text:
Conjugate secondary antibody
Why is the secondary antibody conjugated to the enzyme in ELISA, instead of the primary antibody? Wouldn't it be easier to conjugate the enzyme to the primary antibody?

Making an antibody-enzyme conjugate isn't trivial. By using a primary/secondary set-up you can use the same well-characterised conjugate in combination with many different primary antibodies (as long as these primaries are all raised in the same species). There is also the possibility of some amplification: for example, if the secondary is an anti-Fab then two secondary Igs will bind to each primary.
Response to OP comment
Most primary antibodies in common use are derived from rabbit or mouse, and most are IgG. So, for example, the secondary antibodies goat anti-rabbit IgG and goat anti-mouse IgG will cover most experiments.

In other words; otherwise you would have to make a conjugate for every primary antibody?

Yes, that's right.

@ZafarS: in fact, that is what you do for most immunological techniques, like Western blotting, immunohistochemistry etc.: use an unconjugated primary and a conjugated secondary.

@AlanBoyd Sorry, I still have some doubt whether I grasp secundary antibodies. Every species has (or better: can have) a secondary antibody per animal right? So for example; we can have secondary antibodies for primary antibodies of rabbits, chimps, mice, etc. So that would still be a lot of possible secondary antibodies, but anyway less than primary antibodies.

This answer could be improved with an explanation that many times primary antibodies are monoclonal, providing a high degree of specificity to the interrogation of the protein in questions and reducing off-target binding, while the secondary ABs are polyclonal and will bind to multiple sites on the primary AB, thus increasing the signal, say of a fluorescent marker, HRP, or radioactive probe. Though alluded to, cost and time of preparation are important considerations. You can have a stock of goat-antirabbit secondary ABs that will work with every assay you use a rabbit primary AB.

Another reason that secondary antibodies are used is to look for the production of antibodies by a test animal. Follow me for a second with an example that I think will make it clear.
Our Purpose:
We have identified a protein (call it 'V_Entry') that is vital for Ebola to infect human cells.
We wonder if antibodies against V_Entry will block Ebola infection.
We then use this V_Entry protein as a vaccine in a clinical trial.
Our Question:
Do patients have generate their own anti-V_Entry antibodies as a response to the vaccine. (note: at this point we are not addressing whether these antibodies will be protective or not- that's a separate question)
Our basic protocol:

Day 0: Take blood sample
       Vaccinate patients
Day 14 Take Blood Sample
       Booster Patients
Day 30 Take Blood Sample

To test the ability of the vaccine to generate an antibodies specific to V_Entry, we will assay serum from our cohort via ELISA.
Our Test:
(I'm ignoring controls and other details here to be clear)
Coat ELISA plates with V_Entry protein
Add aliquots of serum from each of out patients at each timepoint.
Wash
Add a secondary antibody conjugated with a detection enzyme
Wash
Add substrate for Enzyme
Allow Enzyme to develop the substrate (usually colorimetric)
Read on a plate reader
Some expected results:

Nothing happens - a control well works, but none of our patients
show antibody generation

Patients have pre-existing antibody that binds V_Entry (maybe these people were already exposed to Ebola?)
Patients have no pre-existing antibody, but they generate antibody in response to the vaccine (control patients not given
vaccine show no new antibody)

Why Secondary Antibody was Necessary:
We can't practically label every antibody made by the patient, but we can use a secondary antibody (perhaps Goat Anti-Human IgG) to detect any human IgG that has stuck to the V-Entry on our plate.
Was this a long run for a short slide?
I considered making a slide for each step of the protocol, but I started wondering if I'm avoiding something...


text:
Is it ok for Chili pepper plant's fruits to fall into its soil?
I wonder if Chili pepper's fruits which fall into the soil near the plant will harm it, since the peppers are so spicy for people.

The spiciness is because human tongues can interact with Capsaicin - an organic molecule that locks into receptors on our papillae and cause a heat/pain feeling. Not all animals have them, and I doubt the soil would be affected since the seeds - where the highest concentration exists - must be planted. However, I can't look up references right now. :)

As @MCM says, the capsaicin molecule isn't intrinsically damaging - its effect upon us is mediated through the TRPV1 (Transient Receptor Potential Vanilloid 1) receptor in the membranes of cells whose function is to sense noxious stimuli such as heat. The binding of capsaicin to this protein causes transmembrane movement of Ca2+ ions which depolarises the membrane, triggering an action potential - a signal to the brain. Heat has the same effect on the TRPV1 protein. In this way the presence of capsaicin mimics the effects of heat, causing a painful sensation.
Have a look at this SE.Biology question.

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text:
Where might I find a list of all recorded instincts by species?
Where might I find a list of all recorded instincts (possibly with all other attributes) by species?
Thanks,
Chenz

What instincts are you talking about?

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text:
How does a tiger have stripes?
A vague question, but let me try to explain. My friend explained to me that in females, some cells use one X chromosome, while all others use the other X chromosome. This can result in some differences of appearance of certain individuals. The Wikipedia page on X-inactivation shows an example. There is a picture there that shows a cat with fur of two colors, each showing in seemingly random groups. My friend had explained that when one cell "deactivates" its X chromosome, all of its descendants have the same deactivated X chromosome, so it makes sense that the similar colors appear in groups on the cat's coat.
But it seems tigers' coats are much more complicated than that. The pattern on a tiger's coat is not completely random. They make very discernible shapes. There are clear borders inside which only black fur grows, and outside of which only orange fur grows. How is this possible?
I'm not suggesting that the patters on tigers' fur is in any way related to X-inactivation, since I know that only applies to female mammals. But X-inactivation seems like a "natural" phenomenon, while the stripes on a tiger (or other animals with complex patters) seem a bit more bizarre. How do the cells on a tiger's body know which color to show and still follow the pattern?

Although not exactly what you ask, but you may want to have a look at this: http://biology.stackexchange.com/questions/3299/how-did-butterflies-evolve-to-have-eyes-on-their-wings/3357

It turns out that this was a question that was answered by Alan Turing in the 1950s.
Turing hypothesized there would be two morphogens, an inhibitor/ activator pair, each of which would produce a one of two phenotypes by activation or suppression of a trait.  He hypothesized that this would produce a pattern like stripes or other patterns (e.g. black and orange stripes).
This year just such inhibiting/activating pairs produce patterns like ridges in the top of the mouth of mice.
In a broad way, this seems like X-inactivation, where there is an X-inactivation center (XIC) that is inhibited or activated when the cell is created in mitosis.  XIC is still hypothetical and undiscovered, but it can create patterns and is non-random.
So I would say that this tiger stripes and X-inactivation may share Turing's mechanism, but the stripes, found in male and female tigers alike is not linked causally to X-inactivation.


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How is olfactory acuity rated/measured?
Acuity of one's sight is rated on the 20/20 scale. An online search appeared to indicate there is no comparable 'standard' to rate olfactory acuity.
How is acuity of the olfactory system rated?

One olfactory acuity rating method that has found acceptance in some studies (despite the commercial-sounding name) is based on "Sniffin' Sticks,"
"a test of nasal chemosensory performance that is based on penlike odor-dispensing devices. It is comprised of three tests of olfactory function: tests for odor threshold, discrimination and identification. Previous work has already established its test-retest reliability and validity in comparison to established measures of olfactory sensitivity. The results of this test are presented as a composite TDI score--i.e., the sum of results obtained for threshold, discrimination and identification measures."
In the paper from which this abstract portion was taken$^1$, subjects were assigned a score based on their thresholds, ability to discriminate, etc., and the findings were said to be internally replicable (consistent from one test to the next).
This is probably not the only rating available but it has been used on other studies and seems to be taken seriously by M.D.s and others who measure such things.
There is no absolute measure of olfactory acuity. People are classed as 'anosmic' if they do poorly enough on the test but that doesn't mean they have no sense of smell (although that might be the case). Likewise people who get a high TDI score are--by definition--people who got the "Sniffin Sticks" right. They might be poor at discriminating a good coffee from a bad one based on smell.
The test seems to do what it was intended to do: quantify relative olfactory acuity in a replicable way.
An earlier study is somewhat reserved. From an abstract: "It is concluded that ‘Sniffin’ Sticks’ may be suited for the routine clinical assessment of olfactory performance."
$^1$ Eur. Arch. Otorhinolaryngol. (2000) 257(4):205-11. Multicenter investigation of 1,036 subjects using a standardized method for the assessment of olfactory function combining tests of odor identification, odor discrimination, and olfactory thresholds. Kobal et al.


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Is warmth/temperature sensed linearly or on a different scale?
I understand that the atmospheric temperature is sensed relative to external body temperature. However, is the sensation of warmth registered linearly, or is it on a logarithmic scale, similar to sound that works on the Decibel scale? Or is it on another scale entirely?

The use of the Decibel scale is only a mathematical practicality, has nothing to do with how our brain perceives sound.

