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Draw simplified phylogenetic tree for kids
I need to draw simple, phylogenetic tree for kids lecture.
I am looking for an online tool where I can enter organisms (e.g., human, wasp, fungus) and get figure of a phylogenetic tree. Tree should be based on how close those organisms are (I don't need genome alignments).
Similar figure producing tool would be perfect.

Just download an existing diagram.. To make a tree you would need to put in reference sequences.

Have a look at this Website. It might be helpful.

@WYSIWYG where can I do so?

You can find images of trees by google search.. but if you want to make a tree yourself you would need some reference sequence. Entire genome is not used for that but some sequences such as 18s rRNA are frequently used. Doing an alignment is inevitable, but the algorithms (such as clustalW) do it under the hood.

you can use http://itol.embl.de to get trees based on the NCBI taxonomy, but you'd have to use a graphic program to make them prettier

As per your requirements I will suggest:
http://www.onezoom.org/

I don't know what background you have given the kids or what level, but here's something we do in a non-majors freshman level biology course that could easily be adjusted. First, to get them thinking about trees and relationships, give them a simple family genealogy (use only 1 parent for simplicity). I use my family tree going back to my grandmother. With cousins, aunts, and siblings, they begin to understand how to interpret family trees. You can substitute the family names with organism names to make it a basic phylogenetic tree.
We teach tree construction simply. We give students a list of six species (fake birds) with DNA sequences that are only 20 nucleotides long. Students have to calculate the number of base pair differences between each pair of sequences which, in our case, range from 2-10 nucleotides.
They then use the pairwise differences to construct their tree, with the understanding that fewer nucleotide differences between organisms means they are more closely related.
You can do this type of activity over a couple of days (depending on time). Then, you can begin to show them trees that become gradually more complex. Because the kids will have constructed a tree and now how it is constructed, they will have a much easier time interpreting larger trees.


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A doctor might give bicarbonate (HCO₃¯) to a patient who is breathing very rapidly. What is the doctor assuming about the patient’s blood chemistry?
The answer is:
The doctor is assuming that the rapid breathing is the body’s response to low blood pH.
(Source: Campbell Biology)
But this answer doesn't make sense. Why would the doctor give the patient even more CO2 if the patient is already suffering from an excess of CO2 that is causing the low body pH?

Bicarbonate is not carbon dioxide. In acidic conditions, bicarbonate will be protonated to form carbonic acid which in turn decomposes into carbon dioxide and water. The net result is the removal of a proton and formation of carbon dioxide.

Bicarbonate is not carbon dioxide. In acidic conditions, bicarbonate will be protonated to form carbonic acid which in turn decomposes into carbon dioxide and water. The overall result is the removal of a proton (ie increase in pH) and formation of carbon dioxide (which accounts for the rapid breathing). The idea behind giving bicarbonate is that it will replenish the buffer.

if a person is both (1) hyperventilating and (2) has a low blood pH then this is a case of metabolic acidosis... in metabolic acidosis the patient compensates by breathing heavy... why? because hydrogen ions are captured by bicarbonate (the conjugate base of carbonic acid) which is then exhaled as carbon dioxide...
metabolic acidosis is not caused by excess carbon dioxide... this is the case of respiratory acidosis... but under respiratory acidosis the breathing is supressed, however tachypnea with frequent shallow breaths could lead to poor removal of carbon dioxide...
here are some causes of metabolic acidosis:
http://en.wikipedia.org/wiki/Metabolic_acidosis#Causes

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Insect identification
It is found in my apartment in Finland. I had to kill it to stop it from getting away before looking for the camera, but it looked pretty much the same alive and intact. It's length is about half a centimeter, and the younger ones look darker. It is often found in dark. Since their appearance, I often notice red and slightly itchy bug bite in the morning. The question is what is this insect?

Where in your apartment did you find them (what environment)?

@fileunderwater I don't know where did they come from, but they are just found on the wood and ceramic floors. The environment is warm and reasonably dry.

It reminds me of silverfish, a common wingless house insect.

yeah, my first idea as well, and the environment fits. I first thought that the legs looked a bit long though. However, environment + movement patterns is a good way to identify them by.

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Classification of glycosidic anomeric bonds (alpha vs. beta)
In the process of studying for my upcoming biochemistry exam, I have stumbled over the classification of glycosidic bonds. I want to be able to distinguish $\alpha$- from $\beta$-glycosidic bonds. Unfortunately, even after reading through this page, I don't really understand how to go about classifying the bonds in e.g. an oligosaccharide.

(Source)
Now, I am inclined to say that both of these anomeric linkages are of type $\alpha$, because the O-glycosidic bond is axial to the respective sugar rings. Is that a correct way of reasoning?

Here's my interpretation, as far as I can get, which agrees with your deduction that both of the O-glycosidic bonds involve α epimers. (If the epimeric carbon has an -OH in the axial direction then this is the α anomer.)
Do you have the name of this compound?
Let's hope that a real glycobiologist comes along.
Supplementary
I'm now not sure that it is even possible to assign an anomeric state to the sugar marked as ?. There is no indication in the diagram of the presence of a -CH2OH substituent on the ring - it appears to have a methyl group instead. If that group was a -CH2OH then the putative anomeric C would indeed be in the α form since it is pointing in the opposite direction from the "-CH2OH" (c.f. the two galactose residues). If ? is a deoxy- derivative of a sugar then it may be that the convention still holds.

Unfortunately, I don't have a name for the compound, I just grabbed an image from the internet that looked roughly like the exam problem I was trying to solve.


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Identifying the inheritance pattern
                      GrandParents                  -- 1
                            |
                            |
                -------------------------
                |S                      |D          -- 2
            ---------                ----------
            |S(A)   |D               |S(A)    |S(A) -- 3
            |S      |D                              -- 4

S = Son
D = Daughter
(A) = Affected with a degenerative disease.
The question is how to identify the type of inheritance of the disease - whether
X-based, Autosomal dominant or recessive. Which sex of fourth generation are likely to have the disease? Does it depend on the disease?

This pedigree can not lead to one absolute answer. There should be more information.

And also, Can you present your ideas on this question?

