)
  Previous Symbols & Names:   NMYC, "v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived"
  Synonyms:   bHLHe37, N-myc
  Chromosomal Location: 2p24.3

Thank you. Both answers help me a great deal. Preceding initial from viral (v-) or cellular (c-). Didn't know that either. Regret that it seems I cannot accept both answers, but thank you both.


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Assembly of metagenomic data
I'm trying to assemble metagenomic data that comes from termite guts. The sequences comes from SOLiD and no paired, so the reads are extremely short (25bp).
I have tried multiple assemblers (CLC, velvet, metavelvet, Meta-IDBA) but all produce few contigs (15 contigs, 1000bp average). The contig output is scarce considering the amount of raw data (5 Gpb).
Has anybody has any success in a task such as this?.
Thanks.

Not sure there is a lot you can do. 15 contigs of 10kb do seem awfully little, though.

This depends on your coverage and the number and relative proportion of species in the mixture.  this seems unlikely to produce results unless the protocol biases the library (rRNA universal primers for instance.)  I think at 25 bp sequences, even 30x coverage would not give full assembly sequences. Typically I believe 25 bp reads are only used to resequence close variants from similar or reference genomes.

The protocol have not been biased, that would be the correct approach. I was just hoping for some new point of view. What do you think about comparative assemble against some other assembled metagenomic data set to compare?. Thanks

Metagenomic data are tricky as novel organisms can't be identified.  But since you are in a bit of a jam you might try blatting your 25mers against a library of a few thousand bacterial genomes (as many as you can get a hold of) and you would get some idea of the distribution of the species in your sample, though rigorous identification would be some work....

Thanks, I was planning to do something like that. I think I'm going to try against some of the known bacteria of termite guts.

yup - better than nothing - plus the reads that do not form alignments will give you some idea of the novel content you are missing....


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Bugs' love for light
Do bugs love light bulbs because they resemble the stars or is it the sun? How do they sense the bulb? What is the purpose of this "brightophilia" that has evolved in insects?

I had previously heard in conversation that insects are actually attracted to the dimmest possible surroundings, which appears to be behind the light.

I think the answer to your question is relatively unknown. The answer I have heard the most often, which is largely the most accepted, is that many insects orient themselves in space using light. So if they are flying at night, the soft light of the moon tells them which relative direction they are going. Light bulbs end up confusing them, because they think they can orient themselves to it, but they are wrong.
http://www.npr.org/templates/story/story.php?storyId=12903572
Additionally, insects do have very similar photoreceptors as humans and vertebrates. Fruit fly eyes are a major research topic because of the similarity of the photoreceptor proteins as well as the amazing genetics that can be done.

This is similar to what I've heard most often, as well. I've always heard that insects use the moon or the sun to navigate, and artificial lights create a false version.

So they carry sextants in their invisible backpacks to follow the celestine map? Did you mean up with "orient" or positioning?


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How does a plant decide when to grow a branch?
As a plant grows, at some point the first branch forms. As it continues, branches grow new branches, and so on, in a seemingly random way. Is it random, or is it driven by the environment (heat or cold, sunshine, wind)? Or is it somehow defined in the plant's DNA, that each branch will grow at in such and such a direction, at such and such a time?
Does this generalize down to successively smaller branches, and eventually leaves?

I answered this in some detail in response to another question... http://biology.stackexchange.com/a/2646/430

Related topics: auxins, apical dominance.

Great answer Richard. Upvoted. You refer to a chaotic process that determines new areas of auxin concentration between meristems as the plant grows, so I guess the simplest answer to my question is "chance, within the confines of a system".  There doesn't appear to be any DNA-style central planning at work.


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Do twins "run in the family"?
My wife and I recently found out that we are going to have twins and so nearly everyone asks if we have a family history of twins.  Now I know that the answer for me is that it doesn't matter—as a man, I have no influence on my wife's tendency to hyper-ovulate.  And, of course, if we turn out to have monozygotic twins (we don't know yet), genetics plays no part.
Therefore the question only matters on my wife's side and only if dizygotic twins are known in her heritage. As it happens, we don't know of any twins on her side.  Given that many factors besides genetics are relevant to twins being born and we only know her family history for a half-dozen generations with any confidence, what are the odds that we would observe twins in her family history if she is genetically predisposed to having them?
Or, to put in another way, can I respond that nutrition and other factors were probably more important than genetics?

I admit to being amused that you say you "only" know her family history for something like 6 generations...:-)

The propensity for heterozygotic twins seems to be driven primarily by genetics, with additional factors playing a role (http://152.98.160.29/contents/p/staff/CV162Lewis_UQ_Copy.pdf', info site):

hormones ("Mothers of fraternal twins tend to be taller, and have earlier and shorter menstrual cycles")
ethnic background (which is really genetic) - African women are more likely than Caucasian women to have them, and Caucasian women are more likely than Asian women to have fraternal twins
mother's age
nutrition
previous births
fertility drugs

I also found a link to a genetic study published in Nature that claims to have linked a DNA region to dyzotic twins, but the Nature website seems to be down - maybe it will work later: A region on chromosome 3 is linked to dizygotic twinning - Nature.
Note that the father does not contribute to the chance of having heterozygotic twins, but a male offspring could pass the gene to daughter.

Do you have a source for: The propensity for heterozygotic twins seems to be driven primarily by genetics?

The Nature site is working for me.  An interesting quote: "Intra-uterine selection may be responsible for the Hardy−Weinberg deviation and we may in fact be dealing with a gene involved in the intrauterine survival of dizygotic twins."  I'm not sure I understand that, but it sounds like this study doesn't link genetics to hyper-ovulation, but survival in the womb.  Most of the information I've read so far point to a genetic link to the number of eggs released instead.

@JonEricson, added a couple of sources. It is my own impression from reading the sources that genetics is the most important. One way to think of it - without the genes for it, there is virtually 0 chance of it happening. In other words, it doesn't seem possible to just eat a bunch of soy beans, let's say, and have twins as a result.

@JonEricson, I don't think they try to establish any kind of causal relationship between the gene and hyperovulation. They simply found a suggestive correlation, but for the purposes of your question that would indicate a strong genetic component, I think. The study was geographically localized, which makes it more difficult to reach a general conclusion. The interesting thing that I noticed: they throw some doubt on the 'maternal lineage only' hypothesis. The quote you mentioned, I think it simply gives an alternative explanation for the disequilibrium in the alleles that they found.