Also, related (although does not answer the question) http://biology.stackexchange.com/questions/371/how-is-temperature-sensed/372#372

Could you precise 'linearly'? In general, it is not a well-defined thing, when it comes to perception, see http://cogsci.stackexchange.com/questions/1751/what-stimulus-features-determine-the-psychophysical-power-law-exponent/1772#1772

A more general answer/comment is that technically almost nothing in biology is really linear.
In a linear relation, when one variable increases the other increases proportionally. In biological systems this typically cannot happen because of physical limits (such as the number of molecules), which tend to produce saturation at some level.
For example, when a substance is "sensed" by the receptors of a cell, sensing would become saturated as the receptors approach maximal capacity. In a similar manner, heat sensing will be limited by a maximal capacity and saturation of the nervous system. This is of course not specific to sensing but is a general characteristic of biological systems, because they are ultimately made of a finite number of components.
That said, sometimes a linear-like relation is observed at a specific range of values. For example, this is a mathematical characteristic of a class of functions called logistic functions. At ranges that are far from saturation, these functions have approximately linear behavior.
In the following example figure I marked (black box) the "linear-like" regime of a simple logistic function y=1/(1+100*exp(-x)):

The human sensation of warmth is not the measurement of static temperature.  Humans detect the rate at which heat is leaving (or entering) their body.  For instance, if you are sitting in your 0 degree car in the morning, your hand in the open air will feels warmer than your hand touching the steering wheel, despite them both being at 0 degrees.
The reason is that heat conduction from your hand to the steering wheel is much faster than convective heat transfer from the air.  So you feel "colder" touching the steering wheel, but it's really that you're losing heat faster.
Scholarpedia's article on temperature receptors:
http://www.scholarpedia.org/article/Thermal_touch#Temperature_receptors

...Cold receptors respond to decreases in skin temperature over a range
of 5-43 °C...
...In contrast, warm receptors signal that skin temperature has
increased...


text:
Is there a term to quantify how spread a character is on a phylogenetic tree?
Is there a term which can quantify how 'spread out' a particular character is on a tree? I want to distinguish between a character which is only restricted to a particular clade vs. a character that occurs all over the tree.
ETA: by 'all over' I meant it may be restricted to a few branches but those branches are spread out over the tree. It need not be ubiquitous. e.g. the character marked in blue on  compared with the case where these three branches are in a small clade.

Probably off topic here, but 'ubiquitous' or 'widespread' should work.

I think that in the general language of trees, 'clustering' might be the word...

I agree with Terdon's terminology in the comment ("ubiquitous" or "widespread").
You can use clade-specific or species-specific for a restricted character.
For the characters that appear in all species of a branch and in a quantitative way you can also provide the estimated age of the last common ancestor to the branch featuring that character. This tool might help you: http://www.timetree.org/

Isn't a character restricted to a clade synapomorphic for that clade? (at least within the groups being considered.)


text:
Can Taq polymerase be used instead of polymerase Vent exo (-)?
Instead of using  polymerase Vent  exo (-), can I go with the usual Taq polymerase?
Do the PCR conditions change (the temperature and master mix concentrations ) in the these two conditions? Do the primers (sequence and concentrations) change if we use vent exo instead of Taq polymerase and vice versa? If the primers are designed specifically for Vent exo (-) how can I modify the PCR conditions so that I can use the same primers (meant for vent exo) using Taq polymerase?

Can you describe what you need the PCR for, what your requirements on accuracy and other factors are?

SNP detection, using ARMS PCR

I haven't done ARMS PCR myself, so my answer is based on theory and there might be other practical factors I overlooked.
The characteristic feature of the Vent exo(-) polymerase is the lack of exonuclease activity compared to the regular Vent polymerase. ARMS uses the fact that a mismatch at the 3' position prevents primer extension. For this to work it is important to use a polymerase without exonuclease activity, as such a polymerase could "repair" the mismatch and the whole method would not work. Taq polymerase also doesn't have any exonuclease activity, so in theory you should be able to use it for this experiment.
The primers don't have to be changed for different polymerases, the polymerase buffer though is different and I wouldn't recommend using the wrong one.


text:
How many people are required to maintain genetic diversity?
Imagine humans were to colonize a distant planet and it was a single one-way trip. How many people would they need to bring?
Obviously 2 is the minimum, but that would result in a lot of inbreeding.
So what number is the minimum number of people you can have in an isolated community and still maintain a healthy diversity?

Without doing any digging, my understanding is that first cousins can really interbreed without too much risk.  So a first estimate that 2 completely unrelated mating pairs from distant parts of the human genetic tree might make a minimal  gene pool candidate.  I can see an argument being made for 8 too.

It depends on how you select the people, if they are carefully selected for genetic diversity you might be able to get away with a hundred, but  you have problems if even a few people die, which is not unlikely in a completely new environment. So even with careful selection and breeding controls you still want a few hundred. the more other things like skills matter the more people you need becasue you can't just select for genetics which brings you closer to 500 individuals. If people are selected more or less at random (genetically) you want more than  a thousand.

The big problem is NO  new genetic material is going to be introduced (aside from mutation), and the population is going to be expanding, dying, and need to continue into perpetuity.  So you need a a lot of initial diversity. This isn't a  lab study where you only need to maintain for a few generations.

Actually it is a very important question for laboratory animals (and, I imagine, endangered species) and was calculated to be 25 couples.
With any number of animals (including humans), there is always some inbreeding happening, but you can reduce it with the number of breeding pairs and careful pairing. When you get to 25 pairs (50 animals) and have complete control over pairing, you can sustain the genetic diversity practically infinitely (especially if you take into account spontaneous mutations).
Of course, such control over who can have children with who (plus whether one is at all allowed to procreate and what will be the sex of their children!) would be questionable morally, so in case of populating a distant planet, we would need a larger group, to provide for sexual preferences, fertility problems etc.
Some information on laboratory outbred stocks.

nice answer - it makes me realize though that there are problems keeping some dog breeds viable - they tend to accumulate too many diseases (link below).  Yet there must be thousands of animals in most breeds that are in trouble.  Is this because controlled breeding is used differently (emphasizing breeding traits vs diversity), because there was few original dogs in the pool, or why?  http://www.nytimes.com/2011/11/27/magazine/can-the-bulldog-be-saved.html?pagewanted=all&_r=0

I am no expert on dogs, but did learn a bit about in- and outreeding. Each dog breed is either open or closed. In a closed breed, only offspring of animals already belonging to this race belong to the race. In an open breed any animal that looks similar enough (or has other important traits, characteristic for the breed) can be a parent of a "breed" litter. Under certain circumstances (e.g. too few animals in the breed, too bad overall health of the breed) a closed breed can be opened and after the problem is solved, closed again.

How did people arrive at this number? The linked article doesn't seem to explain it.

It's just mathematics. If you pick two outbred mice/rats etc. and mate them, the offspring is about 0,5-1% more inbred than their parents (meaning both their copies of any gene are a tiny bit more likely to be inherited from one ancestor mouse). If you have enough animals, this effect is smaller than the effect of other phenomena, such as genetic drift (compare with the assumptions behind Hardy-Weinberg equilibrium). I don't know the exact equasions behind those numbers, I just know, that this was calculated and such-and-such numbers are used.

I don't think it's that bad to control who has children with who. It's not like you're controlling who is in love with who or who is having sex with who. You're just making sure people use protection and get inseminated with the proper sperm when they're ready for children.

Have you considered women's point of view? That in this scenario somebody decides to use a woman's body to generate some number of children and you cannot decline, you are literally forced into pregnancy? Pregnancy and childbirth, which, even with modern medical advancements, are an important cause of death for women?
I guess the people who board such a ship can make this kind of a decision, but their children would not be given any choice with regard to bearing a second generation.

The sentence When you get to 25 pairs [..], you can sustain the genetic diversity practically infinitely is wrong IMO. At equilibrium, genetic diversity is a simple function of the effective population size. There is no minimum size to sustain the genetic diversity practically infinitely. There is some genetic diversity with only 2 people and there is more genetic diversity with 50 people and even more with 100k people and the is no such as THE genetic diversity

I'm not an expert, but after reading more about it I would say between 500 - 1500 couples without trying to control the pairing.
I don't know where Dan Horvat took these assertion:

To maintain healthy genetic diversity and establish enough different
alleles to allow for sustainability of the species. I don't remember
the exact number but I think for humans it was something between 1000
or 10000, and if you get below that number the species will likely go
extinct by natural causes.

but it seems to be supported by the evidence of past bottlenecks in human population, like the Toba Cathastrofe Theory. The human population is supposed to had a maximum of 3,000–10,000 surviving individuals. I am very optimistic and take the minimum: 1500 couples. It left to match that amount with Dan's source.
The exact answer would come by the designer of the life and DNA. ;-) That info seems to have been leaked by the creator's son in a conference. Thomas has taken note from his words:

I shall choose you, one out of a thousand, and two out of ten
thousand, and they shall stand as a single one.

It seems to me that it is talking about genetic diversity, and the minimal proportions are those: 1/1000. That's why I take 500 couples as minimun.
By the way, in the previuos versicle it seems to says that that selection would be in the moment when the human race has finally ended evolving to the intended social and morphological status (very rare indeed):

When you make the two one, and when you make the inside like the
outside and the outside like the inside, and the above like the below,
and when you make the male and the female one and the same, so that
the male not be male nor the female female; and when you fashion eyes
in the place of an eye, and a hand in place of a hand, and a foot in
place of a foot, and a likeness in place of a likeness; then will you
enter the kingdom.

Going back to science, it seems that not to much effort should be made to control the pairing, because we seem to have a subconcient attraction for those individuals of the other sex that present better histocompatibility with us. In the case of humans given by odor and appeareance (mostly simetry).
Also the genetic diversity is supposed to be reached faster, if the environment is more aggresive. Normally a big mutation and adaptation happen after hostile and persistent environment over near 40 generations, something observed with the Peppered moth evolution
So I suppose that if you use well cared laboratory animals, the number can be 25 couples. But if you use a natural hostile enviroment the genetic diversity could be reached sooner.
It might be that if you build a nice human space station in another planet, maybe you need 25 couples, but if you let them nude with no technology and fig leaves you need fewer couples in order the species to survive more adapted (Although you might got many failed attempts)
Another point to consider, is how valuable are those animals for genetic studies?, how much is the study affected by the captivy of their population?, resembles their growing places the natural environment?, how hostile are these environment? resembles this environment the natural population dynamics ? how many generations ago their ancestors had a natural environment ?
Laboratory animals might have less genetic diversity and might need more couples.

The distinction between this being the correct answer and the one chosen, has to do with the level of genetic preselection. I agree that a minimum of 1000 "randomly chosen" people would be required, as one must not forget the impacts of homosexuality and varying levels of "fidelity" in mating pairs.