Short answer
As said @Biogirl, "This pedigree can not lead to one absolute answer". We miss information in order to answer this question.
Long answer
Should we make the assumption that the allele causing the disease (A) necessarily come from the lineage you draw or can it come from the partners of the second generation (offspring of GrandParents)?
Then, depending on your answer to this question...
If yes (= if the allele causing (A) comes from the GrandParents):

This genealogy is impossible if the type of inheritance is as simple as you suggested (either recessive or dominant, no epigenetics, no epistasis, no effect of the environment, no protein-mediated disease via the vomb,... even if it can be autosomal, sexual or mitochondrial genes)

If no (= if the allele causing (A) do not come from the GrandParents only)

Everything is possible (from the space of possibilities that you suggested)

some possibilities would be more probable than others (depending especially on the allele frequencies)

We are missing some information, but (by what I recall from my little inheritance genetics knowledge) it looks X-based. I will make up some of the missing information.
Lets say, an "affected X" is H (I wanted to use x, but it will be harder to see), HY will be diseased, XH will be carrier, but not diseased. XX/XH means unclear if carrying.
Grandparents:               XY-------------XH
                                    |
                           -------------------
                           |                  |
Parents&Partners      XH---XY                 XH---XY
                         |                        |
                     ---------               ----------
                     |        |              |         |
F1                  HY       XX/XH          HY         HY
                     |        |
F2                  YX       XX/XH

The F2 son is not carrying (because he is healthy). The F2 daughter could be carrying if her mother was, but even then does not have to. Unless her dad was also carrying it.
Please correct me, if I am totally off.

This would be one possibility. I guess you say that it looks like the disease is X-linked because all sick people are males but we only have three sick people. Among three guys, the probability that all have the same sex is $\frac{1}{4}$! Moreover, for your tree to be likely you would need that the allele causing the disease is present in high frequency in the population (which is rather rare for a X-linked disease)! I think it is better just to say that we don't have enough information to infer an inheritance type.


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Neuroscience: zapping an axon connected to thermoreceptor
Let’s say an experimenter has an electrode that can give a shock to a single axon. She takes that electrode and zaps an axon connected to thermoreceptors in the hand of her subject.
I) What would the subject’s perception of the stimulus be?
II) Why?
III) If she zaps that axon AND ONLY THAT AXON so hard that it destroys the axon, would the subject feel pain?

Hi! Welcome to the site. The question you have asked is classified as homework question. You need to show your efforts - what you thought, what you tried to search, etc. You should write what you think can be the answer.

I and II depend on the type of electrical signal applied to the axon. for III, most receptors can perceive other sense as well, so for example striking a vision receptor may produce the perception of light (even in complete darkness) - my guess is the you would feel pain, even if you could isolate the destructive signal away from nearby pain receptors.
search "action potential" in duckduckgo.com, it will get you going.

Can you please add some references?


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Why do the neuron pathways decussate?
I learn about the brain right now, and there are crossing of neuron pathways everywhere; in the thalamus, the medulla oblongata, the pyramidal tract... And I don't understand why? What is the reason to connect - for example - the right foot to the left part of your brain?

Possible duplicate: Here and especially here.

Crossing or decussation is a lot more robust against wiring errors than their seemingly simpler same-sided wiring counterparts. See here for the research carried out to establish this and for more detail.


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Transition/Transversion ratio
I'm taking a bioinformatics class and at this point we are just going over basic stuff about molecular biology. Half of the class is doing reading/research on our own, so there isn't much class time to ask questions or go over examples. One topic is transition/transversion ratio, and I'm not 100% sure I'm understanding it. Do you just compare the first symbol of string 1 to the first symbol of string 2? What if the two symbols you're comparing are the same? Do you just ignore it? Let's say string 1 is ACGATG and string 2 is TCAGTG. Would the ratio be 2/1?
Here are the comparisons I made.
Transitions: G-->A, A-->G,
Transversions: A-->T,
Neither: C-->C, T-->T, G-->G
Is this correct or am I completely on the wrong path?

You are almost on the right path.
This schematics from Wikipedia is quite clear in my opinion.

Slightly more chemical explanation (which you do not necessarily need to do bioinformatics, however I think it is always better to know exactly what you are dealing with outside of the computer!)
The idea is that you have four basic nucleotides: cytosine and thymine are called pyrymidines and adenine (A) and guanine (G) which are called purines. Pyrymidines are characterised by a 6 carbon azo-ring which is called a pyridine, while purines have a larger double ring, formed by a pyridine ring + an imidazole ring.
A transition is defined as the passage purine -> purine or pyrimidine -> pyrimidine.
A transversion is the passage purine -> pyrimidine, or viceversa.
These mutations can be caused for instance by certain chemicals, such as alkylating agents, or by ionizing radiations.

In your specific example, given the sequences
 ACGATG
 TCAGTG

You have 3 mutations:
A -> T
G -> A
A -> G

So you have 1 transversion (from the purine A to the pyrimidine T) and two transitions (between the purines A and G).

Thanks! That's pretty much what I thought, but nice to get confirmation.


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Gene pool simulation
this simulation, you sampled the gene pool without replaceing beads in the beakerafter you drew each one. Thus, f(A) and f(a) in the gene pool changed slightly after each bead was drawn. For example, if you begin with 50 light and 50 dark beads, the probability of drawing a dark bead the first time is 50/100 = 0.5. THe beaker would then contain 49 dark beads and 50 light beads, so the probability of drawing a second dark bead becomes 49/99 = 0.495. Does this make your simulation slightly less realistic? In small natural populations, does one mating change the gene pool available for the next mating, or not? What biological factors must be considered in answering this question?

Homework questions should show some effort to answer them yourself.

non-replacement may work in the case of strictly monogamous/monoandrous society..

I am not sure I'm answering your question but I hope this will help.
There are two main models of genetic drift in biology: Moran model and Wright-Fisher model.
The Wright-Fisher model implies picking $N$ beads (where $N$ is the population size) with replacement in order to form the new population. Therefore, the change in allele frequency (due to genetic drift) follows a Poisson distribution.
$$\frac{2N!\cdot p^kq^{2N-k}}{k!(2N-k)!}$$
The Moran model consists of the following: At each time step you draw two beads. One disappear from the population and the other replicate in order to keep a stable population size.
The two models yield to similar results. Moran model runs twice as fast as Wright-Fisher model.
I don't fully understand your model. You say that in your model you pick one bead at a time. What do you do with this bead? How do you construct your population at the next time step? Do you allow changes in population size? Can you please try to develop how you defined your model. If it is a computer simulation you might paste the important part of your code, that might help.
Haldane and Kimura both worked a lot on these models of genetic drift. For example, they provide different ways of calculating the mean time to fixation of a given allele given their selection coefficient $s$ starting from a given initial frequency $p_0$. Also some work has been done on genetic drift in population where the population size changes over time. Some work have been performed considering more or less complex probability density function for the number of offspring per individual. This kind of literature is very interesting but sometimes ask for quite good knowledge in mathematics (especially for Kimura's articles).
I once asked this question concerning the different models of genetic drift and their assumptions but I didn't get an answer yet.