I think it would help if some of your comments were added to the answer.  I particularly appreciate: "it doesn't seem possible to just eat a bunch of soy beans, let's say, and have twins as a result."  On the other hand, the practical aspect of my question is really a statistical one.  Are the genes for twinning very rare or do they just rarely produce twins?

Nutrition and environment don't have a huge affect, if any, that I could find. Age can, as women above 35 have a greater propensity for bearing twins. http://en.wikipedia.org/wiki/Twin#Fraternal_.28sororal.2Fdizygotic.29_twins
However, because fraternal twins can be the result of a gene on the X-Chromsome, the answer is yes in this specfic case. http://genetics.thetech.org/ask/ask86  If a mother is, herself, a fraternal twin then her chances of bearing fraternal twins is 2.5x higher than normal and it can be inherited from the mother's side even if she's not a twin herself. It's definitely not guaranteed, as the normal chances are so low to begin with, but there is definitely an increase.
However, for all other types of twins I have not yet been able to find anything implying there's a genetic component.

Hmm... I read those references as well and my impression was that nutrition did have a significant effect.  The age factor sounded more like a function of fertility treatments than age itself.  (We were actually trying to hold off on more children as it happens--our birth control failed.)  It does seem like a reasonable thing to point out is that my wife is not herself a twin.  But I'm more curious about the question of whether searching back through the family tree is a waste of time, statistically speaking.

I am still catching up on this topic but there are (atleast) 3 documented towns with greater than average rate of twinning: Cândido Godói, Kodinhi and Igbo-Ora. A published study on the Brazilian town might also be of help. It might be informative to look at familial twinning in these examples as beginning clues.


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Are the cytosol and extracellular fluids electrically neutral?
I've found several sources that state that overall, the cytosol of a cell is electrically neutral. The extracellular fluid is also purportedly electrically neutral. How can that be when we have membrane potentials?
Also in that regard, how do the ion transporters that set up the membrane potential know when to stop pumping ions to get a certain potential set up?

Membrane potentials are caused by different concentrations of ions on opposite sides of membranes in micro-environments along the membrane. The membrane can be, overall,  electrically and chemically neutral with small areas that have differences in electrochemical gradients.
For cells to produce these potentials they have proteins embedded in the lipid membrane. Ion pumps are the main players in creating potentials and gradients; through active transport (the use of ATP) the protein moves ions from one side to the other. When the concentration of that area of membrane is at one concentration the proteins are held in one conformation (active or inactive) and when the gradient is changed or meets a threshold the protein changes conformation and becomes activated or inactivated. So the actual electrochemical gradient dictates when the proteins are transporting.
There are also other proteins/messengers that are produced which can interact with the transmembrane proteins that keep them in one configuration or another to facilitate the production of an action potential. Once again, when this specific concentration is met the signaling molecule/transporter will become inactivate or activated.
This is just stuff I recall from some classes. Honestly, wikipedia is a fine general knowledge source. And more detailed than my explanation.  http://en.wikipedia.org/wiki/Membrane_potential#Ions_and_the_forces_driving_their_motion

Thanks for your answer! I didn't know about microenvironments and just assumed it meant the whole cell would be at these different voltages. Regarding second question, are you saying that the sodium-potassium pump would be regulated by both sodium and potassium concentrations?

Good response.  If you look at a neuron, you will see that it has a lot of surface area and its easy for a small portion of it to have a strong potential while the rest of the cell would hardly feel the difference.

@GorgeHomless Basically. Proteins are effected by what environment they are in, ie. temp, pH, salt, etc. These factors affect the bonding that makes proteins a certain conformation. So when the concentration is at a specific level, meaning the environment has changed, the bonding and interactions of the amino acid side chains will be altered; the protein will change shape. So, when sodium or potassium or other ions are in high concentration they interact with the protein & enviro, disrupting or enhancing bonds, making the shape change. Hopefully that answers the question and makes sense :)


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Digital Genomic Footprinting for ENCODE
I'm reading over the ENCODE Nature papers, and one of the papers referred to is "Global mapping of protein-DNA interactions in vivo by digital" by Hesselberth et al[1].
Genomic footprinting is a massively parallel variant of DNAse I hypersensitivity screening, which I feel I have a good handle on, but I don't understand this paragraph from the beginning of the results (the troublesome part is in bold):

To visualize regulatory protein occupancy across the genome of Saccharomyces cerevisiae, we coupled DNase I digestion of yeast nuclei with massively parallel DNA sequencing to create a dense whole-genome map of DNA template accessibility at nucleotide-level. We analyzed a single well-studied environmental condition, yeast a cells treated with the pheromone α-factor, which synchronizes cells in the G1 phase of the cell cycle. We isolated yeast nuclei and treated them with a DNase I concentration sufficient to release short (<300 bp) DNA fragments while maintaining the bulk of the sample in high molecular weight species (Supplementary Fig.1). These small fragments derive from two DNase I “hits” in close proximity, and therefore their isolation minimizes contamination by single fragment ends derived from random shearing. Because each end of the released DNase I ‘double-hit’ fragments represents an in vivo DNase I cleavage site, the sequence and hence genomic location of these sites can be readily determined by sequencing (Supplementary methods).

There's a reference to another paper by Sabo et al.[2] about genome-scale DNase assays using microarrays in that paragraph that I'm reading, but if someone understands the biology well, I'd really appreciate an answer.

Hesselberth JR, Chen X, Zhang Z, Sabo PJ, Sandstrom R, Reynolds AP, Thurman RE, Neph S, Kuehn MS, Noble WS, Fields S, Stamatoyannopoulos JA. 2009. Global mapping of protein-DNA interactions in vivo by digital genomic footprinting. Nature Methods 6(4): 283–289, doi:10.1038/nmeth.1313.
Sabo PJ, Kuehn MS, Thurman R, Johnson BE, Johnson EM, Cao H, Yu M, Rosenzweig E, Goldy J, Haydock A, Weaver M, Shafer A, Lee K, Neri F, Humbert R, Singer MA, Richmond TA, Dorschner MO, McArthur M, Hawrylycz M, Green RD, Navas PA, Noble WS, Stamatoyannopoulos JA. 2006. Genome-scale mapping of DNase I sensitivity in vivo using tiling DNA microarrays. Nature Methods 3: 511-518, doi:10.1038/nmeth890.