I guess than homosexuality and fidelity might have also to do with epigenetics and the needed dynamics of the population.
In some fishes like: "Lythrypnus dalli" , even the genre of the individuals changes at a morphological level according to the necessities of the population. (https://www.sciencedirect.com/science/article/pii/S002209810400680X)

Also it might be that less individuals and good conditions  for expanding the population generates less "fidelity".

At the contrary, an excess of genetic diversity in a population (if such concept exists) might generate more fidelity.

I think the issue of epigenetics throws this answer into debate once again. This reminds me of my biggest issue with the book The Transhumanist Wager, which was centered around a very Libertarian tenant of "worth".
Without knowledge of the way in which every aspect of human genetics (including epigenetics) works, how can we possibly establish the "worth" of a given set of base allele, and thus determine minimum viable population? If such a bottleneck were forced (through disaster or "choice") would such a resultant population still be considered "human" by today's standards?
I would say that Humanity must still be defined by more than the sum of our current knowledge of genetics.
I believe these questions are something that are very often missing from the debate around The Singularity [establishing an artificial intelligence beyond the intelligence of humanity]. Most argue that such an event would be the end of humanity, but I disagree; as any intelligence created by humanity would not be so stupid as to destroy the diversity of intelligence that essentially established its baseline. In this line of thinking, personally I believe it would be more along the lines of the ideas presented in the movie Her, in which such Intelligence(s) would establish a way to remove themselves from direct human control, but ultimately observe/compare/contrast humanity as "wild stock" useful for error-correction, and a seperate line of modeling.

Inbreeding isn't negative at all, so one couple would suffice for colonization.
Inbreeding fixes recessive traits and the ones displaying unwanted traits can be culled. Actually, inbreeding is one of the most potent weapons of evolution, it speeds things up greatly. We went through a major bottleneck event ourselves and lived to tell the tale.
The exact number of individuals needed for a healthy species that will survive X number of generations depends on the species though. To maintain healthy genetic diversity and establish enough different alleles to allow for sustainability of the species. I don't remember the exact number but I think for humans it was something between 1000 or 10000, and if you get below that number the species will likely go extinct by natural causes.
Of course, everything is completely different when you have full control over who mates with who. But still, in the above example of 1 couple, they can successfully start a seemingly healthy population, but due to low genetic diversity they - as a species - won't be able to respond to, say, increased radiation, changes in atmosphere, a virus, bacteria, shortage of food, etc. That's why 1 couple is basically enough, but to ensure longetivity of the species 25 couples is far from enough.

And if the undesirable trait is recessive, how do you cull it?  Queen Victoria had the allele for hemophila, and after a few generations, it was in all the European royal houses, with multiple people suffering from the disease.

You cull a trait by simply not procreating the specimens who have that trait. But, first of all, some genetic diseases are not noticeable before old age so you can't know about them unless you study the genome, and second of all it isn't ethical (or desirable, but that's a different story) to cull humans. Especially if it's the Queen. In case of haemophilia, a female can be the carrier but rarely has the disease. It just shows up with certain males down the blood line and in that day and age they didn't know why.

Actually, that's a much more complicated case. The short answer is: you can't be completely certain you've culled the recessive allele. You can diminish it's frequency and this has been done in a neat way in the Mediterranean with thalassaemias (a group of diseases related to sickle cell anemia) - young couples with non-negligible risk were tested and if both carried the gene, they were advised against having children or given access to abortion if the fetus turned to be sick. Given stricter control, reduction could be achieved fasted, but when the allele becomes rare, it gets more difficult.

Dan Horvat's scenario is only theoretically feasible. People have, on average, 15 damaged genes that may lead to a deadly disease. The first couple (and next generations, too) would have to produce lots of children in order to give them a good chance of findinf couples who can have healthy children. Much more likely this scenario would result in a population with uncommon genetic diseases being common, like in Finland (which artificially created a series of bottlenecks from the 17th century, a fascinating story), read more here: http://www.cs.sjsu.edu/~khuri/Aalto_2010/Norio_2003.pdf

Hey, Dan. Where did you got these numbers from: "1000 or 10000" ?

The reason similarity is bad is the more genetically similar the population the more likely a single disease will wipe them out. That is before you get to things like recessive traits.

You only need a single female. The space ship could carry a database of genetic material in the form of frozen sperm and eggs. The first female would impregnate herself to breed and raise as many daughters as she can, using as much genetic variety as possible. The daughters would do the same once they can.

Welcome to Biology.se. You should always add references for your claims.

I didn't mean to convey the scientific insight that the OP was presumable looking for; I was hoping that would be clear. This answer points out a logically valid alternative interpretation of the question.

In this case yours is probably more suitable as a comment

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text:
Can paper/plastic currency serve as a medium for pathogens?
http://www.nytimes.com/2009/12/15/health/15real.html seems to indicate for a surface, to serve as a medium, the following properties are relevant

animation
humidity
temperature

The article however does not elaborate on the properties a surface must possess to serve as a medium - albeit i would figure it may vary from one virus/bacterium to another.
The same article also states
... when objects in a hotel room — light switches, telephones — were contaminated
with a  cold virus, 60 percent of healthy volunteers picked up the virus when they
touched one of the objects an hour later. Eighteen hours later, the transmission rate
was cut in half.

When currency changes hands we rarely ever know whether it may , within a reasonable timespan, have passed through an agent/carrier.
Sir Dumpty loves to sneak off with a currency note to get me to chase him. He is protected; another member of his species may not be so protected. For that matter a person infected with, say, the common cold virus may have passed a note/coin/card to the vendor at the store within a minute of sneezing/coughing into his/her hand. What if the same person , instead, suffered from TB?
So ... can currency serve as a medium for transmission of pathogens?

It's going to vary wildly, for example Hepatitis B can survive 7 days outside of a host.  Furthermore, some bacteria such as Bacillus antracis can produce endospores and survive for years.

its always a good idea to wash your hands when you handle money.

TB is perhaps a poor example as it is actually quite difficult to contract without spending extended time with someone actively infected.

Who the heck is Sir Dumpty?

@arboviral: That's my canine son

@Everyone Ah, that makes sense.

@Everyone While you're around - is there anything else you wanted to see in the answers?

TB is an extremely poor example, because as has been mentioned, it usually requires prolonged contact.
But lets go with something with a low required infectious dose, that's friendly to surface contamination, and persists in the environment: Norovirus.
Can norovirus serve as a medium for pathogens? Absolutely. To be blunt, almost anything will serve as a medium for the right pathogen with some level of efficacy. This is a presentation from the New York Federal Reserve on what contaminates money, but given the outlandish things that can be contaminated with infectious material, there's no reason to suspect money isn't among them.
Wash your hands.

The same may be said for any of the pathogenic E. coli which can persist on surfaces (including plastic) for a day or two.

Yes. Salmonella, Staphylococcus aureus and Escherichia coli have all been isolated from paper money. There is a review article here on money (paper money and coins) as a source of infection but it's unfortunately behind a paywall.
Exactly how important money is as a source of infection and for which pathogens is more complex. As you note in your question, material will be important too, making answers to this question also relevant to the subject (although it hasn't been answered yet).


text:
Evolution in 37 years, is it possible?
I am confused, can evolution ( speciation ) really occur in such a short time ?

In 1971, biologists moved five adult pairs of Italian wall lizards from their home island of Pod Kopiste, in the South Adriatic Sea, to the neighboring island of Pod Mrcaru. Now, an international team of researchers has shown that introducing these small, green-backed lizards, Podarcis sicula, to a new environment caused them to undergo rapid and large-scale evolutionary changes."

Here is a short video featuring the scientist.
Two related articles:

http://www.sciencedaily.com/releases/2008/04/080417112433.htm
http://news.nationalgeographic.com/news/2008/04/080421-lizard-evolution.html

Edit: I asked a similar question previously about two people having 44 chromosomes and their possibility of creating a new species. You might like to read/answer that as well:
Can two humans with 44 chromosomes produce viable offspring?

Evolution just depends on the amount of selective pressure.  The classic selection for antibiotic resistance is just a single generation. It may seem artificial, but it is adaptation in a single generation.  Also wanted to add this link: yeast become multicellular in a 60 generations. http://www.scientificamerican.com/article.cfm?id=test-tube-yeast-evolve

I am confused, can evolution ( speciation ) really occur in such a short time?

Well, Evolution and Speciation are not the same. Evolution is the adaptation of an existing species to an environment over generations. Speciation is the development of a new species, and the definition of "species" can vary depending on who you talk to - but a very commonly accepted one is that two individuals cannot produce fertile offspring.
However, the answer is still Yes. Evolution can occur in as little as two generations because that's all the time it takes for a change in the DNA to be exhibited in the newest generation. For instance, Lactase Persistence - which allows the bearers to ingest dairy products without digestive stress into adulthood - has evolved at least twice in humans in separate groups. Both are the result of either one or two point mutations (single changes in a Nucleotide within the DNA). The result is that at one point in time for each appearance of lactase persistence, a child was born that could drink milk into adulthood while their parents and cousins could not.
That is evolution; the child was better adapted to the resources available, and because lactase persistence either...

Provided a significant advantage over their kin in the environment (which is likely, as being able to digest milk in an agrarian society opens up a new source of energy)...

or

Didn't hinder the child's ability to grow and produce fertile offspring of their own...