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Which restriction enzyme would i use?
Plasmid pBr322 includes two genes that confer antibiotic resistance: a gene for ampicillin and  a gene for tetracycline. The cutting site for the restriction enzyme BamH1 is in the middle pf the tetracycline resistance gene. The cutting site for the restriction enzyme Pvu1 is in the middle of the ampicillin resistance gene.
If you were using a cell culture plate that contained ampicillin, which restriction enzyme (BamH1 or Pvu1) would you use to cut the plasmid and excise the gene you wanted to insert?
Attempt:
I would assume you need to use Pvu1 since the cutting site is in the ampicillin resistance gene, but the correct answer is BamH1. Why?
Any help would be awesome! Thanks!

Remember than Pvu1 cuts in the middle of AmpR, and when you insert your gene you'll be disrupting its function, meaning that any transformed colonies will no longer be able to grow on Amp-containing media. This is why you want to cut with BamH1 - the disruption to the TetR gene is irrelevant, and it leaves Amp resistance in place.
The point of growing on antibiotic-containing media is to select for cells that have taken up your plasmid - cells that haven't can't grow.

I would go with BamH1 enzyme as the cut site in pBr322 is BamHI 375 and ss you are plating  it in a ampicillin plate you need the ampicillin resistant gene to be intact for screening so by using BamHI you will not disrupt the Amp resistant gene


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Are there any bacteria that can receive ultrasound signals?
I'm looking for an example of bacteria that could receive ultrasound (at any ultrasound frequency) signal and possibly perform some (re)action afterwards.

... well it can break open the cells and kills them ...

I know but maybe there is some ultrasound frequency that doesn't kill bacteria.

I'm going to post a quick answer here, really a thought piece.
Usually to detect a sound wave you need a sounding board about the wavelength of the sound.
Bacteria are on the order of a few microns in length.
Ultrasound frequencies range from 2 to 200 MHz (and up I assume).
To have a wavelength on the order of 3 microns, a 100 MHz wave would be needed.
So only on the very high end of the range.  If bacteria make sound though, they probably are on this frequency range.
I wonder if this has been looked at?  Not sure it has.  While in biology you never say never - if a bacterium really needs to pick up a wave it might have a clever adaptation to do so, but in the 100MHz + frequency range seems more likely.


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When did human and animal blood became distinguishable from each other as forensic evidence?
Since a few decades ago, DNA testing became an important tool in criminal forensics, and a lot of information can be gathered from a single drop of blood or from a few cells.
Even before that, blood type could be used even in the early 20th century, to at least exclude 3/4 of possible suspects.
However, when did it first became possible to distinguish between human and animal blood, and what method did they use? Is there information about the first time it was used as evidence in a trial for forensic purposes?
I would suspect it was not sooner, or not much sooner as the discovery of the ABO blood types at the beginning of the 20th century. There are modern, much more accurate methods, and the introductory parts of such papers likely mention the early history, but they are behind paywalls.

Huh. I assumed this would be easy to look up but I've spent a few minutes Googling and come up with nothing. +1!

(Kinda) Related: The Uhlenhuth test (antigen-antibody precipitin test) [ https://en.wikipedia.org/wiki/Uhlenhuth_test ]. You might wanna give the Wiki article on the man himself a read too [https://en.wikipedia.org/wiki/Paul_Uhlenhuth ] ..it's pretty interesting O:)

I'm confused about the "evidence in a trial" part. Are you saying a perpetrator splashed chicken blood at the scene? That a cow committed a crime during which some of her blood was spilled? How would that be relevant in a court of law? In any case, blood of animals often looks different than human blood. In medicine, drug seekers often come in complaining of kidney stones, which are very painful and often require narcotics. The first test for kidney stones is looking for blood in the urine. If it's present, and we think it's trickery, we just look at it under the microscope...

...because they used to carry a bit of blood with them and slip it into the cup while giving a sample. The most common blood (chicken) has nucleated RBC's. Bovine blood  cells (e.g. steak) are unequal in size and have less central pallor. Etc. So I would imagine the first time someone noticed the difference between human and other blood was when microscopes came into widespread use. Now they do something trickier, which I won't elaborate on, to put human blood into the sample, but still easy to catch.

@anongoodnurse : you are right, I had more in mind when it was practical enough to use it in forensics, for example, they find a bloody knife, is it human blood and must they investigate more thoroughly, or can they discard it...


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Are there any methods to quantify H2O2 (hydrogen peroxide) which don't rely on horseradish peroxidase?
I can't use HRP since my substrates interfere with it and I need a real-time method because I want to measure kinetic parameters of some oxidases.

Titrate it with Potassium permanganate? http://phs.prs.k12.nj.us/rcorell/LabREDOXAnalH2O2.pdf

I'm sorry, I forgot to mention that I need a real-time method because I need to measure kinetics parameters for oxidases.

Amperometric detection of H2O2 can be performed without HRP, and gives high-resolution real-time readings.
You will find many different type of electrodes that are used in the literature to detect H2O2, including for instance MnO2-coated carbon paste microelectrodes or gold electrodes derivatized with cytochrome c.
Commercial electrodes also exists. For instance these from WPI are based on derivatized carbon fibers (although they do not specify with what, so I would not exclude HRP...)
Another option is that of using the H2O2-sensitive dye H2DCF (dihydro-dichlorofluorescein).

Thanks to your suggestion (H2DCF) I looked more into it and I found several other options: dihydrocalcein AM, dihydrorhodamines, dihydroethidium and Europium-tetracycline. All of them seems to not require another enzyme. Any experience with one of these?

No sorry, I actually found that while looking for amperometric detection and I thought I would add it as another option. The thing that I would start and check is their specificity, I am under the impression that they are ROS detectors rather than H2O2 detectors, but I may be wrong.

For a purely chemical assay, Manganese dioxide (MnO2) will react to produce oxygen from hydrogen peroxide, which can be detected spectroscopically or by means of direct chemical analysis.
I think the enzymatic assay is less environmentally challenging and produces colorometric results directly, which is probably why it is ubiquitous.

To measure the kinetic parameters of oxidases you could also look into measuring the oxygen concentration directly. Oxygen sensors are much more common than H2O2 sensors, and I know small setups (1 ml samples) based on a fluorescent dye based probe are available.

can you please tell me more about this fluorescent dye probe for measuring oxygen?