Is it the emboldened section that is causing a problem? Or the previous sentence about yeast? (I can help you with the latter.)

The section in bold is what's confusing me.  The rest is provided as context.

After reading the paper cited I think the logic goes like this: DNAse I will create free ends at accessible sites in the genome. However shearing during subsequent DNA isolation is also a source of free ends, and these represent noise in the analysis. You have to put in a lot of energy to shear DNA to very small fragments, so I infer that mild shearing during DNA isolation is very unlikely to create a new end that is near to an existing DNase I-generated end. Therefore, under the conditions used, any small fragments are much more likely to have been generated by two closely-spaced DNase I hits. By limiting the analysis to these fragments the noise from shearing is minimised.
Now that I've written this answer it doesn't seem like much more than a rewrite of the emboldened sentence, but I hope it is helpful anyway.

This is very helpful.  I didn't understand what "random shearing" was, or how it would add error to the results.  If I'm understanding correctly, random shearing during processing of DNA is unlikely to generate fragments that are relatively short (300 bp), which means that the 300 bp fragments are, with high probability, coming from short segments of DNA that have been clipped by DNase twice.

Yes that's right. Large DNA molecules are easily broken by physical handling. The low-tech way of doing it is to pipette up and down but if you Google "DNA shearing" you'll find lots of companies selling equipment that use shearing to produce random fragments in a desired size range.


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Why animals can move and plants cannot in general?
To clarify, I think the answer should be able to explain:

What are animals?
What are plants?
What's the difference between animals and plants (How do biologists differentiate them, if they differentiate them by moving ability of course it's simple, but we know they don't)?
How do those differences affect their evolutionary paths so that most animals can move around and most plants cannot? I know there are exceptions, but that's just the exceptions that show the rule.

Animals and plants are both classified as Eukaryotes, and as such can form large, complex, multi-cellular organisms. There are several major differences at the cellular level that distinguish the 2 Kingdoms (Animalia and Plantae). Without getting technical, the most crucial difference in relation to your question is that plants contain chlorophyll, and as such can generate their own food using sunlight.
This is very important when you consider that plants (by definition, those Eukaryotes that contain chlorophyll) have therefore evolved to be very efficient at converting sunlight to 'energy', whereas animals have evolved without this option and have to eat what food they need. So they have instead evolved mechanisms that allow them to forage, or even to hunt, for their food.
At some point, a unicellular organism incorporated chlorophyll, leading to multicellular plants in the course of evolution. The ancestor of animals evolved independently from the last common ancestor of plants and animals. Therefore, plants and animals are quite diverged, e.g. in mating 'rituals' (in plants this involves flowers and seeds - whereas in animals there are mating and gestation periods), and systemic changes, such as the immune system and the circulatory system (these are generally much more complex in animals than plants). All of which has stemmed from the difference in evolutionary pressures applied by the choice of food-source.
As you have pointed out, there are exceptions to all rules, so not all plants have chlorophyll, but as a rule it is the case! (Wikipedia: "Some plants are parasitic and may not produce normal amounts of chlorophyll or photosynthesize.").

Also, plants get their nutrients via their roots, so it is quite handy for them to stay in the ground! :)

Awesome answer. Not all plants have chlorophyll? I guess I'll look at wikipedia then.

So what's exactly biologist use to differentiate plants and animals? Chlorophyll?

@Jim Thio: think of red algae for instance

@nico the rhodophyta (red algae) all have chlorophyll, they are red because they also have red accessory pigments. An example of a plant lacking chlorophyll is the parasitic Hydnora africana

@Richard Smith: I was pretty sure there were deep sea red algae without chlorophyll, but maybe I just remember wrongly

@JimThio generally plants and animals look sufficiently different that biologists don't need to find "the one trait" that differentiates them - there are usually many differences, different cell structures, different molecules (like cellulose, chitin, glycogen...)... But nowadays there is a very simple way of differentiating animals from plants on the off-chance it isn't obvious from their appearance: DNA. The plant and animal kingdoms have diverged long enough ago that they have very different DNA. It would also help recognize freakish combinations or previously-undiscovered kingdoms.

Plants are multicellular organisms that utilize diffuse inorganic molecules (CO2, NO3, etc...) for energy and growth and thus they have evolved anatomical features that maximize the efficient concentration of these molecules (i. e., the root - shoot).
Animals are multicellular organisms that utilize concentrations of organic molecules for energy and growth (i.e., food) and thus they have evolved anatomical features that maximize the efficient harvest of these molecules.  Note that not all animals move.  There are many sessile filter feeders.


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Productive turnover and generations in the fruit fly
I was reading about the Lenski experiments on the evolution of E. coli bacterium and Dr. Elders's experiments on the evolution of the guppy.
These two experiments absolutely fascinated me, and seemed to happen relatively quickly by evolutionary standards. It was mentioned in the book that the fruit fly's productive turnover time is especially short.
I am extremely interested and would very much like to conduct an experiment into the evolution of the fruit fly, in much the same way as the Lenski and Elder experiments when I'm older.
Just so I can get a good idea, as I can find nothing on the internet, how long would it take for the fruit fly to get through, say, 10 generations?
Also, what would be the best way to go about beginning an experiment like this? Would there be certain people to contact? Would you need certain qualifications?

I love the subject of experimental evolution! Give me some time and I'll write more about it.

It is one of the most amazing things

What do you mean by you couldn't find anything on the internet? Drosophila generation time is explained here?
Your other question is a bit off-topic here but I'll give all advice I have heard myself:
You can leave out a banana skin and catch some fruit flies, then do the experiment in your kitchen :) Joke aside, unless you perform the experiment independently it will probably take a long time and it's well possible that you won't be able to do it at all (unless you become some famous scientist). I'm not familiar with the experiments you mention, but if you require equipment and/or funding, you will need a qualification and/or a good explanation why people should give you money or let you use their equipment for this experiment.
I don't know what stage of education you are at, but it sounds like you are still at school ("when I'm older")? Most countries have some schemes where students (below uni) can apply for young researcher kind of things, so you could try and google that. Apart from that, the best bet is probably to try and get into a uni with good facilities and research programmes for their students. What you study shouldn't matter so much as long as it's science.
In response to Marta's commment: if you understand the experiment and you think you can gather everything they used at home, nothing speaks against just doing it on your own. Just make sure you don't let those flies swarm your house ;)

Quite discouraging. As far as I know one don't need very expensive equipment to experiment with natural selection (especially among fruit fly!). Creativity and a lot of patience would be much more needed.