...it has persisted in the populations where it initially evolved.
Speciation is a little trickier, but that's because there isn't a known qualitative way to differentiate species at the genetic level quite yet. It could be a few key gene changes, it could be a whole genome difference of 10%, or a million other factors. Practically speaking, though, Speciation is simply the result of accumulated genome changes that at some point prevent the members of one group from producing fertile offspring with their ancestral group.
Because we simply don't know how much of or where the genome has to change, it's certainly possible that speciation could occur in the same time period as it takes to evolve: Two generations.
Since I'm doubting the wall lizards have a generational time of >37 years (don't mistake it for lifespan, humans can reproduce in our teens - even if we live into our 80's), it's definitely possible that the wall lizards could evolve (and potentially speciate) in such a short amount of time.
With organisms that have a very, very short generational time - like E. coli or other bacteria - you can observe the Evolution of populations in days or hours.

Clarified with your correction.

I want to underline 1 fact about speciation, although you don't object to this. Speciation doesn't necessarily mean the lack of ability to produce healthy offsprings. For instance, Lions and Tigers ( Two different species) can reproduce healthy offsprings (Liger and Tiglons), but they don't mate in the nature. So speciation also requires the lack of inclination to mating with the other.

@MCM I have updated the question. You might like to answer the referenced question as well, please do :)

@Comptrol: the problem lies in the hazy definition of species. Often you would hear that two different species cannot produce fertile offspring, for instance.

@Comptrol - Regarding "ligers" and other such combinations, usually the "Do not reproduce and produce fertile offspring" also runs with the caveat "in the wild" when you're talking about more 'official' definitions of species in Biology. Since Tigers and Lions do not reproduce in the wild the definition fits for them, but it doesn't work for other creatures. Hope that cleared it up a bit.

@MCM - would you be against editing "Evolution is the adaptation of an existing species to an environment over generations." to "Evolution is a change in the characteristics of a population over generations." The existing sentence describes the response to selection, but evolution occurs by drift, mutation, and migration

Evolution can occur in just one full generation
Strong selection will rapidly reduce the gene frequencies of genes which cause negatively selected phenotypes. This reduces the likelihood of unfavourable genotypes occurring in the next generation.
(I regard generation here as the complete cycle of one individual being born to the point at which they successfully give birth/sire young).
Population genetics explanation:
Imagine a population in which LOC1 is a locus affecting a phenotypic marker allowing perfect identification of genotype at that locus. There are two alleles at LOC1, A and a. This gives rise to three different genotypes, AA, Aa and aa  which occur in the population in equal proportions. Those individuals with AA exhibit a certain trait, whilst Aa and aa individuals do not. If only the AA genotypes are allowed to mate then the following generation will only contain AA genotypes at LOC1 (assuming no mutation).
For more population genetics read Principles of Population Genetics and then Introduction to Quantitative Genetics.
Genetic drift caused by using 5 Pairs
The new population was started with just 5 pairs of individuals. This means there is huge potential for fixation of alleles via drift with in the very first generation. I ran a (basic) genetic drift simulation in R just now. Out of 5000 replicates 4709 went to fixation (Single locus, two alleles, using 30 generations of 10 individuals).
Environmental change can cause hidden genetic variation to be exhibited
Molecular regulators which affect the expression of traits can respond differently depending on environmental influences. This point is summarized nicely by the opening lines of this paper- thanks to @leonardo for this point.

Hsp90 is a molecular chaperone for many signal transducers and may
  influence evolution by releasing previously silent genetic variation
  in response to environmental change. In fungi separated by 800
  million years of evolution, Hsp90 potentiated the evolution of drug
  resistance in a different way, by enabling new mutations to have
  immediate phenotypic consequences.

Evolution and speciation are different things
These are just the simple wikipedia definitions, for better ones then consult the literature:

Evolution is the change in the inherited characteristics of biological
  populations over successive generations.

For a good thorough introductory text on evolution I recommend Evolution by Mark Ridley (not to be confused with Matt Ridley - popular evolution science writer).

Speciation is the evolutionary process by which new biological species arise.

Speciation, thanks to a long fought debate over species concepts, is also an ambiguous process. What some species concepts would define as two distinct species, another would call one species, and another may call them 10 species! Seemingly everyone who specializes in the study of speciation would have there own twist on a species concept so don't expect that argument to resolve any time soon! It's not advanced much since Dobzhansky wrote this.

The species concept is one of the oldest and most fundamental in
  biology. And yet it is almost universally conceded that no
  satisfactory definition of what constitutes a species has ever been
  proposed.

When does evolution occur? and when is change not evolution in such a short time?
I've put this bit in because what I find is a strange, but common, question people ask is

"species X has changed/adapted to novel selection very rapidly, has
  evolution really occurred?"

The way people ask this makes it sound like they want a certain amount of evolution to occur before we can say something has evolved. To me saying evolution has occurred means that some change has occurred, via any of the mechanisms of evolution, which results in one subset of individuals being different from another it is compared to (spatially or temporally separated). You could ask if such strong evolution can really occur over a short time period, but the answer is obvious - yes it can. If it has occurred then why do you think it is exceptional? what is your alternative explanation for the differences seen?

You can also look to the work on heat-shock protein 90 (Hsp90) and specifically the scientist Susan Lindquist for human evolution within one's lifetime.

also; the fact they only introduced five pairs means there could have been a lot of change in the first generation via genetic drift - I'll edit that, and some examples of rapid evolution, in to the answer soon - thanks @leonardo


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Do plant-plant interactions inhibit growth?
Plants produce lots of compounds that inhibit (kill or irritate) microorganisms and insects.  They have defenses against plant viruses and infections.
What kinds of compounds or hormones to plants use to regulate the growth of other nearby plants?  I have hear of ethylene, but I would like to hear about more specific compounds that might be known that work against specific species or kinds of plants?

The phenomenon you are asking about is allelopathy.
Remarkably, it has its own journal - Allelopathy Journal (ISSN:
0971-4693) published since 2009 and currently at volume 30, issue 1.
Here are the titles of the papers from the most recent issue:

In-vitro assessment of allelopathic effects of wheat on potato.
Allelopathic effects of sunflower on seed germination and seedling growth of Trianthema portulacastrum.
Effects of simulated acid rain on the allelopathic potential of invasive weed Wedelia trilobata.
Allelopathic effects of Brachiaria ruziziensis and aconitic acid on Ipomoea triloba weed.
Effects of Butia capitata pyrenes extracts on the germination of lettuce seeds.
Effects of root exudates from crop plants on the growth of Fusarium oxysporum f.sp. niveum.

So, if you have specific questions, this might be the place to look.

thanks - this helps quite a bit - i know nothing about plants!


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Possibility of orthogonal view for a creature?
Just a pure curiosity: Does there exist a creature with an orthogonal view to the world instead of perspective? What would be an optical explanation for possibility/impossibility?

I guess this depends more on how the brain processes the signal rather than on how the eyes detect it. So technically, it might be possible but I'm not sure if there is a way to know. You can't go around asking animals how their brains work :)

@OndřejČernotík Nice points. Still eager to know more :)

Many creatures have eyes on the sides of their head where they cannot have both eyes simultaneously look at the same target. For example whales. Chameleons are well known for having independently moving eyes (though they can align them for binocular vision)

Since all the significant processing of vision occurs in the brain's occipital lobes there is no problem with optics.

spiders usually have two rows of 4 eyes each, so they are not really vertical, but more hemispherical at least.  They eyes don't see very well...  in the case of jumping spiders they seem to lose the top row...

The answer depends on the distance between eyes, and width of the objects you are viewing.
The view of a separate object is close to the orthogonal view when the width of the object is equal to the distance between your eyes.
Hence the creature that has variable distance between eyes, and has large maximum distance between eyes, has most possibilities to view objects in orthogonal view. Snail comes to mind when I try to think about animal with variable distance between eyes, but its maximum distance between eyes is not that large.
When object is narrower than distance between eyes, you see it in "anti-panoramic view". You will see both left and right side of the object, which is impossible both in orthogonal view and in panoramic view.
Speaking about whole 180 degrees wide visble scene (wider for some animals), the answer is No. You cannot view the whole scene without perspective view, unless you have large number of "eyes" (sensors) that are spread over a large plane. There is no such animal, but you can artificially construct such "perceptor plane" using large number of photocameras.
When looking at the objects of width equal to distance between eyes, if your brain can direct eyes such that their viewing axes are parallel, and could integrated two pictures, then it would view perfectly orthogonal view. This is not what our brain normally does, though. But even with non-parallel view axes of eyes, what we eventually see when brain integrates different pictures the result is not par from orthogonal projection.


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Is there a normal human melatonin concentration to light level curve?
I'm looking for a graph or a curve that would show the typical concentration of melatonin in blood or saliva for humans over 24 hours. It would be good to know the photoperiod for the same human as well.
I know that melatonin release is inhibited by blue light, perceived through the retina, with melanopsin being the photopigment that signals suprachiasmic nucleus to suppress melatonin release. This is why it would be great to see melatonin data alongside light exposure data.
Thank you for any hints on where I can find such information!

Found a few samples here: http://ars.els-cdn.com/content/image/1-s2.0-S0024320503008142-gr2.gif this shows the nocturnal melatonin peak, which is apparently very important for well being


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How do infectious bacteria determine when their numbers are high enough to attack a host?
When you get sick, you generally don't contract enough bacteria at once for them to succeed in battling your immune system, right?  Their numbers must gradually increase in the host's body before they know that they can attack.  How does that work?

I think the current answer to this for bacterial infections is quorum sensing.  Quorum sensing is a signalling pathway in bacteria which senses a molecule that the bacteria themselves secrete.  When the concentration of the quorum signal reaches a certain level, the bacteria interpret this as their population density reaching some threshhold.
Bacteria are always around - even infectious Staph, as described in the other answer, the bacteria are always being cleared out by the immune system, but when they find the right place where they can get critical mass, they dig in, form a biofilm and secrete toxins, which can help them divide more successfully.
This is a description of the process from a paper on Staph infection, a common bacterial infection in humans.