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Is there theory that connects longevity, time-scale of environmental disturbance, and adaptation?
I'm thinking here about environmental disturbance or like climate change-driven warming. It seems as if there are two macroevolutionary ways to deal with environmental change:
1) Have short generation times, and evolve fast. For instance, the mosquito Wyeomyia smithii is under selection by the warming climate in North America and it has shown an evolutionary repsonse. The response is "detectable over a time interval as short as 5 years" (Bradshaw and Holzapfel 2001).
2) Be hardy, and 'try' to wait out changes. No real-world example to cite, but imagine a long-lived tree growing in an area that has become to warm for its seeds to effectively produce seedlings.
It seems intuitively like strategy 1 is better in the case of ongoing climate warming. However, we could easily imagine a 5-year hot spell followed by a return to the normal as part of natural weather variation. Perhaps in this situation strategy 2 is better.
Essentially, having a longevity/generation time/hardiness that matches the time-scale of the disturbance would be important – if the disturbance is long (or unidirectional) compared to your lifespan, evolving fast seems best; if the disturbance is short compared to your life, it seems best to wait it out.
So the question is, is there theory that deals with this? I suspect that I just need to hit the population genetics books again or something; or perhaps there's a massive tome by Gould I should be reading?

 Bradshaw WE, Holzapfel CM. 2001. Genetic shift in photoperiodic response correlated with global warming. PNAS 98: 14509–14511.

Found this question, which seems related: http://biology.stackexchange.com/questions/378/has-there-been-any-observation-of-species-adapting-the-evolution-process

Not exactly matching your question, but I think that the idea (from stochastic demography) that life histories should be buffered against environmental variability in influential vital rates (Pfister, 1998, Morris & Doak, 2004) can be related to this issue, even if it is mainly (originally) dealing with stationary environmental fluctuations.
In general, fluctuations in vital rates cause the stochastic population growth rate to decrease. This can be described by Tuljapurkar's approximation (Tuljapurkar, 1982):
$$log \lambda_s = log \lambda_d - \frac {1}{2\lambda_d^2} \sum_{i,j} V(a_{ij})S^2_{ij}-\phi$$
where $\lambda_s$ is the stochastic growth rate, $\lambda_d$ is the deterministic growth rate based on average conditions, $V(a_{ij})$ is variance in vital rates (here matrix entires) and $S^2_{ij}$ is sensitivity in vital rates. $\phi$ represents covariances between rates, which can be important, but can sometimes be ignored for simplicity. This equation shows that the effect of variability in vital rates on stochastic growth rate (which can be interpreted as a measure of fitness) is a product of sensitivity to change and the amount of variability.
Because of the negative consequences on stochastic population growth, selection is expected to minimize variance in population growth rate. Pfister (1998) predicted (based on an evolutionary argument and the equation above) that a species should have smaller temporal variances in the life history traits it is most sensitive to. Therefore, across species, there should be a negative correlation between the sensitivity and the temporal variance of vital rates. This also means that the evolution of life histories and the tolerance of species to variability in environmental conditions are shaped by their life-history patterns.
A consequence of this is that in a long-lived species (as an example), you should find larger variabilty in juvenile survival than in adult survival, since population growth rate is more sensitive to variability in the latter. The lower variability in adult survival can then be seen as an expression of "hardiness" to variability in environmental conditions, and this theory can therefore be used to understand likely evolutionary trajectories of different species, also under a climate change scenario. The ways to minimize the negative effects of variability in population growth in this theory is to either be hardy in important traits (change in environmental conditions doesn't translate much into variability in vital rate) or to decrease the sensitivity in vital rates that vary a lot (which amounts to modifying the life-history pattern of the species). Your question mainly deals with longevity, and this is influenced by both maturation age and adult survival. Therefore, this theory can be useful to think about which species should develop a "hardy" strategy.
However, this answer completely ignores tipping-points in environmental tolerances, nonlinear responses and the genetic variation that selection can act on.
Related articles you might want to check out are Van de Pool et al (2010), Morris et al. (2008) and Doak et al 2005.


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How are Raunkiær's plant life forms viewed today?
At the beginning of the 20th century, Raunkiær proposed a typology of plant life-forms based on where they bear their buds, roughly as:
cryptophytes: belowground
hemicryptophytes: at the surface
chamaephytes: close to the surface
phanerophytes: projected above the surface
Are these still held to be useful / biologically meaningful categories? Is there a different typology preferred (eg. tree/shrub/subshrub)? Or are people moving toward gradients of quantified traits instead of typologies (eg. measuring plant height, specific leaf area, etc.)?

Oreotrephes, it all depends on the needs. Reproductive schemas don't exclude shape schemas. There has been, however, a shift to cladistics in classification, which means to give scientific names ONLY to monophyletic groups, i.e. groups that include all the descendants of a single ancestor - and only its descendants. But we still use tree/shrub distinction and epiphytes, for instance, but that's to describe the ecology of species, helping identify them, not to classify them on these grounds alone.


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How many honeybees are there, and how has the number changed across time?
How would you begin to estimate the world population of the European Honeybee (Apis mellifera)? Would recent colony collapse disorder show up as a blip? How about the spread of A. mellifera from Europe to Asia and the New World?
Ideally, I'd love to see a chart with estimates of the kept and feral populations of A. mellifera across time. I realize that this is a tall order; but given that we have available to us:

the complete genome,
current data from agricultural organizations, and
historical and archaeological records,

it seeems that with a combination of genetic and historical methods this shouldn't be impossible. Or is it? There seem to be plenty of articles arguing about A. mellifera's African or European origin, but none that I see that mention actual population sizes.

1 billion hives
(at 10,000-50,000 bees/hive this is 10-50 trillion bees)
Managed: 100 million hives
Based on country-level data from FAO, supplemented  for a few countries with Apiservices, in 2011 there were about 80 million managed hives. Because FAO lacks any data for some countries, and other countries under-report (for instance US figures don't include hives kept for pollination service and hives kept by small-scale operators) a reasonable round estimate of managed hives in the world is 100 million. (This implies a 128% correction to the FAO numbers). (Aizen and Harder 2009 give context on FAO figures).
Wild/Feral: 900 million hives
Wild/feral hives of Apis mellifera are difficult to count via direct observation. Jaffe et al 2010 use a genetic sampling method, and also report a reasonably strong correlation between the total number of hives (managed and wild) per square kilometer and the mean annual temperature of the area.
I used the best fit line from their data to estimate the "hive-carrying-capacity" by country using (the admittedly very general) land area and mean annual temperature. Then I subtracted the number of managed hives from the carrying capacity to estimate wild hives.
Although this formula probably overestimates large, cold countries and underestimates Africa (the formula gives 211 million feral hives in Africa when literature suggests closer to 300 million), in general, it seems to give not unreasonable estimates in comparison to the literature. Globally, this formula gives an estimate of 984 million wild hives. Given that land area included desert and other unsuitable habitat, it seemed reasonable to round down, and I took 900 million as my estimate.
Historical Populations