I'm not aware of what experiment they carried out there so I wrote my answer trying to stay on the safe side, assuming that it was a full-out scientific project :) Of course, experimenting is well possible on a small scale especially with these little ones.

Yes I'm still at school, I'm 16. I'm well aware of the length of time it would take and why would you need to be a famous scientist? Also, if Elder and Lenski gave reasons for wanting invested money (if they did at all), I'm sure I could give the same reasons. But yes, overall, rather discouraging

You would need a good explanation why you want to repeat the same experiment. And being famous has the advantage that people tend to give you access to things more willingly - and may not ask for as many explanations if you ask for things :)

@Armatus but one have to do something to become famous. It's not something that just come to you when you get older :)

Yup, and there's an excellent video on ted about that :) http://www.ted.com/talks/lang/en/richard_st_john_s_8_secrets_of_success.html


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Do egg laying animals experience a pregnancy?
Does a female animal that lays eggs experience a pregnancy-like period of time, where she will feel and behave differently as if she were fertilized and her body is prepared to lay a fertile egg, not a sterile egg (like the chicken eggs we eat)?
For example,

does the egg takes more time to be formed?
is it different in size?
maybe the animal will feel hormonal changes that cause it to increase body heat to help her sit on the egg, etc.?

Can you elaborate on what you mean by "fill deferentially", as it's not very clear what you are trying to say there.

And can you also clarify what "pregnancy-like period" refers to? A "period" can refer to two things :P And the short answer is yes, but I don't fully understand the question.

@jonsca, jello, "deferentially" was a typo, the hour was late and I was tired. "Pregnancy like period" - a period of time, when the animal will fill/act differently than every-day, or have changes to her body that are do not happen unless she is going to lay a fertile egg.

@IlyaMelamed See if that's closer to what you were aiming for.

@jonsca, yes it's.

I think this varies quite a bit.  many egg laying species are periodic and have a mating season (e.g. sparrows, salmon).  Others create eggs continuously (e.g. chickens, ants).

@shigeta, in guess that this means that a full answer will need to touch on both types. For example what happens to a sparrow or a salmon that doesn't mate on its season, and as asked before is there a difference between laying a fertile and an infertile egg from the POV of the chicken/ant.

In oviparous animals the egg retention phase in the uterus is brief. After fertilization eggshell mineralization is triggered but it seems the initial triggers of the pathway is not understood. The uterine fluid is rich in calcium and bicarbonates and calcium carbonate, in the form of calcite, precipitates around the egg. Shell mineralization is quite a rapid process and there are some specific proteins involved in this pathway. Have a look at these:
http://www.ncbi.nlm.nih.gov/pubmed/22201802
http://hera.ugr.es/doi/15773115
In ovo-viviparous animals the egg is retained in the uterus for a longer time and embryo is quite developed when the egg is laid (happens in boas). You can call it a sort of "pregnancy".
However progesterone pathway exists in birds and is involved in oocyte maturation
Oxytocin pathways also exist in birds, acting through oxytocin homolog Mesotocin, and perhaps they cause development of maternal care as they do in mammals.
This article talks about effects of oxytocin on birds but not exactly about its role in maternal care.
However i believe that the shell size and mineralization time shouldn't differ much between unfertilized and fertilized eggs in oviparous animals.

So your answer is that the animal doesn't feel any serious change between laying a fertilized and an unfertilized egg?

i dont know in what sense you are talking about.. parthenogenesis or what they do with chicken in poultry.. i think the behavioral response will be the same but observations in poultry chicken can be misleading..
there is a practice called forced-molting which poultry industry adopts in order to increase the egg yield.. during molting the reproductive tract of the hen again becomes capable of egg-laying.. So definitely there is some endocrine response after egg laying and perhaps the hen doesn't "know" if its a viable egg or not


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How are synaptic vesicles brought to the synapse?
I'm reading about how synaptobrevin is used to identify synaptic vesicles for tethering near the synaptic cleft. Since neurons have a synapse and dendrites, I'd like to know how exactly  the vesicles get moved from the Golgi to the synapse.
As far as I can tell, they are transported along microtubules by dynamins as opposed to floating freely in the cytosol (correct?). If so how do the dynenins identify synaptic vesicles - would they form a SNARE complex that gets released near the synapse or by some other means?

In eukaryotic cells you can assume most things not to be floating freely. Enzymes and smaller molecules just diffuse, but all organelles and even big proteins are in constant contact with the cytoskeleton. (Source: Conversations with lecturers)

Or the membranes, of course.

You are looking for a review on vesicle cargoing along the cytoskeleton. This open access article is the most recent I found on the subject.
From the abstract:

How synaptic cargos achieve specificity, directionality and timing of transport is a developing area of investigation. Recent studies demonstrate that the docking of motors to their cargos is a key control point. Moreover, precise spatial and temporal regulation of motor-cargo interactions is important for transport specificity and cargo recruitment. Local signaling pathways Ca2+ influx, CaMKII signaling and Rab GTPase activity regulate motor activity and cargo release at synaptic locations.

M. A. Schlager, C. C. Hoogenraad: Basic mechanisms for recognition and transport of synaptic cargos. In: Molecular brain. Vol. 2, 2009, p. 25. DOI:10.1186/1756-6606-2-25. PMID 19653898. PMC 2732917.

Nice review. Although it is quite unlikely that that link will be removed... could you improve the answer by quoting relevant passages or summarizing the important information?

Thanks for the link, looks like it's Rab GTPases that attach them to microtubules.


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Why do stranded marine mammals die so quickly?
Mammals have lungs, so do marine mammals. Nevertheless some marine mammals seem to die rather quickly when they strand on a beach.
As they have lungs and can breath while on land, why do they die so quickly? Not being in water only restricts them from food.
Do they maybe try to get back into the water so rudely that they get hurt by rocks and/or break bones? Pressure difference doesn't seem to be a problem as they can jump out of the water as well.
I was wondering after reading this article on stranded pilot whales that got spot but died rather quickly after.