S. epidermidis is considered part of the of the normal human microbial flora, while S. aureus is usually regarded as a transient member. Colonization by either species usually does not lead to adverse events. However, when these organisms or their extracellular products are allowed to breach the epithelial layer, serious disease can result (1). S. aureus has many cell surface virulence factors (such as protein A and clumping factor) and secreted exotoxins and enzymes that allow strains to cause a myriad of infections. These diseases range from relatively benign furuncles and subcutaneous abscesses to scalded skin syndrome, sepsis, necrotizing pneumonia, and toxic shock syndrome (TSS). While no single cell surface virulence factor has been shown to be uniquely required for mucous membrane attachment, once colonization occurs, numerous secreted exotoxins, including the pyrogenic toxin superantigens and exfoliative toxins, definitively cause serious human disease. Other secreted exotoxins, such as the four hemolysins (α, β, δ, and γ) and Panton-Valentine leukocidin have also been suggested to contribute to significant illnesses. S. epidermidis does not possess the array of extracellular toxins that S. aureus does, and its primary virulence factor is considered to be its ability to form biofilms.
To improve their ability to cause this variety of human disease and to occupy numerous niches within the host, staphylococci have developed quorum-sensing systems that enable cell-to-cell communication and regulation of numerous colonization and virulence factors.

Viruses are typically simpler - as @MattDMo describes. They seem to rely on finding an environment where they can infect more cells at such a rate greater than the immune system can clear them out.  For influenza, this is more of a 'shock and awe' offense where they infect and multiply quickly, trying to outpace the immune system.  Another virus like HIV will actually multiply so slowly that the immune system can't find the host cells, allowing HIV to slowly spread over the host cell population.
Here's a bonus topic... When they were looking a cholera in the 1990s they found that V cholerae bacteria actually take up phage with toxins in them that convert benign bacteria to virulent ones (that cause dysenteric cholera).  They do this by conveying both the pili that attach to human cells and the toxin that causes the violent G.I. reaction of dysentery.  I think this is not unusual for bacterial diseases.  (the reference is Science 272, 1910-14 BTW).
This has lead to a suspicion that bacteria might be even adapting to infectious phenotypes through genomic changes.  This study had sequenced the genome of C difficile from 486 patients and found that relatively few of them really were capable of patient to patient infection:

The results of the study indicated that, although transmission between patients is likely to occur, it actually happens at relatively low frequency. In particular, concerns that healthcare teams were spreading infection between different hospitals seem to be misplaced. One exception to this general finding is that there were a large number of cases of infection from one particular strain that does appear to have been due to patient-to-patient transmission, emphasising the epidemic nature of this lineage. Notably, this strain has declined in UK hospitals in the last five years.

Great!  Thanks a lot -- this is what I was looking for.  Here is a very interesting TED video about the subject matter: http://www.ted.com/talks/bonnie_bassler_on_how_bacteria_communicate.html

@Hypoxide this is a great talk - highly recommend it too.   There is another topic of interest regarding bacteria - they modify themselves to become virulent.  I've added a note to the bottom of the entry above...

Infectious agents like bacteria, viruses, fungi, etc., don't know when to "attack" or produce pathogenic substances, they just do it under their preferred conditions, and your body's immune system either succeeds in fighting them off immediately, or it doesn't and you get sick. Your body is constantly confronting and clearing potentially dangerous microorganisms without your ever being aware of it. Every breath of air, mouthful of food, or contact with your mucus membranes is a possible infection, if not for your innate immune system.
However, sometimes pathogens get past the first line of defense, or are otherwise able to evade it, and in the time it takes for the adaptive immune system to engage they are building up their numbers and gradually getting to the point where you realize that you are sick or otherwise infected.
Interestingly, many of the symptoms of sickness you often feel - being tired, feeling sore, having a fever or localized redness/inflammation - are actually caused by some of the effector chemicals or cytokines released by your own immune system, and not by the infective agents themselves.
For example, lipopolysaccharide or LPS is a major component of the cell wall of Gram-negative bacteria, including such pathogenic species as E. coli (food poisoning, urinary tract infections), Neisseria species (bacterial meningitis, gonorrhea), H. pylori (stomach ulcers), and Salmonella species (food poisoning, typhoid fever). LPS on its own does not cause fever or inflammation, for example, but when bound by certain immune cells (B-cells and macrophages, mostly) it rapidly and overwhelmingly promotes the generation and release of pro-inflammatory cytokines like TNFα and IL-1β. These proteins then act on target tissues to allow the inflammatory response - swelling, pain, increased temperature, redness, etc. - and recruit immune cells to fight whatever invaders must be there.

I would have thought this was the universal answer, but shigeta gives some fascinating examples of bacteria that do use environmental information to "choose" a stealthy vs. aggressive strategy. I would imagine your answer is still applicable in most cases.


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Questions regarding ELISA
I have recently peformed an ELISA (Enzyme-linked immunosorbent assay), but I still have some questions, let me first outline what I did:

We had a number (20) of tubes containing fake 'bodily fluids' , namely saliva. One of these tubes contained the Epstein-Barr virus, which on its turn causes Pfeiffer's disease, aka the 'kissing disease' (so we basically conducted an experiment to see how fast the virus would spread within a class if everybody started kissing each other, if you don't mind the crudity).
Everybody mixed their saliva with the saliva of 3 other people, so at the end everybody had a tube with the saliva of 4 different people in it.
Since we worked in pairs of 2, every duo got a microtiter plate with 12 wells in it: 3 wells for a positive control, 3 wells for a negative control, 3 wells for the fluids of 1 of the duo and 3 wells for the fluids of the other one. You pippete in (is that correct?) the fluids accordingly.
After a while you rinse and clean the wells with wash buffer.
Then you pippete in the primary antibody in each well.
After a while you rinse and clean the wells with wash buffer.
Following this you pippete in the secondary antibody (conjugated with the enzyme HRP).
After a while you rinse and clean the wells with wash buffer.
Finally, you add the enzyme substrate (TMB) to each well. This causes a blue color if when in contact with HRP. The positive controls must come out blue, the negative must come out colorless, and the other wells can go either way, depending if you have the virus.

I hope this is not to crudely explained, again. These are my questions concerning the experiment:

What do the components of the acronym 'ELISA' actually stand for? Does immunosorbent refer to the binding of the antigens to the wells? My English isn't too good, and these acronyms and abbreviations often seem foreign to me (nevermind that they are foreign since I'm not English, you get the point I hope).
When you pippete in the saliva in the wells, what actually sticks to the wells? All of the antigens in your saliva? Because it's hard to believe that they make special microtiter plates for every single antigen seperately. I assume it is only the antigens, since the primary antibodies attach to the antigens only, so there is no need for the microtiter plate itself to bind to antibodies.
How would we get the primary and secondary antibody? This is my assumption: The primary antibody we get is by injecting some antigens of the Epstein-Barr Virus into a human and then taking a serum. The secondary antibody could be gotten by injecting a random human primary antibody into ANY animal, irrelevant which anyimal, and then taking a serum. After that you conjugate an enzyme to the secondary antibody. Is this correct?

ELISA is Enzyme-Linked ImmunoSorbent Assay (capitalisation to point out source of acronym).
You can read about the various ways to do an ELISA here.
In your case this was probably an indirect ELISA. All ELISA techniques make use of the fact that proteins stick to plastic. In your case the protein components of the saliva, including the virus (the viral coat is proteinaceous) will stick to the wells. After rinsing out the sample the wells are treated with another protein (usually bovine serum albumin (BSA)) to completely block all available protein binding sites. At this stage these wells will no longer bind protein non-specifically, but will bind anti-EBV Ig because of the presence of the EBV particles bound to the plastic. This bound anti-EBV can then be detected with a secondary antibody. The protein complexes will build as follows:
plastic/EBV/rabbit anti-EBV/goat anti-rabbit IgG-HRP conjugate
It would also be possible to do this experiment as a sandwich ELISA. In this format the wells would have been pretreated with anti-EBV serum (or purified anti-EBV IgG) then blocked with BSA. At this stage these wells will no longer bind protein non-specifically, but will bind EBV because of the presence of the EBV-specific antibody. Once samples have been incubated in these wells (so that any EBV can bind to the antibody coating the wells) another antibody (raised in a different animal) is added, and this will bind to the EBV that has been captured by the original antibody that coats the wells. This latter antibody is then detected with a conjugate. The protein complexes will build as follows:
plastic/mouse anti-EBV/EBV/rabbit anti-EBV/goat anti-rabbit IgG-HRP conjugate
Your description of how to get the antibodies is basically correct, except that the primary antibody will probably have been raised in rabbits or mice, and certainly not in humans.
Added later: I didn't read the first question carefully enough. An ELISA is an assay because it measures something. It is based on a binding reaction mediated by an antibody-antigen interaction (immunosorbent). It is enzyme-linked because the secondary antibody is present as an antibody-enzyme conjugate. It is the amount of this conjugate that remains bound at the final step which is what is measured - the assay is set up so that the amount of this enzyme is a measure of the amount of the original molecule that is being assayed.

So, if I understand correctly, the primary antibody of mice and rabbits will also respond the same way as human antibodies to the Epstein-Barr virus?

Yes, any animal will generate an antibody to any antigen, as long as it isn't recognised as "self". So for example you could not raise an anti-rabbit-IgG in a rabbit. The coat protein of EBV is just another antigen as far as a mammalian immune system is concerned - if it is foreign, there will be an immune response.


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Are humans hardwired to continue gathering resources after the costs outweigh the benefits?
An animal will stop foraging in a berry bush if the perceived cost of searching for berries remaining is greater than the cost of finding another bush which isn't as picked over. People do the same thing on websites. We'll stay on a website searching for our information berry if we feel it costs less than jumping to another website bush.
If we had significant resources such that the cost of predatory/foraging behavior out-weighed the energy benefit from gaining more resources, would we stop? There seems to be a biological and cultural drive to keep getting more stuff. As people, could we ever reach a point where we're satisfied? The logic says yes, but common sense says we're hardwired to feel compelled to never stop gathering resources.