1961-2011
FAO statistics date to 1961. I plotted their numbers, with the 128% correction for each year. I assumed that during this time the number of wild bees has remained virtually unchanged, at 900 million, because it was defined by mean temperature and land area, which have not changed.*
1650-1961
This period represents the globalization of Apis mellifera. Before 1600, there were no European honey bees beyond their native range (Western Eurasia and Africa). However, once established in new areas (the usually cited first beehive in the USA in 1622), Apis mellifera rapidly spread in both managed and feral populations, in North America (17th c), South America (18th c), Australia (19th c) and East Asia (20th c) (Crane 1999)
.
I used carrying capacity of native range countries (just about 35% of the carrying capacity of the globe, or 350 million hives) as a before-1650 estimate,  and then assumed a geometric increase of about 2% per decade in available land area (ALA), as Apis mellifera bees and beekeeping made their way around the globe.
To estimate the number of managed bees during this period, I assumed a human:hive ratio of 35:1**, and modelled hives based on historical estimates of human population, multiplied by the ALA for the decade. The 1650 estimate was 5 million managed hives.

*Although diseases, pests, and pesticides have been reported to affect feral populations, I didn't find any solid information on this. For instance, feral populations of Apis mellifera mellifera and A. m ligustica have been widely reported to be in decline in the USA, but at the same time, feral populations of Africanized honeybees (Apis mellifera hybrids) have been rapidly spreading. Even with 90% losses in the USA, Canada, Japan, and Europe (areas affected by varroa) my estimates would only be decreased about 10%. However, it's also possible that land-use change has greatly affected feral bee populations (Moritz et al 2007).
**This wasn't a totally wild guess. I first calculated the human:hive ratio for 1961-2011. This ratio was increasing - there were 71 people / hive in 2011, and 47 in 1961. Initially, I assumed the rate of change in the ratio to be constant, but this led to unrealistically large estimates for historically managed hives. However, the rate was clearly increasing (just, perhaps in a nonlinear way I didn't want to estimate), so I decided instead to compromise on a number less than 47 and greater than 4. I decided on 35, as it produced what seemed like a realistic estimate of 5 million hives in 1650, compared to around 20 million today for Eurasia and North Africa (excluding sub-saharan Africa where wild-harvest remains important and likely was even more so in the past).

 Aizen MA, Harder LD. 2009. The Global Stock of Domesticated Honey Bees Is Growing Slower Than Agricultural Demand for Pollination. Current Biology 19: 4–4.
 Crane E. 1999. The World History of Beekeeping and Honey Hunting. Taylor & Francis. (Chapter 12).
 Jaffé RR, Dietemann VV, Allsopp MHM, Costa CC, Crewe RMR, Dall'olio RR, Rúa PPDL, El-Niweiri MAAM, Fries II, Kezic NN, et al.. 2010. Estimating the density of honeybee colonies across their natural range to fill the gap in pollinator decline censuses. Conservation Biology 24: 583–593.
Moritz R, Kraus FB, Kryger P, Crewe RM. 2007. The size of wild honeybee populations (Apis mellifera) and its implications for the conservation of honeybees. Journal of Insect Conservation


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Are there dangers to Teflon and aluminium cookware?
I've been reading some articles on the internet about dangers of Teflon and aluminium to the body.
My family say I'm just exaggerating the situation, and maybe I am, though I'm not sure because not everything on the internet is true. They always tell me that if aluminium were dangerous then why would the government allow the use of aluminium bottles in drinks.
Are there strong references and facts to support dangers associated with aluminium or Teflon cookware? If aluminium or other chemicals enter the body from cookware, are they naturally eliminated, or do they remain in the body?

I was recently taught in a module on chemical toxins that the Al in deodorants was more concerning because it was more readily being absorbed in the blood and that heavy deodorant users had higher circulating levels of Al in the blood.  I'm looking into actual sources now.  This question may also need some rephrasing to be sure it is not a personal health question.

I think that teflon that is still teflon is pretty darned chemically inert... the dangers are in teflon that has been damaged by heat and in the production of teflon which uses horrible chemicals... also Al metal is less dangerous than Al+3 compounds... and even then, most aren't soluble at all, but some give good routes to ingestion especially antacids.

@Daniela Diaz, I've edited the question so as to make it more useful to other users, and taken a stab at answering it below. I hope the edited question still reflects your intentions.

@Oreotrephes Your edition is perfect. Thanks so much.

The US Department of Health and Human Services has a nice set of factsheets on aluminum. In brief, and to specifically answer your questions, they point out that:

Aluminum occurs naturally in air, water, soil, and plants.
The amounts of aluminum that we encounter in pots and pans are considered to be safe for healthy people. Cooking acidic foods in aluminum pots increases the amount ingested, but is still considered to be safe; and it still represents many times less aluminum than in over-the-counter antacids, which are also considered safe.
Much of the aluminum we ingest leaves ones body naturally through the digestive system (that is, feces), and is not taken up into the bloodstream. The small amount of aluminum that makes it to our bloodstream is mostly quickly eliminated in urine. Those with kindey problems may not process this bloodstream aluminum as quickly.

Nonstick pan coatings are a little more difficult, probably because they're so diverse. Cookware isn't even mentioned as a source on the factsheet for perflouroalkyls, the chemical which has been mentioned in connection with nonstick pan health issues. The US Environmental Protection Agency FAQ says:

Consumer products made with perfluorochemicals include some non-stick cookware ... Consumer products made with fluoropolymers and fluorinated telomers, such as Teflon and other trademark products, are not PFOA. PFOA is used as a processing aid in the manufacture of fluoropolymers and can be also be produced by the breakdown of some fluorinated telomers [NB. I assume they mean overheating nonstick pans]. The information that EPA has available does not indicate that the routine use of consumer products poses a concern.

This is one of the articles I read: http://www.globalhealingcenter.com/natural-health/concerned-about-aluminum-dangers/                                              It contains some references and basically my concern is the part where it says that aluminium accumulates in different parts of the body and it causes problems with calcium absorption and demineralization, and also that is bad for the brain.

Well, it's always good to see citations. However, I would approach with a cautious eye any article that ends with an appeal to buy a product from the author.