I'd assume that old, sick, or otherwise weakened animals have a much higher chance of getting stranded at all, which adds to a quick demise.

In the case of whales, I always thought that it was something to do with the fact that they rely upon buoyancy to support their weight and this seems to support that view:

When whales, including small whales or dolphins become stranded on beaches
  they suffer from the pressure of their own weight on their organs,in the
  water they are weightless.  They also suffer from overheating as they have
  blubber that insulates them in the water and outside of the water causing
  them to overheat.  This is why we place wet towels and cold water on their
  fins and flukes when do they strand to help keep their body temperature
  down.  Unfortunately most stranded whales do not survive once they have
  beached themselves.

That's not exactly true, you are generalizing. For example seals are marine mammals (that's a rather large non-official group I think)  and they don't die so quickly.
Anyway, breathing is not the only thing necessary for survival. If you leave a human inside a 50°C room he can still breath but won't live for long.

I said "Nevertheless some marine mammals seem to die rather quickly when they strand on a beach.". So I was not generalizing on species. It's true that breathing is not the only thing necessary for survival, otherwise they wouldn't die, my question aimed to find out what was the other crucial thing for survival on such short time frames.

@StevenRoose That would depend between animal. I believe most of them require their skin to be moist or they get sunburns.


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Do dogs have something different about their physiology that allows them to pant without hyperventilating?
I was wondering this as I considered how effective panting would be for humans as a means of cooling.

This article quotes a professor of respiratory physiology that says "dogs are built to pant just right. The mechanics of their lungs and chest set a precise rate for panting that minimizes the amount of work while maximizing cooling power." They also don't breathe fully when panting, so they can still cool themselves without increasing gas exchange. This is different than humans, who will hyperventilate to get rid of carbon dioxide (or you can intentionally hyperventilate and cause respiratory alkalosis).

What about panting with breaths that are only slightly more than the amount of dead space?

Not knowing the physiology or the literature, I can say based on personal observations that dogs, even when extremely hot or exhausted, mix in a routine of deep inhales and exhales to their panting.  Perhaps this prevents unwanted side effects of their cooling mechanisms.

Our physiology is quite different. I guess their larger surface-area tongue is one obvious difference, and the fact that they have limited sweat glands. I actually thought they had none, but this article states that they have them on their feet.
Another fun fact there is that they don't just use panting -- they can apparently  constrict/dilate vessels in their face and ears..


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Predators faking to be not hungry?
I believe that there are predator/prey combinations where the prey can easily spot that the predator is not hungry and will not try to flee from it. I’m thinking, for example, of gazelles who will happily graze in sight of sleeping lions. (Please correct me if this is already wrong.)
It seems to be sensible (in an evolutionary sense) for the predator to not put unnecessary stress on the prey. First question: Are there predator who actively signal that they are not hungry, e.g. by a certain sound?
And my second question: Is there such a combination where the predator will, in times of severe hunger, pretend not to be hungry in order to more easily catch a prey?

It seems to be sensible (in an evolutionary sense) for the predator to not put unnecessary stress on the prey. What leads you to believe that?  I don't know one way or the other, but what is the evidence in that direction?

I suppose that the reason why gazelles could graze in sight of sleeping lions is because the prey are aware of the predator's presence. That's why gazelles do not came close enough to be catched. Also lions quickly learn that there is no point to chase a prey if it already notice the threat. I'll make it an answer when I find adequate references.

@jonsca: Naive thinking maybe, but isn't it in the interest of the predator that the prey population thrives?

I would suggest that the behaviour of the gazelles you are citing is perhaps over simplified. There will likely be temporal and spatial dynamics in their behaviour... Prey will probably spend more time concentrating on observation when they know there are predators around. There will also be likely peak times during which hunting occurs (in savannah systems it tends to be dawn and dusk) and prey would be more cautious at these times.
It seems to me that the prey would not be judging the hunger of the predators but instead they learn the consistent patterns in the level of risk associated with being near predators. This could be genetic in its cause. If there is a gene (or genes) which determine when a prey individual is most likely to be out in the open grazing then the higher probability of predation at certain times would reduce the frequency of the genes which cause that choice.
There could also be fluctuations over time as the predators learn that the prey have become less cautious, which then causes predators to take advantage of unsuspecting prey, which you might be interpreting as the "faking" behaviour... it is not a deliberate fake, more taking advantage of the risk taking behaviour of the prey (as time passes without attack they will become more brazen). To the best of my knowledge there are no examples of the deliberate fake but predator prey dynamics are not my specialism.
Overall, I think you are asking a question based on learning and information use of repetitive patterns in behaviour of predators by prey, and have interpreted these behaviours in an over complex way (see Occams Razor).


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E. coli values for [enzymes], [metabolites] and kinetic rates
In my attempt to create a metabolic model of E. coli, I have found a comprehensive list of metabolic reactions and their stoichiometry. The one I am currently using is E. coli model iJO1366 (more here). What I have not yet found is a comprehensive list of kinetic rate constants associated with these reactions. I also require a data source of concentrations of these enzymes and metabolites at steady state in E. coli. Where can I find information on concentrations and rate constants?

why do you want to compile this?  Flux analysis is looking pretty useful and does not require all this data.

I found SABIO: http://sabio.h-its.org/

I would advise you to use the SMBL for iAF1260 E. Coli with a COBRA toolbox on MATLAB. It has all the constants you are looking for optimized for the steady state and have been extensively tested for simulation of single and multiple genes deletion / mutation. Even if you want to stick with your model you will be able to copy the constants from there.
However depending on what you are doing you might not be satisfied by the whole models, since the they are computationally too complicated to simulate and optimize and lead to computationally unstable results, especially when you try to simulate colony collaborative mechanisms.

Do you have any literature to support your claim of computational instability?

This is my personal experience. When you use the COBRA toolbox, you use an external module for linear optimization to get your "objective" function. When I computed the base model from iAF1260 E.Coli, it worked well, just as a system of two bacteria living together. But as soon as you started to perform single or double gene deletion analysis, your objective function maximum started to behave erratically. You could make it bit better with it by using a different external linear optimization module, but still no analysis was possible.

This work was based on this paper and I had an impression that the authors run into pretty much the same limitations: only qualitative analysis is provided with the computational model, whereas they could have gone quantitative with this model and had quantitative experimental results.