I really think this is so.  This has been studied by behavioral economists quite a lot - Daniel Arielly's book "Predictably Irrational" and the work of Daniel Kahneman might be a good direction to browse if you feel that interested in it.

Good edit, @DQdlM. I changed the word consuming to gather because it seems we'll never stop consuming, but would we stop hunting/foraging if we knew the cost was more than the benefit? I was the one who originally used the word "consuming" in my post. My fault. Thanks for the edit. :)

It's called "addiction", or "obsessive-compulsive behaviour". Unfortunately not every behaviour is explained by rational calculation.

There are cases where such behaviors are clearly hardwired or due to the way our brain learns.

The answer to your question is very sensitive to the time frame you are interested in.  Assuming the costs and benefits you describe are referring to fitness (i.e., survival and reproduction), then the situation you are describing is one in which a particular behavior has lowered fitness (i.e., costs outweigh benefits).
There are several possible outcomes in this case.

Evolution. If the behavior is not plastic (i.e., it cannot change in a single individual), the there would be selection pressure against those individuals that exhibit the behavior.  If the behavior is heritable then evolution would cause a reduction in the frequency of the behavior over time.
Lowered Fitness. If you are not interested in evolutionary time scales but the behavior is not plastic, then the outcome would be no change in behavior but a reduction in the survival and reproduction success of individuals with the behavior.
Change in Behavior. If the behavior is plastic (i.e., it can be changed by a single human) and the current situation provides the appropriate information about the state of the behavior, then the behavior will change.  The key here (as with optimal foraging models) is that the appropriate cues have to be present to change the behavior.  Often organisms use proxy cues to trigger behavioral shifts.  For example certain caterpillars use day length to trigger shifts in developmental pathways (diapause vs pupation) when what really matters is temperature.

So the real answer to your question lies in the further questions of whether consumption is plastic (or hardwired as you say) and if it is, whether a situation provides the appropriate cues to indicate that we have acquired enough resources.  Those are rather complex questions that, as far as I know have not been answered definitively in the general sense that your question implies.

Wow, it's so hard for me to think in all these biological perspectives. Now it's apparent I don't have a very strong foundation in biology ("schema") to put all these ideas. Thanks for your insight. :) Clearly there's lots I can learn!


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Good place to ask health based questions?
I like the development of biology.stackexchange.com, but it is still in an early stage and far from perfection. While we develop it further, could you guys help me finding places to ask questions related to health and biochemistry in general?

Since this question is more about the Q&A site rather than an actual question on the topic, I think this belongs on meta.

Health: ask your doctor.
Biochemistry: ask here, there are already >100 biochemistry questions.

Thanks, but what if I want to ask health questions from a student - not pacient - viewpoint? That is, I want to find papers, data and literature about certain topics. Do you/someone here know?

In that case you're still the closest to on-topic here. I don't think we have any professionals for medicine here yet but as a fellow medical student I might be able to help. Plus there are people with extensive knowledge on human biology, which tends to cover a lot of health topics.


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What chemical or biochemical agents do plants use to inhibit each other's growth?
As I just learned, allelopathy is the action by which plants regulate the growth of other nearby plants.
I have hear of ethylene is a general signal for growth and fruit ripening in particular, but I would like to hear about more specific compounds or proteins that are known to be allelopathic agents and how specific can they be - lots of plants ignore each other and just grow over each other.
@AlanBoyd has pointed me to a journal, but as its not open content, I'm hoping for a next level review of the mechanisms and actors in this topic...
thanks in advance!

A classic example is juglone from Black Walnut tree roots. This review from 1973 discusses juglone and allelopathy, inhibiting growth of other trees. This 1961 paper describes juglone's effects as able to sedate or at depress movement of Daphnia magna, leopard frogs, perch, catfish, goldfish, mice, rats and rabbits. That led to work testing juglone on cancer cells.

As with the massive variety of compounds that serve to protect plants against insect and animals, resulting in a wide range of poisons, antibiotics and other natural insecticides, allelopathic compounds are highly varied with different methods of action: some merely prevent germination while others are effectively herbicides.
One example is Alliolaria petiolata. In that species the allelopathic substance is not known, but is thought to ahve a fungicidal effect that impedes mycorrhizal development, which would seriously affect the development of many species.


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Are serotonin levels in humans affected by light?
I'm reading this Wikipedia article on light therapy  and noticed a peculiar statement:

The production of the hormone melatonin, a sleep regulator, is
  inhibited by light and permitted by darkness as registered by
  photosensitive ganglion cells in the retina. To some degree, the
  reverse is true for serotonin, which has been linked to mood
  disorders.

If I read this correctly, when melatonin is suppressed, serotonin is released? This makes some sense. I'm interested if there is any scientific backing to serotonin being affected by light levels.

You might want to look into seasonal affective disorder which is possibly related to this.

I'm not sure about humans, but this is true of many vertebrate's retinas. There is experimental evidence showing light-inhibited production of serotonin. This article reviews how serotonin is regulated in response to day lenght (as well as fasting/feeding cycles). The authors suggest a mechanism in which serotonin and ghrelin integrate signals from fasting/feeding and night/day together.

Nowak JZ, Z Urawska E, Zawilska J. Melatonin and its generating system in vertebrate retina: circadian rhythm, effect of environmental lighting and interaction with dopamine. Neurochem Int. 1989;14(4):397-406.
Kirsz K, Zieba DA. A review on the effect of the photoperiod and melatonin on interactions between ghrelin and serotonin. Gen Comp Endocrinol. 2012 Nov 1;179(2):248-53. doi: 10.1016/j.ygcen.2012.08.025. Epub 2012 Sep 5.

The second article looks really nice. Is there a place where I can take a look at it for free?

No, but if you give me your email I can send you a PDF.


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Which Enzymes are Responsible for the Biodegradation of Beta-endorphin?
Which enzymes are responsible for the biodegradation of the endogenous opioid peptide, beta-endorphin?

As far as I have been able to find out, there isn't a definitive answer to this question.
β endorphin is a peptide, and it would seem that there are numerous brain peptidase enzymes that are implicated in the hydrolysis of β endorphin and other peptide neurotransmitters. These include aminopeptidase N, membrane-dipeptidase A, angiotensin-converting enzyme and neutral endopeptidase (also called enkephalinase).
For an early (1984) review of this topic see here; there doesn't seem to be a more up-to-date review, but there is quite a bit of literature on the effects of inhibitors of these various enzymes.


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Chromosome 2 fusion?
I read this article by Jeffrey Tomkins and Jerry Bergman claiming to debunk chromosome 2 fusion. Is there anything wrong with these conclusions?
" 1.The reputed fusion site is located in a peri-centric region with suppressed recombination and should exhibit a reasonable degree of tandem telomere motif conservation. Instead, the region is highly degenerate—a notable feature reported by a previous investigation.

In a 30 kb region surrounding the fusion site, there exists a paucity of intact telomere motifs (forward and reverse) and very few of them are in tandem or in frame.
Telomere motifs, both forward and reverse (TTAGGG and CCTAAA), populate both sides of the purported fusion site. Forward motifs should only be found on the left side of the fusion site and reverse motifs on the right side
The 798-base core fusion-site sequence is not unique to the purported fusion site, but found throughout the genome with 80% or greater identity internally on nearly every chromosome; indicating that it is some type of ubiquitous higher-order repeat.
No evidence of synteny with chimp for the purported fusion site was found. The 798-base core fusion-site sequence does not align to its predicted orthologous telomeric regions in the chimp genome on chromsomes 2A and 2B.
Queries against the chimp genome with the human alphoid sequences found at the purported cryptic centromere site on human 2qfus produced no homologous hits using two different algorithms (BLAT and BLASTN).
Alphoid sequences at the putative cryptic centromere site are diverse, form three separate sub-groups in alignment analyses, and do not cluster with known functional human centromeric alphoid elements."

I've also heard them say that there has to be a fusion in every living thing that evolved or evolution isn't true.  Is that true or not?
The article is here

Part one
Part two

You are describing two processes - one of general fusion happening now and then throughout history (which is common) and one of specific fusion, that was supposed to happen at a certain time in human evolution history (which is not sure, but possible).

@Jeff , could you include the reference to the story  you are asking about?

Thanks!  Let me take a crack at this, though @jkadlubowska has it in a nutshell here.