Teflon® is a brand name for a man-made chemical known as polytetrafluoroethylene (PTFE) and it has been used since 1940s (discovered by DuPont Co.). Perfluorooctanoic acid (PFOA, also known as C8) is another man-made chemical and it is used in the process of making Teflon and similar chemicals (known as fluorotelomers), although it is burned off during the process and is not present in significant amounts in the final products.
Teflon itself is not suspected of causing cancer, but PFOA has the potential to be more of a health concern because it can stay in the environment and in the human body for long periods of time. Studies have found that PFOA is present at very low levels in just about everyone's blood in the US and it can be found at low levels in some foods, drinking water, and in household dust. It can be higher in areas due to contamination. People can be exposed to PFOA from fabrics, ski wax or carpeting which has been treated to be stain resistant. However non-stick cookware is not a significant source of exposure.
Studies in laboratory animals have found that PFOA exposure increases the risk of certain tumors of the liver, testicles, mammary glands, and the pancreas in these animals. Overall, well-conducted animal studies do a good job predicting that cause cancer in humans exposures. But for PFOA, there are clear differences in the way the body of laboratory animals and humans handle this chemical. Because of these differences, it is clear that the process chemical to cause cancer in animals also occur in humans.
Human studies have shown that people with workplace exposure to PFOS have a higher risk of cancer of the bladder and kidneys.
Several national and international agencies studying various substances in the environment, to determine if they cause cancer (carcinogens, substances that cause cancer and help cancer grow). However, at this time, these agencies do not formally assessed whether PFOA can cause cancer. The US Environmental Protection Agency (EPA), an electronic database that contains information on human health effects from exposure to various substances in the environment, has not officially classified PFOA as to its carcinogenicity.
Other than the possible risk of fumes from overheating the pan, there are no known risks to humans using Teflon-coated cookware. When PFOA is used to make Teflon, does not occur (or not present in very small amounts) in a Teflon-coated products. Because the way by which people may be exposed to PFOS are not known, it is not clear what steps to take for people to reduce exposure.
Currently, EPA states:

"Consumer products made with fluoropolymers and fluorinated telomers,
  such as Teflon and other trademark products, are not PFOA. PFOA is
  used as a processing aid in the manufacture of fluoropolymers and can
  be also be produced by the breakdown of some fluorinated telomers. The
  information that EPA has available does not indicate that the routine
  use of consumer products poses a concern. At present, the EPA does not
  recommend any steps for consumers to take to reduce exposures to
  PFOA."

Source: Teflon and Perfluorooctanoic Acid (PFOA) at Cancer.org


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All or none phenomenon
Let's say that the threshold potential of a neuron is +40 mV to make a muscle twitch. Now suppose we have two signals of +20 mV. So, this signal will cause the twitch in muscle because it has reached the threshold potential.
Suppose that we have many signal of +20 mV. Will this cause a lot of twitch, the same twitch or no twitch at all in the muscle? In other words, how will the twitch be greater?
Please be a little simple.

Are the stimuli arriving all at the same time or sequentially? If the latter, how far apart? You may want to look at this: http://en.wikipedia.org/wiki/Summation_%28neurophysiology%29

Is the question something like: Given the mecanism of threshold potential, how can we produce various ammount of intensity of muscle contraction?

I think you are asking about cooperativity.  In many biological systems the action of many individuals are coupled together such that when an individual is activated, the others are more likely to act as well.
The classic example of cooperativity is hemoglobin a protein which has four sites to bind oxygen (one in each of four protein subunits).  When there is enough oxygen present for a single binding site to bind oxygen, the other three will have an increased affinity for oxygen.  This makes the binding curve relatively steep.  Take a look at the graph.

When one oxygen is bound, three others also become bound. The more individuals in a cooperative system, the sharper the curve becomes until a very small change in a few individuals creates a very large effect very quickly.  "all or nothing" as you say.
Muscle contraction also is cooperative.  In this case there are many individual muscle fibers, both the myosin thick filaments, and the actin thin filaments.  Each fiber consists of chains of interwoven individual proteins.  When a myosin individual protein acts against a thin filament other myosins in that filament and those on other thick filaments that are bound to the same thin filament will react to the change in tension and also be more likely to activate and pull.  This causes the entire muscle to quickly start to contract together.  Most researches feel that all the various other factors contributing to muscle contraction, calcium release and uptake, other proteins that are associated with the thick and thin filaments etc, are cooperative as well.  A search for 'muscle contraction cooperativity' will give many references like these.


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Pollinator mating system in orchids
I came across three terms in an article on pseudocopulation. However I don't quite understand what it means.
They are:
1) solitary and haplodiploid
2) social and haplodiploid
3) diploid
These are mentioned in reference to pollinator mating systems in orchids. Could anyone please explain the above mentioned terms?

Can you provide a link to the article you read so I have context. I assume from the terms that the terms refer to the insect pollinators but I would like to be certain before I answer.

As 3cat already stated, the terms actually refer to the pollinators. While solitary and social describe the behavioural traits (see this wikipedia article), diploid and haplodiploid give information about the chromosome number of the pollinators (see here and here).
The descriptions in the article depict different combinations of both characteristics.


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Can rats pass on memories of a maze to their offspring?
A friend of mine told me once about a documentary movie he saw some years ago. On this movie he saw scientists talking about particular experiment. This experiment involved rats and probably electrical traps. The rat had to get to the cheese, there were traps on the shortest route to it, and obviously it got shocked few times. What is interesting is that my friend says that when they took its offspring (probably born later) they avoided those traps.
I'm aware that its not how "genetic memory" works. Its not memory of individual, but of species (so it requires evolution). This is what I'm trying to explain to him, but he says "he knows what he saw".
Anyway maybe someone here is aware of such an experiment. I believe that he is wrong about something (or conclusions drawn where changed later), so I would like to find out more about it.
To sum up:

Its not Tryon's Rat Experiment
It involved: rats, traps (probably electrical), more then one path to cheese, rat's offspring and some sort of memory/learning amongst rats.

This Nature Neuroscience paper published this week suggests that rats can pass on learned smell sensitivities to their F1 and F2 offspring. This is surprising stuff, so I imagine there will be a lot of close scrutiny and good conversation over the next few weeks. Here's a nice summary of the results from a National Geographic blog.

Here is a pop science article talking about "transgenerational epigenetic inheritance." Also, there is good evidence that another smart animal, crows, pass info between generations -- though this is perhaps due to a complex but subtle language that crows have rather than a genetic phenomenon...