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How do trees use Adhesion and Cohesion to move water against gravity?
I have an AP Bio class where I have to name 3 properties of water and I chose adhesion and cohesion for one of them. I'm having trouble finding out how exactly trees use adhesion and cohesion to move water. There is a lot of different answers out there on the net. How do trees use adhesion and cohesion to move water against gravity?

In high school, we did an experiment that showed this.
Basically, if you take a glass of water, and let it sit out, perhaps in front of an open window, it will eventually lose water due to evaporation. It may take a few days/weeks to really see a large difference, but the level will go down. But, if you take a few flexible straws, put them in so the bendy part is submerged, the water level will drop much more quickly. (I'm not exactly sure if the bendy straw part is really that important here. Logically, I don't think it is, but I haven't done the experiment so I can't really say.)
The reason the straws cause evaporation to happen more quickly is because as wind blows across the top of the straws, it pulls some of the water with it. And because, as the last person said, of cohesion and adhesion, the column of water is pulled up with it and thus it evaporates faster.
Similarly, these fluid mechanics are why toilets and siphoning work. When you siphon, you create a low pressure area inside the tube, like you are sucking out of a straw. Because of this low pressure, liquid is pulled into the tube. If you fill the tube with liquid, and turn the tube down toward the ground so the liquid starts coming out the end, the force of the liquid coming out of the tube creates low pressure in the tube again, thus causing more liquid to be sucked up.
This is very similar to how trees work. In the stomata, or the pores in the leaves that allow the leaves to "breathe," wind helps to pull the water out of the pores. But because of the decrease in pressure cause by the liquid being sucked out of the pore, water gets pulled up the tubes in the tree (xylem).

The mechanism is called "capillary action". It requires a tube of a small diameter and happens because of the adhesion of water to the walls and the cohesion within the water (=surface tension).

Its important to add that the driving force for the actual water movement is the gradient in water potential in the system (atmosphere is dry, while the mesophyll of the leaf is wet). The plant expends no energy to move the water.

Trees don’t use either adhesion or cohesion to move water against gravity.
It is impossible to “suck” above 10.3 m, which is equal to our atmospheric pressure.
Air Pressure is pushing up the xylem Micro-tubes - which have a lower pressure / vacuum at the top (created be evaporation from the leaf).
This “siphon effect” is powered by Air Pressure, pushing up a closed tube.

It has to do with heat transfer and Newton's Law of thermodynamics.  Matter that is heated will always travel to a cooler location.  The roots are like a sponge, soaking up water from the ground.  The water moving through the capillaries causes friction = heat,  These heated water molecules collide with carbon atoms and form CO2, which is expelled trough the leaves in summer, but is negligible in winter.

I don't buy this explanation. Trees don't have leaves in early spring and water comes up the tree with no problem. Also, if water was put under enough pressure to get sucked up a hundred feet, it would have so much heat that it would become steam. It's why buildings that are super high need pumps every so often to get it to go up.
I have a theory. In a tree you have different parts of the trunk. Heart wood, sap wood, cambium layer, and bark. I think because the heart wood and bark aren't taking up water, they aren't expanding like the sap wood is. The cambium layer is very slippery and let's the tension between the bark and sapwood to slip past each other. I think the expanding sapwood eventually gets squeezed and osmosis does the rest.

have any references to back up the claims you're making?

Trees don't have leaves in early spring and water comes up the tree with no problem you mean "no leaves = no gravity". buildings that are super high need pumps every so often to get it to go up so pumps don't use pressure to push water. Welcome to Biology.SE, but you seriously need references

I somehow discovered that in some trees with thin bark, I could place my ear on the bark and hear the movement of the water in the tree.  It was not a continuous flow, but with hesitations like spurts or pauses.  I thought there might be a valve system to keep the water from coming back down.  But by saying it was pulled up by evaporation from the leaves, I can't explain the pauses.

Hello Martha. Welcome to [biology.se]. Your answer is not really addressing the asked question. Even if it did, your answer is based more on personal experience and not validated facts. You can [edit] your answer so that it provides relevant points that address the question or else it would be deleted.


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Are there any substance that are more dangerous at low dose than at higher dose?
It is commonly admitted that

The dose makes the poison

which means as a person, the more I take a substance, the more risk I take for my health.
There is even an indicator called LD50 (see Median Lethal Dose), which specifies the 'lethal dose' at which 50 percent of subjects will die.
This might seems a stupid question but: are there any substances for which it is more dangerous to take at low dose than at higher dose? For example, you have to ingest at least 1µg of XXX because if you ingest less you will have health problem...

Oxygen comes to mind. A low dose is much more harmful than a large one :).

sugar, water, protein, ... these all have an optimal range of healthy doses- too much OR too little can be harmful.

Dihydrogen Monoxide is a brutal killer.

several ingested poisons can be more harmful in low doses because in large doses they naturally trigger a vomiting response.

Yes. Taking antibiotics (and by extension antivirals and antineoplastics) at low doses is dangerous, as this creates an evolutionary pressure to evolve antibiotic resistance (or rather, incorporate through horizontal gene transfer). This is dangerous because an infection resulting from these bacteria will then be harder to treat.
In the paper "Experimental evolution of resistance to an antimicrobial peptide", Perron et al. gave E. coli the chance to evolve resistance against a novel antibiotic. When given a high dose initially, most bacteria died. When exposed to low doses, the bacteria evolved resistance in 600 to 700 generations.
For the same reason it is strongly advised to finish a course of antibiotics even after symptoms fade.

+1 although I don’t think this is what OP was referring to because the effect is indirect rather than there being a toxic effect of the antibiotic of the host which decreases with increased dose.

I agree, but my answer is true to his original question

This is a bit of a news flash - the answer is probably yes.
Reading through recent Nature articles this one popped up: Toxicology the learning curve.
Where there are some intriguing examples of low concentration only toxic effects.
It might be worth a read. The preface gives a review of the idea, going back to the 16th century physician Paracelcius that the toxic properties of anything increases monotonically with dosage.  This is reflected in most of the answers and its one of the few things which toxicologists universally expect to see.
A research group at U Missouri-Columbia is claiming that endocrine disruptors have non-monotonic toxicology curves, meaning that toxic effects actually decrease with greater dosage.