Regarding the Papers referenced above:
If the authors maintain that the evidence at the site of fusion is not clear and that explanations as to how this happened are flawed that is possibly concedable.   They would need to do more homework than these papers.  The discussion of vestigial centromere sequences and telomere motifs being inverted is interesting, though contrary views have been written up elsewhere.  I'm not going to review that evidence as I think its not primary to the question at hand...
I would point out that the centromere and telomere sequences are highly repetitive - they are so repetitive that they are often associated with unreliable sequencing in a typical genome build.  While its possible some will be found in future builds of the human genome, such sequences are just as likely to have been excised during mitosis or by mutation.  There would be strong selection pressure for them to be excised quickly; having two centromeres on one chromosome would probably be a fatal trait and the same is probably true for telomerase susceptible sequences in the middle of a chromosomal arm is too.  A lot has happened at the point of fusion and 150 kB of DNA seems to have included itself which is not from the original Chr 2A or 2B.
I think there is some confusion here: The fusion models examined do not predict the fusion from the local configuration of bases.  The main evidence for fusion has always been the fact that the two pieces of human chromosome 2 are nearly identical to chromosomes 2A and 2B of apes - typically 96-98% identical.  The genes are almost entirely in the same order, the inter-genic regions are very similar All along the 2A/2B length - millions of bases.  The site of fusion ad models for its occurrence is merely confirming what we already - there are two chromosomes somehow stuck together.  Since both papers focus on the site of combination and do not adequately address this primary piece of information, they seem to be missing this point.
The chances are infinitesimal that human chr 2 were to resemble those of other primates at random.   This is what you say in science when you mean 'impossible'.  One simply doesn't see a segment of DNA the size of Chr 2A and 2B being so similar for such a length when we look at rats, dogs, worms or any more distantly related living thing.  But for every primate the relationship corresponds to humans the same way.  In addition studies show that these highly similar blocks of DNA sit right next to the site of fusion and show a crossover where the fusion probably occurred.  Some recent hominids - Neanderthals and Denisovans had the chr 2 fusion as well.
I have to say is that there's always a chance that chromosome 2 fusion did not happen though in my view there's a tremendous amount of evidence that it did.  The second most likely explanation is that all the other apes had their chromosome 2 break into 2 pieces at some susceptible site.
I don't quite agree that chromosome 2 fusion is an indispensable or even leading piece of evidence that means that humans and the other primates are interrelated.  That question is a different kettle of fish and the relationship between Human chromosome 2 and the chromosomes of other primates is just one contributing point.  All the other chromosome sequences in primates are the same, and nearly every gene in human beings is closer to primates than to other animals.  If they had not found chromosome 2 fusion in the genome sequences few if anybody would have worried about it.
As to your last question - I don't know if its necessary that chromosomal fusion must occur in every living thing, but it appears that it has.  In fact what we see as we look at all the diverse chromosomes being sequenced, is that most chromosomes have been merged or rearranged over and over again.  Over long periods of evolutionary time, a typical chromosome looks like a patchwork quilt stitched up from pieces of other chromosomes.  These relationships are called synteny, which reaffirm the thesis that all living things came from a single point of origin, if you go back far enough.  Really, the fusion point of Chr2 is interesting because its a relatively new event; by picking through the pieces we might find some understanding of something that appears to be a common phenomenon in genome dynamics.

The above image comes from a review of methods to identify syntenic regions.  It identifies regions of human chromosome 7 and similar regions of mouse chromosomes, identifying regions on mouse chromosomes 6, 9, 11, and 12 with substantial similarities as well as a little bit of chr 2.  Hu chr 7 is 158 million bases long, so even a small band (> 1/1000th of the full length) on this chart means 100,000s of bases.
If all these syntenic relationships are considered together they can construct chromosomal rearrangement events that compare with the phylogenetic tree and typically verify speciation events that separate the two organisms being compared.
Whoops - just found this.  Take a look at this Biology.SE question: it refers to Robertsonian translocation where the long arms of several of the chromosomes chr 14, 15, 16, 21 and 22 are known to sometimes fuse, resulting in viability.  The answer there is useful - these variants don't tend to produce offspring, but it only takes one time.  Its only happened once in the past 5 million years or so.  So another point of view there.
That should't discourage the authors from trying again.
All this being said, as a scientific question I'd rather have a discussion like this, based on evidence and facts that anyone can evaluate.  The authors did quite a bit of homework and read some of the literature that is out there.  This is the right direction some of the creationists are taking here and I personally hope that they keep at it.
If science is to have any merit (or fun) at all, its because any idea can be called into question and be re-evaluated at any time by anyone.

I'd really like to give you more than just one upvote.

Thanks for this.  Can you tell me, was the fusion of "two chromosomes" actually predicted before it was demonstrated in Chr 2, or was it discovered first and then taken as evidence in support of the lineage?

It was known. When you localize genes in humans and then in chimps the broad idea of a chromosomal fusion is referenced from 1995 on the wikipedia page http://en.wikipedia.org/wiki/Chromosome_2_(human)

This reply needs to contain a number of links to qualify each of my claims. Unfortunately this site won't allow me to include more than two links because I am a new user. Please see this post which contains the same response and all the necessary links as well.
I would be very careful trusting any claims published by the young earther Jeffrey Tomkins. In my experience, each of his claims needs to be thoroughly researched because I have found him to be less than rigorous (sloppy) in at least one other paper he has published. He has faced similar accusations from others in the past.
I'm not saying dismiss everything he says: I'm saying take all of his claims with a grain of salt, expect there to be exaggerations, errors and misleading claims (he has a young earth creationist agenda)
If you are ever concerned about anything he writes, you will need to look at the evidence for yourself. I will attempt to answer your questions here.

In a 30 kb region surrounding the fusion site, there exists a paucity of intact telomere motifs (forward and reverse) and very few of them are in tandem or in frame.

This is true, but it isn't surprising (at least not to me). To quote popular science blogger, Carl Zimmer:

The ends of chromosomes are very vulnerable places. If they simply dangle loosely, DNA-cutting enzymes can nibble away at them, destroying the genes they encounter. The dangling end of one chromosome can also get attached to the dangling end of another, fusing chromosomes together. We are mostly protected from such changes thanks to special proteins called telomerases. They tack on little repeating bits of DNA, which form a loop–a telomere–so that chromosomes end as a hairpin curve, rather than dangling ends.

It is this loop that prevents chromosomes from undergoing the type of fusion that we see in the second chromosome. Now telomeres naturally shorten and become mutated with age. If we encountered two fused chromosomes (with the telomeres joined end to end) we should expect that this could only happen where the telomeres are short enough and mutated enough to allow this to happen. Only when they can no longer form that protective loop, can they become fused.
Experiments like this have shown that defective telomeres with few repeats are vulnerable to chromosome fusion.
Here is what the fusion site actually looks like - the highlighted repeating elements (TTAGGG and CCCTAA) are those that are still perfectly formed. If I relax my criteria a little and also highlight those repeating elements that have just one single mutation, this is what the fusion site looks like. To raise doubts that what we are looking at here are a series of repeats of "TTAGGG" joined to a series of repeats of "CCCTAA" is either asinine or dishonest.

Telomere motifs, both forward and reverse (TTAGGG and CCTAAA), populate both sides of the purported fusion site. Forward motifs should only be found on the left side of the fusion site and reverse motifs on the right side

(Note: it is CCCTAA not CCTAAA)
This is just pure nonsense, I am tempted even to call it a lie but I can't be sure. I have looked into this claim by searching through the 20,000 bases that surround the fusion site.
In those 20,000 bases there is exactly 1 instance of TTAGGG that occurs before the fusion site and 1 instance of CCCTAA that occurs before the fusion site (No more than we should expect to occur by chance alone in any sequence this long).
After the fusion site (and away from it), there is 1 more instance of CCCTAA and 3 more instances of TTAGGG (No more than we should expect to occur by chance alone in any sequence this long).
Don't take my word for it. Here are 20,023 bases that surround the fusion site.

The 798-base core fusion-site sequence is not unique to the purported fusion site, but found throughout the genome with 80% or greater identity internally on nearly every chromosome; indicating that it is some type of ubiquitous higher-order repeat.

This sounds like more rubbish (even a lie perhaps). Using BLAT to search for the actual sequence, there is no location in the human genome except for this place on chromosome 2 where we see a sequence of repeating TTAGGG joined to a sequence of repeating CCCTAA. If the authors claim to have found another site like this, why have they not linked to it?
We could also use BLAT to search for an idealised sequence of perfect repeats. Once again, the only hit that includes both the TTAGGG and the CCCTAA is in this exact location on chromosome 2.
We do unsurprisingly find sequences of repeating TTAGGG but what makes this fusion site unique is that those repeats are followed by repeating CCCTAA - that isn't found anywhere else in our genome of over 3 billion base pairs.
Think about that for a moment. A sequence with a signature as unique as this, found in the exact place where scientists expect to find it!

No evidence of synteny with chimp for the purported fusion site was found. The 798-base core fusion-site sequence does not align to its predicted orthologous telomeric regions in the chimp genome on chromsomes 2A and 2B.

First of all, this claim doesn't even make sense. The 798 bases he talks about are just the telomeric repeats. If they are telomeric repeats then they will be found on the telomeres of chromosomes 2A and 2B. Perhaps he made a mistake here and was talking about the wider region surrounding this fusion site?
It is true that there is a lack of synteny in the wider region surrounding this.
This became well understood with the sequencing of the gorilla genome. There was a paper published explaining how this happened in 2012. If you prefer, here is the layman's explanation with diagrams.

Queries against the chimp genome with the human alphoid sequences found at the purported cryptic centromere site on human 2qfus produced no homologous hits using two different algorithms (BLAT and BLASTN).

This isn't true either. Where does he get this nonsense from? I have downloaded the alphoid sequences from the defunct centromere on human chromosome 2 and used BLAT (against Chimpanzee Feb 2011) to find their homologs in the chimpanzee. Unsurprisingly they are exactly where we expect to find them on chimpanzee chromosome 2B - where there is a functional centromere.
Think about that for a moment. The very same sequences that form a functioning centromere on chimpanzee chromosome 2B are found exactly where we expect to find them at a defunct centromere on human chromosome 2.
I am busy constructing a detailed write-up on this. I will update this post to provide a link to that.

Alphoid sequences at the putative cryptic centromere site are diverse, form three separate sub-groups in alignment analyses, and do not cluster with known functional human centromeric alphoid elements."

I can't comment on the first claim but it seems irrelevant anyway. I can tell you that these alphoid sequences occur frequently at centromeres all over the human genome from X to 22. More importantly they are appear almost exclusively at centromeres. For example, alphoid 2 appears at centromeres on the following chromosomes: 21, 9 (twice), 11 (twice), 20 (twice), 7 (3x), 22 (5x), 16, 14, 15, 5.
It appears once at an unexpected location on chromosome 9 where there isn't a centromere, but that exact location is rich in other alphoid sequences suggesting that it too is a defunct centromere (or was perhaps duplicated from another centromere).
This will also be covered in that detailed write-up I mentioned.
edit (2 Oct 2015):
I promised to follow up on this post with a detailed write-up on the fossil centromere on chromosome 2. I've done that now (A year and a bit later) - you can find the information I've compiled on the centromere here

You can add the links into the comments and we can add them for you. Just state where they should be located.

every claim should be taken skeptically in science really...