The phenomenon you're talking about was a fad in the 60's, called 'interanimal memory transfer'. It started out when James McConnell performed a later-discredited experiment in which he found that if you chopped up flatworms which had been exposed to some stresses, and fed them to other unexposed flatworms, the unexposed worms became wary of the source of stress quicker after eating their dead companions. He jumped to the conclusion that a 'memory molecule' was being transferred, and that the cannibal worms gained the food worms' memories of the stress.
People then started looking to see if they could:

repeat the experiments
find the same phenomenon in other animals

In the first case, nobody could replicate the experiments in worms, but because McConnell was such a PR genius he managed to convince the public that his results were valid (see Rilling, 1996 for more on this).
In the second case, Frank et al. (1970) and others tried working with rats - I think this is the experiment you're talking about in the question. They found various interesting results including that if you trained rats to run through a maze by using particularly stressful negative reinforcement (like electrocution), then those rats' children would be able to learn the new maze much faster. However, Frank et al. didn't make the same mistake as McConnell - first of all they wondered if the parent rats might be leaving a scent trail. So they used duplicate mazes with the exact same design, putting the children into clean mazes. The children of adults who had already learned the maze continued to outperform the control rats - the explanation was not scent trails.
Next they wondered whether it might be that the second generation rats had been born with a higher wariness as a result of the stress their parents suffered; i.e. it could be a hormonal transfer from mother to child (e.g. cortisol, the stress hormone).
Frank et al. tested their hypothesis by torturing some rats for a while (rules about animal welfare were not strict in the 70's). They would lock some rats in a small jar and bash them about for a long time, then kill them, chop them up, and take out their livers. They fed the livers to other rats, and found that after eating the livers the other rats learned the maze much faster. They interpreted the results in what now seems a sensible light: the stressed rats were producing high concentrations of a stress-signalling molecule. When those rats either had children or were fed to other rats, they passed on high doses of the stress molecule. This raised the alterness and wariness of the receipient rats so that they were much quicker to learn which parts of the maze were dangerous.
There is no evidence that the child rats actually 'remembered' the maze - they still had to find their way around, but they were extremely wary of the electrocution plates and so avoided them, finding the safest way to the end. This is not a case of genetic memory.

 Frank B, Stein DG, Rosen J. 1970. Interanimal “Memory” Transfer: Results from Brain and Liver Homogenates. Science 169: 399–402.
 Rilling M. 1996. The mystery of the vanished citations: James McConnell’s forgotten 1960s quest for planarian learning, a biochemical engram, and celebrity. American Psychologist 51: 589–598.

That was probably part of the fad to test Lamarckian ideas, wasn’t it?

@KonradRudolph yeah I think that whole thing was started as a result of McConnell's charade. I came across a reference to this when reading Carl Sagan's Demon Haunted World the other day, where he cited it (the flatwork memory thing) as an example of high-publicity pseudoscience.

It also inspired a scene in THX1138 (early George Lucas film) where children are being fed their lessons through an IV bottle.

Did Frank et al. (or someone else) actually measure concentrations of "stress molecules"? I didn't read the paper, but based on your answer it sounds like a lot of speculation.

This is somewhat unrelated, and for that, I apologize, but I find it truly fascinating, and I believe you will too.
Zebra finches are a song bird that have become a popular model organism for behavioral research. They have a very stereotypical pattern for song learning: at about 70 days after hatching, the baby male song bird starts to listen to his father's song, copy it, practice it, and ultimately learn it. Female birds do not have a courtship song to learn.
Interestingly, if the baby male bird does not learn their father's song, they end up just kind of screeching, and never singing a song. This, in nature, makes them unable to court a female.
But in the lab, this research group did an experiment, where they took these screeching males, let them grow to adulthood, then teach their child as best as they can. The child, wanting to learn a song, takes what it can from the father. After 4 generations of this, the group was able to get de novo song production from these birds.
Unbelievable!
De novo establishment of wild-type song culture in the zebra finch - Fehér et al. - Nature, 2009

Very interesting! I have not had the time to read through the article yet, so I do not know whether they address this, but I wonder what happens if then you expose those 4th generation birds to birds that sing normally. Who would they choose? A screeching one or a singing one?

https://www.facebook.com/ScienceNaturePage/videos/1319435594855362/
I’m not sure if this is the right link, but there was a video on Facebook called “memories can pass between generations DNA” posted by hashem al-ghaili, it is 4 minutes and refers to an experiment where mice passed on maze knowledge to their offspring...

Welcome to Biology.SE! It isn't clear that this adds anything to the existing accepted answer. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best) — Facebook is well known for spreading misinformation and a video is not a good scientific source. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thanks!

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Is Schoons Hard Shell muskmelon a hybrid?
Would Schoon's Hard Shell muskmelon be considered a hybrid as I have read it was a cross between a Bender's Surprise and a Honey Rock.

Do you have a reference for where you read it?

Goldman surmises that Schoon's Hard Shell is a variant of the Bender, so would have been bred from the Surprise, Irondequoit, and Tip Top, all of which were from the Sill's Hybrid.
In that sense, I suppose it's a hybrid. I'm guessing that you're asking because you want to know if you can save the seed; that is, if Schoon's Hard Shell will breed true or will lose its characters in subsequent generations.
I can't find any specific detail on that, but given that it's sold by Seed Savers Exchange, I'd guess that it is a good candidate for seed saving, as long as you make sure it's not crossing with related species in your garden. Seed to Seed has detailed info on melon seed saving.

Goldman A. 2002. Melons. Artisan Books (p. 76)

Whealy K. 2012. Seed to Seed. Chelsea Green Publishing (p. 103)


text:
Chemoautotrophy in large organisms?
The major nutritional mechanisms include chemoautotrophy, heterotrophy (including parasitism and saprotrophy) and photoautotrophy. All of these modes of nutrition developed first in prokaryotic ancestors, and gradually, through the course of evolution, these prokaryotes formed complex eukaryotic, multicellular organisms. Some of these complex descendants (the majority of Kingdom Plantae) possessed the photoautotrophic mode and some (the majority of Kingdom Animalia, some of Kingdom Protista & Kingdom Fungi) possessed the heterotrophic mode.
My question is, since all the three modes developed quite early in evolutionary history, why didn't any chemoautotrophic multicellular, eukaryotic organism develop? (Or, if they did, why did they not form a wide-diverse group as the organisms with other two modes of nutrition did.)
(One possible reason could be lesser availability of chemoautotrophic substrates, but I have no proof, nor any argument to support this.)

i think its because organisms with more genes to regulate are not as competitive as organisms with many many genes and phenotypes. i.e. If there's a lot of sugar available from eating plants, making your own slows you down.

@shigeta There's also an advantage to ingesting and internally digesting biotic material - once you've eaten, you're no longer in competition with your neighbors those nutrients, so your meal can't be cut short by crowding.

@satwik-pasani While they would still probably be considered heterotrophs, there are a variety of insects that spit gastric(-like) juices onto prey and externally digest them, then suck up what's left.