Nature is kind enough to allow access to this image.  The three curves on the right show a decline in drug effect as concentration increases.
Endocrine hormones act at very low dosage - testosterone, estrogen, pituitary and thyroid hormones are some examples.  We'll probably be hearing more about this in the future, rather than less.
While this is still controversial, its made news because it is the sole class of compounds which really behave this way.  notably the first curve is for BPA (Bisphenol A) - the plastcizer which is common in pool toys and toy inflatable balls and drink bottles but the FDA has flagged for closer study.

No. The influence of dose–response relationship on toxicity is one of the fundamental properties of (bio)chemistry, and follows directly from the fact that concentration influences the reaction rate: a chemical reaction between two or more agents is a stochastic process where agents have a certain chance of interacting based on physical proximity (and other factors). The higher the dose, the higher the chance of two agents meeting, and a reaction taking place.
This has two interesting consequences:

Homeopathy doesn’t work.
Although not all substances show a clear dose–response curve (simply because they are always reactive no matter their dose), toxicological studies which fail to show a dose–response relationship are met with scepticism. A recent example of this is the GMO toxicity study undertaken by the French scientist Séralini. One of the many flaws in this paper cited by other scientists was precisely this lack of dose–response relationship.

Example of something always reactive no matter the dose?

@David No, sorry. “no matter the dose” is also stretching it a bit – you always need some minimal amount, it’s just that the steepness of the curve varies.

thanks for the clarification; as written it can be interpreted as "homeopathy" doesn't work, except when it does. On another note (more as a clarification for readers than as a correction to you) the GMO study is a poor example to use. Because of the many flaws, any inference is limited (e.g. my primary conclusion is that there is insufficient information to conclude anything about the relationship dose-response relationship).

No. The influence of dose–response relationship on toxicity is one of the fundamental properties of (bio)chemistry...?!?

@Lo Unclear? It means that things get more toxic with increased dose, never the other way round.

@Konrad Rudolph: there are plenty of example of substances having different effects at different doses (steroid hormones, for instance), and dose-response relationships are not always going up. A diet low in vitamines is as bad as a diet high in vitamines

"concentration influences the reaction rate": Usually, but there are zeroth order reactions. Of course not forever, it stops if the reactant is gone, but reactions exist that have a fixed rate for a large range of concentrations.

I think the best answer is right now would be
Probably no, but we're not certain
The question of non-monotonic dose-response is still being discussed and debated. You will find a good example of this at EFSA

First of all, that is an excellent question! Secondly, please excuse the lack of thorough sourcing for this post. I only like to share some pointers...
Q: Can substances do more harm in a mammal at a lower dose than at higher dose?
A: Yes.
Some may know the example of the blood thinner, and widespread NSAID Acetyl-salicylic acid (Aspirin). I will use this example because Aspirin is one of the most known and used drugs in the world, with a long and interesting history. As being part of the class of nonsteroidal anti-inflammatory drugs (NSAIDs) it has recently gotten a bad wrap for blocking an enzyme which is crucial for prostaglandin synthesis and processes that maintain  a healthy stomach wall in the presence of an potentially harmful bacterial and chemical milieu. On a sidenote, as an acid, Aspirin actually hardly dissolves directly in the acidic stomach.
To quote wikipedia (DOR: 28/09/2012):

Salicylates are excreted mainly by the kidneys as salicyluric acid
  (75%), free salicylic acid (10%), salicylic phenol (10%), and acyl
  glucuronides (5%), gentisic acid (< 1%), and 2,3-dihydroxybenzoic
  acid.[148] When small doses (less than 250 mg in an adult) are
  ingested, all pathways proceed by first-order kinetics, with an
  elimination half-life of about 2.0 to 4.5 hours.[149][150] When higher
  doses of salicylate are ingested (more than 4 g), the half-life
  becomes much longer (15–30 hours),[151] because the biotransformation
  pathways concerned with the formation of salicyluric acid and salicyl
  phenolic glucuronide become saturated

Aspirin can interfere with a lot of drugs, including Ibuprofen. The known list of drugs is so high, in part due to the widespread application of aspirin, and in part due to the chemical composition of this very small drug with two functional groups. A functional group is a sort of chemical feature that determines how and with what probability a chemical interacts in a given milieu.
As a certain metabolic degradation pathway may get saturated, other pathways can take over and lead to different potentially harmful metabolites resulting in damage to the excretion/clearance organs such as the liver (hepatotoxic) and kidney (nephrotoxic).
A metabolite is the product of metabolism ( a weak back-referencing definition). metabolic pathways are a sequence of chemical reactions within a cell, and metabolism is the entire set of metabolites and pathways.
Liver/Kidney Toxicity is believed to result from an interplay of a) high concentrations of metabolites or direct toxins (=parent chemicals) within specialized high-concentration-forming cells, and b)  the non/covalent  binding of cellular macromolecules to interfere with their normal function and/or production of reactive oxygen species (ROS).
Another example (from memory) is the interaction pharmacokinetics of theobromine (from cacao) and other xanthines (unverified).
There are many more examples. I hope this example and mechanism serves you well as a starting point...

From a biochemical standpoint:

In fact drugs may act differently at different concentration thresholds at different times at different places within an organism and its cells that make it up. Evolution exploited this very early on and used it for things like body segmentation along defined axis during development.
Drugs may interact with each other differently at different levels of concentrations, say as binary, ternary, and higher order complexes. The rate of formation of such complexes is denoted through the dissociation constant - which is a type of equilibrium constant such as pH is.
The dissociation constant describes the propensity of a chemical species to separate reversibly and, - this is crucial! - is concentration dependent. This is accounted for by the use of so called activities or the apparent concentrations, as a result of incomplete hydration of the chemical and other effects of a "crowded environment". Now don't just think of chemicals, but macromolecules as well. In immunology for instance new molecular features can arise on the surface of a macromolecule, due to the association (complexation) with a small molecular drug. This in turn can lead to an immunological reaction, even anaphylaxis ( a so called Type I hypersensitivity reaction) and ultimately shock. Such drugs are classified as haptens.

Important in an organisms sensitivity and susceptibility to drugs however, is the current allometric growth rate and types of organs and cells available. As such a fetus is more susceptible than an adult.
I hope a simple yes accompanied by this admittedly to-long to really read post gave you some insight into what scientist across many, many fields are dealing with. Naturally, the issue is more complex.
Personally I believe the issue of dosing and drug reactions will improve significantly over the coming decade...