I've been able to add the links myself now :)

There's skepticism, and then there's refusing to consider extremely well-evidenced conclusions, simply because one doesn't like the conclusion.  With Young-Earth Creationists, you have to figure the latter is what's happening.

I promised to follow up this post with a detailed write-up on the fossil centromere. I have done that now. It turns out that there is an abundance of evidence for this centromere. You can find that here

If one looks at the sequence map in detail, at the fusion point we find both telomere and pre-telomere sequences. And what is particularly compelling, is that these main groups occur in the correct order.  That is, first you see a pre-telomere sequence, then a telomere sequence. Then we see the telomeres inverted and the inverted pre-telomeres after that. This is exactly what would be predicted for a chromosome fusion.  Yes, one can quibble (as Tomkins does) that within a particular group that the sequences don't "look exactly as they should".  But this would be consistent with ideas proposed here.  That these sequences MUST have undergone significant mutation in order for the fusion to even occur!  And then of course one would expect mutations to continue after the fusion event as part of normal evolution.


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Which Enzymes are Responsible for the Biodegradation of Noladin Ether?
Which enzymes degrade the CB1-specific endogenous cannabinoid 2-arachidonyl glyceryl ether? (Noladin ether)

Noladin is an endocannabinoid. The best-characterised members of this family of molecules are Arachidonoylethanolamine (AEA; anandamide) and 2-arachidonoylglycerol (2-AG). The degradation of these endocannabinoids is reviewed in:

Pamplona, FA et al. (2012) Psychopharmacology of the endocannabinoids: far beyond anandamide. Journal of Psychopharmacology 26:7-22

These endocannabinoids are inactivated via a reuptake system that is present in both neuronal and glial cells, although the protein responsible has apparently not been identified.
AEA is then metabolised to arachidonic acid and ethanolamine by fatty acid amide hydrolase, while 2-AG is converted to arachidonic acid and glycerol by monoacylglycerol lipase.
Because of its ether linkage, noladin cannot be a substrate for either of these enzymes. However the review also describes other possible pathways of endocannabinoid metabolism involving oxidation by cyclooxygenases, lipoxygenases and P450 cytochromes. These are the best candidates for the further metabolism of noladin, but there is apparently no direct evidence for this.


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How do warm-blooded animals keep their temperatures constant?
Warm blooded animals like us keep their temperature constant irrespective of their surroundings. But how do they do that? Energy should be supplied from the inside. I assume that reactions like making ATP from glucose are exothermic. That means in winter our body reacts more. Water is absorbed by those reaction.We should need more water in winter. Which is contradictory with our real life experience.
On the other hand what prevents cold blooded animals from making heat? Don't they need ATP? Do they use different types of reactions to make energy? Do they have different evolutionary path? They don't seems very different from us.

It's a process called homeostasis - have a look at this Wikipedia entry: http://en.wikipedia.org/wiki/Homeostasis

Since there seems to be several distinct sub-topics in your question, I will answer them one-by-one:
1). There are a variety of mechanisms that allow endothermic animals to maintain thermal homeostasis in a cold environment. The main ones are:
a). The shivering response: When the core body temperature of a endotherm drops below a critical value (36.8C in humans), it causes the posterior hypothalamus to stimulate certain skeletal muscle groups (especially around vital organs) to start to "shiver" rapidly, generating heat.
b). Compared to ectotherms, endotherms have more mitochondria per cell, thus allowing them to have a higher metabolism. Since metabolism always generates heat, an [general] increase in cellular metabolism will cause an increase in body heat.
c). Many endotherms have layers of insulating matter, such as fur, blubber, feathers…etc, allowing them to preserve body heat. In addition, endotherms can also route blood away from  capillaries via vasoconstriction of arterioles, reducing the area in which heat can be lost.
d). As mentioned by Memming, brown adipose tissue also plays a role in temperature regulation. Thermoregulation-based metabolism in brown fat causes the P+ in the electron transport chain to go through thermogenin instead of ATP synthase. This process generates heat, but no ATP.
e). Some endotherms, such as penguins and arctic wolves have countercurrent exchange in their capillaries. This is when warm arterial blood "passes" some of its heat to cooler veinous blood. This feature allows some of the heat normally "wasted" into the air to be recycled back into the body.
Note: Though it is true that endotherms are able to keep their body temperature constant irrespective of their surroundings (ignoring extremes), they do this at a cost of requiring significant amounts sustenance. Most endotherms require much more sustenance than ectotherms.
2). Your second sub-question is very interesting. Though it is true that generating heat will require substantial amounts of carbohydrates/fats/...etc, it does not necessarily mean that the net consumption of sustenance in cold environments is greater than that in normal environments. In most cases, endotherms in cold environments will have exhibit significantly less activity than when in an optimal environment. The decrease in activity when in a cold environment will likely balance out the increase in thermo-regulation based metabolism. This likely explains why people tend to drink equal or slightly less amounts of water when in cold environments. One more thing: some reactions heat-generating reactions (like the alternate ETC pathway) do not require water. Glycolysis and Krebs actually generates water (not to say that there is a net gain in the body :))
3). In truth, nothing "prevents" ectotherms from generate heat. They simply do not have the cellular "machinery". Ectotherms metabolize in ways very similar to other organisms, using molecules like ATP, glucose, fat…etc. Unlike endotherms however, they spend very little of their energy on temperature regulation. As a consequence, their overall metabolic rates are dependent on the external temperature. The point is this: A substantial portion of endotherm sustenance is used to generate heat. Only a small (if any) portion of ectotherm sustenance is used to regulate heat. As a result, endotherms require much more nourishment than ectotherms.
4). I am not entirely certain what you mean by "evolutionary path", but I will just say this: In many ways, endotherms and ectotherms are organisms that have found different ways to the same problem; how to regulate body heat for maximal survival and reproduction. Basically,
ectotherm- more dependent on environmental temperature, requires less sustenance
endotherm- less dependent on environmental temperature, requires more sustenance
5). You are quite correct. The cellular and genetic components are very similar. Some morphological aspects seem to be shared as well.

Sources:
Cambell & Reece (2010) Biology (9th ed)
Swan, K. G.; R. E. Henshaw (March 1973), "Lumbar sympathectomy and
  cold acclimatization by the arctic wolf", Analysis of Surgery 177 (3):
  286–292,
Guyton & Hall (2006) Textbook of Medical Physiology. (11th ed)
Romanovsky AA. (2007). Thermoregulation: some concepts have changed.
  Functional architecture of the thermoregulatory system. Am J Physiol
  Regul Integr Comp Physiol. 292(1):R37-46.

Here answers a part of your question. Warm blood animal burns more food in the winter, so they can keep their body warm. They are not consuming much more ATP in the winter, just a bit more. Usually they have mechanism to reduce the heat loss, like growing hair. How do you know that you need to drink more water? You should know that you area also sweating less in the winter.
The cold blood animal has a mechanism encoded in their gene to prevent them keep warm in the winter. It is a evolution result so that they dont have to consume much foods and so ATP in the winter. It means that they belong to a different branch of phylogenetic tree thus has a different evolution path.

There's always shivering, and also the brown adipose tissue that generates heat to keep the core temperature regulated. Extra mitochondria in brown adipose tissue can be used to generating heat without producing ATP. As @jackweirdy mentions, this is a negative feed back involving hypothalamus.


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HIV Rapid Tests
The hiv antigens that are used in the oral rapid tests, are they infectious? The tests do not contain any actual virus but I am curious if the antigens themselves could somehow create the virus on their own if they get into the bloodstream? Like do they contain all of the parts needed for replication inside them? (Not the actual virus but the antigen).

nope - the test contains antibodies to HIV proteins, but nothing from HIV itself.  The 'antigen test' tests for antigens, it doesn't itself contain any antigens.
Antibodies are proteins that animals (like humans) produce to fight of viral and bacterial infections, they don't come from viruses.
Even if the test did contain HIV proteins, it could not infect anyone.  You really have to have the HIV RNA, and almost certainly the rest of the virus too,  to cause any infection.

Okay. but the proteins don't contain that RNA do they? Sorry I am not very good at this stuff and get easily confused.

@Sarah: no, RNA and proteins are two completely different things. Anyway, there is nothing from HIV in the tests.

@Nico: Oh okay. Yeah I was just curious because of what I read about the hiv antigen. It kind of scared me because I wasn't sure if those were infectious or not. So just for clarification: proteins and rna are two separate things. The proteins do not have the RNA inside them and without the RNA there can be no infection?

@Sarah: Exactly. The test contains something (an antibody) that -if present in the sample- binds to HIV proteins.

No, the protein components of viruses may be able to initiate the infectious process, i.e. injection, but if there is no RNA or DNA, there is no virus to inject into the target cell. Hence none of the viral genome's action such as replication or transcription will occur and the cell itself will remain unchanged.
However, some effects of viral infection are actually part of an immune response of some kind, and these are often triggered by viral proteins themselves.

By taking proteins produced by bacteria and virii and then introducing them with a Carrier the body will mount an immune response and react when the real danger is presented. This is called the Hapten-Carrier effect, and is how we make many vaccines. The Innate Immune response is first, and the Adaptive Immune response creates the "memory" of the encounter so it can effectively fight the actual bacteria/virii/etc.


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Does Doxylamine have any Influence on the Monoaminergic System?
Does doxylamine have any affects on the monoaminergic system? Specifically I am interested in adrenergic or serotonergic activity but additional information on its dopaminergic activity won't hurt either.