Maybe I'm misreading your post, but I don't see any example of a substance that is more harmful at lower doses in your post.

I may be missing something here, but I can find no mention of how lower doses of aspirin are more harmful than higher ones in your answer. I assume that one of the metabolites it gets broken into activates a different pathway and can lead to toxicity. Is that what you mean?

Correct, I didn't include a specific example only an example mechanism. Substances acting differently at different levels is well known within the concerned fields of science. Substances/Drugs which are toxic at low levels cannot be approved nor are they generally appealing for studies. Substance's "dualism" can offset the LD50. The post also doesn't discuss how substances can be toxic at low dose or discerns entantiomeric purity (e.g. thalidomide) and/or entantiomer-specific pathways. Specific examples may best be extrapolated from systems-biological and/or chemotherapeutics literature...

The question is not about substances acting different at lower concentrations but specifically about being more harmful/dangerous at lower concentrations. Your examples don't fit that, strictly speaking you're not answering the question that has been asked.


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Where would Saccharomyces cerevisiae be found in highest concentrations in environment?
I have bakers asthma specifically to 'Sc' yeast, and know to avoid bakeries, breweries, etc...
I have figured out to not disturb rotting leaf piles, and fermenting bark mulch. Where else?
What percentage higher are concentrations in say Florida, as opposed to New York state?

interesting question.  aerosol yeast and fungi must vary a log with the weather, humidity and this sort of change in condition.

Here is a link to an interesting article which reports a survey of wild isolates of Saccharomyces cerevisiae in China.

Wang, Qi-Ming, et al. (2012) Surprisingly diverged populations of Saccharomyces cerevisiae in natural environments remote from human activity. Mol Ecol 21: 5404-5417

A relevant quotation from the article:

In addition to grapes and oak tree (Quercus spp.) bark, S. cerevisiae was successfully iso-lated from a variety of damaged fruit collected in orchards or markets in different provinces of China; from the bark of different deciduous trees; forest soil and rotten wood collected in primeval, original secondary and planted forests located in different regions covering temperate, subtropical and tropical climate zones from northern to southern China. Unexpectedly, the success rate of S. cerevisiae isolation from fruit samples (6.5%) was lower than that from tree bark (16.5%), soil (10.8%) and rotten wood (9.2%) samples. S. cerevisiae was more frequently isolated from forest soil samples (success rate 13.7%) than from orchard soil samples (success rate 9.1%). Among the fruits giving positive S. cerevisiae isolation, grape samples showed the lowest success rate.

Table S2 in the supplemental information records isolates as follows:
climatic zone    sites   isolates
__________________________________
tropical           5       20
subtropical        2       14
temperate          13      51

Superficially, from this it looks as if there would probably be little difference between New York state (humid, continental) and Florida (humid, subtropical).


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How does the stem-loop cause intrinsic transcription termination?
In this animation, towards the end (about three quarters) the process of transcription termination is shown. It states that the transcribed RNA forms a hairpin loop (or stem-loop), which halts the transcription process.
My question is, why does it halt the transcription process, considering that the RNA polymerase moves in the opposite direction of where the stem loop is created? Does it somehow change the RNA conformation such that no further bases can be added? Interpreting it as a physical obstacle doesn't seem to make any sense here.

There are two mechanisms of transcriptional termination in prokaryotes.  The one shown here is "rho-dependent" because it involves rho, a DNA-RNA helicase that loads on and unwinds the RNA from the DNA, terminating the elongation by the polymerase.  Check out [1] which shows a model for how rho multimers move through the RNA.
The other mechanism involves just a hairpin. The paper [2], especially Page 23, part C, shows how "rho-independent" or "intrinsic" termination works.  Basically, the hairpin slows down the polymerase and destabilizes the transcription bubble, allowing the intrinsically-weaker A:U bonds to fall apart.
There is no requirement for a hairpin in rho-dependent termination, and I think the movie is mixing them up.

 Geiselmann J, Wang Y, Seifried SE, von Hippel PH. 1993. A physical model for the translocation and helicase activities of Escherichia coli transcription termination protein Rho. Proceedings of the National Academy of Sciences of the United States of America 90: 7754–8. [pdf]
 Datta K, von Hippel PH. 2008. Direct spectroscopic study of reconstituted transcription complexes reveals that intrinsic termination is driven primarily by thermodynamic destabilization of the nucleic acid framework. The Journal of biological chemistry 283: 3537–49. [pdf]


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Linkage and LD: quantitative or qualitative?
My understanding is that the concept "genetic linkage" can be expressed in quantitative form, like:
A predisposing gene X was found in close genetic linkage to Y.

And that linkage disequilibrium (LD) is a quality, like being pregnant, you are either in LD or your are not:
A predisposing gene X was found in close genetic linkage to Y and in
linkage disequilibrium with Z.

Is this correct?

Linkage disequilibrium (LD) occurs when there is a non-random association or correlation between genotypes. Note I used the word correlation; this is a quantitative trait.
Some genotypes may well correlate perfectly (R=1), i.e. they are always inherited together. Others may not be in 'perfect' linkage (e.g. R=0.9), but are still considered to be in LD because there is a strong correlation between the genotypes (I think 0.8 is generally seen in published papers as the 'cut-off').
The correlation coefficient is derived from the D' value - this (simply) denotes the observed vs. expected frequencies of the genotypes (whether they are in linkage or not). Therefore either value can be used, but I think it is more common (and more interpretable) to express the correlation coefficient (or to be more precise, the coefficient of determination, R^2).
If you'd like an example: I might be interested to know if any SNPs are in LD with rs10757278 (located on 9p21, associated with heart disease). Using SNAP (by the BROAD) I can input my search, choose my options (e.g. use 1000 genomes data, and an R^2 cut-off of 0.8) and search. ~5 SNPs are found to be in 'perfect' LD (R^2=1), but a further ~40 are still considered to be in linkage with the input-SNP because their R^2 values are above 0.8.
So in summary, both statements can be used correctly, but it is always more informative to state the degree of linkage (otherwise it might be assumed they are in perfect correlation).

This is a good explanation with a fine example. It can be added that the r^2 value can be between 1 (complete LD) and 0 (zero, no LD whatsoever as with markers on different chromosomes). Yes, we and many others use a cutoff of r^2 > 0.8 to denote strong LD. However, values of 0.4 and above are not to be discounted as having no LD.