I've been thinking about this question for a few days and along the lines of @ThomasIngalls comment, the simple answer is that cooperation between organisms has such a huge advantage in selection that any chance a eukaryote would become a chemautotroph would simply not adapt fast enough to compete with those that are already holding these niches.
The chemautotrophs I'm aware of are usually archaeabacteria.  They are optimized to grow slowly and have a large number of genes that can break down the unusual chemical compounds to grow in an inorganic often anoxic environment.  These bacteria have genes evolved from the chemautotrophic earliest days of life on earth.  They live deep within the earth, under ground, in volcanic vents.  There are animals that live in some of these environments, but its simply too easy for these to use the bacteria that are already growing here readily rather then re-evolve the genes to do it by themselves.
Eukaryotes are already symbiotes - they used bacteria to create ATP and photosynthetically fix carbon to the extent that they absorbed them as mitochondria and chloroplasts respectively.  If eukaryotes were under a tremendous amount of selective pressure, some of them might absorb symbiotic chemautotrophs, but without such pressure, it doesn't happen when you are competing against plants with roots and animals that eat for their energy.
Forming systems of organisms is much more stable than having individual species that can do it all.  This question is actually similar to other questions that ask why we don't have metal armor, run as fast as cheetahs, etc.  Evolution doesn't actually create super animals that are completely self contained.  The ones that reproduce the best are the ones that can actually spread out the risk of survival and contribute to an ecosystem.
It kind of makes me think of human beings - the only superorganism on the planet in this regard.  We don't really need to compete against any organism - we are in fact killing most of them out there without really thinking about it.  That might now turn out to be good for us long term.


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How do animals/plants change for each season?
The question pretty much sums it up. How do animals/plants change for each: Spring, Summer, Autumn, and Winter?
A detailed explanation on distinct behaviour and appearance changes would be nice.

i'll answer the mechanism for plants as of now.

I flagged this question as "too broad" because, well, isn't it ? Could you maybe give some reason why you're asking this or share some research you've already done on the question to help people orient their answers more precisely ?

There are various parameters that describe change of seasons such as day length, temperature, humidity. But it can be assumed that most of these parameters ultimately depend on one parameter- day length.
The response of plants towards the length of day/night cycle is called photoperiodism (which dictates spring flowering).
This article explains the effect of a gene called CONSTANS(CO) on spring flowering. CO is post transcriptionally regulated by cryptochromes and phyochromes.

The circadian rhythm in CO mRNA abundance was proposed to represent a photoperiod response rhythm, in which exposure to light coincides with CO expression only under LDs (Long Day) and thereby triggers flowering.
......
We propose that early in the day phyB promotes the degradation of CO whereas in the evening cryptochromes and phyA antagonize this degradation and stabilize CO protein,

However, my knowledge of plant molecular biology is not that great and I would advise that you refer the mentioned article and the cross references cited in that.

Thanks for the reply, can't wait for the follow up on animals.


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About validation process of phenological study
I have recently done a phenological study using remote sensing techniques. Now I need to validate my results and my methods, that is, to determine if the phenology estimated from remote sensing is suitable to describe phenological events or not. However, I don't have empirical phenological data from the ground to do validation.
Are there any other ways to validate the phenological signal from remote sensing, that do not require empirical data from the ground?
Thank a lot

What phenological trait are you trying to measure and in what type of environment?

...and what type of remote sensing data are you using?

I obtained onset of green-up, maturity plant growth, off-set of green-up, grown season length and I used NDVI and EVI data extracted from MOD09A1.

Update your Q with this info and it will be easier for other to answer it.

idea 1) It's possible that some subset of your area has higher-scale / better resolution aerial photographs available. Could you find these and use them to test your model?
idea 2) What geographical area / timescale are you looking at? For certain areas/times, you can get a bit of data on phenology from dated herbarium specimens (ie pressed plant collections). So, for instance, you might select a few plant species that you think are good indicators of whatever phenology you're modelling, search for them on GBIF, consider only those specimens that match your geographical area, and look at what time of year the collections have been made. Then you could look at the first, or last, or various quantiles of phenology. It's not ideal data, but each specimen represents a very direct data point (that is, you know there was at least one individual that had flowered / leafed / whatever at that exact date and georeference), and it's available without getting your feet dirty.
idea 3) Again depending on your geographical area and what measure of phenology you're interested in, you might even be able to use non-aerial photographs, if they're dated.


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What are the most well-understood vocal animal languages?
Just as the Bee dance, for a "language", I mean that there are vocal pattens, or "grammar".
In the nature, there are many intelligent animals like human beings.
Bird songs, whale songs, dogs?
In fact, bird vocalization includes both bird calls and bird songs. There are Parrots, hummingbirds and songbirds,...
I wish to know the most well-understood vocal animal languages. Which species?

"most well-understood" is rather subjective, this question doesn't really fit the Q&A format well. It is also cross-posted on CogSci, so I'm closing it here on this site.

@MadScientist Why subjective? Apis mellifera is one of the most well studied animals, if not THE most. Is this subjective? I know of some African monkeys that we know have distinct words for "snake", "eagle", "hierarchy above", "hierarchy below". I know some whales can repeat exactly the same song one and a half hour long. I think the question is very interesting, and it will have different answers here than it will on CogSci, and probably very interesting answers. So I vote to reopen it.


text:
Polymorphism in cnidarians?
To me, the phenomenon of polymorphism in cnidarians is particularly troubling. I gather that it essentially refers to existence of various different forms or  kinds of individuals, i.e. zooids and polyps in one species. But when we refer to the cnidarian Physalia, as an animal, aren't we actually referring to a colony of individuals? Physalia consists of several "entities" including gastrozooids, dactylozooids, and the float, and since each of these is a distinct "organism", therefore is what we refer to by saying Physalia is actually a colony of phenotypically distinct forms of the same species?
Therefore, can "animals" like Physalia or Gorgonia or Pennatula be thought of actually as "colony-beings" which always contain several individuals in group?

It seems like your question might contain two separate and linked issues, both of which are perhaps equally confusing and equally interesting. They're both really discussion questions in a sense, but they've also both been dealt with in the literature in thoughtful ways, so here's a stab at an "answer".
Issue One: how does your species concept deal with polymorphism?
This may depend on which species concept you're using. And, to some extent, the choice of which species concept you use depends on what kind of organism you're dealing with (for instance, organisms that reproduce asexually have a whole different set of issues and challenge several species concepts).
Various papers by Kevin de Queiroz deal very well with species concepts. In 'The General Lineage Concept of Species'  (which is also summarized on this page), he argues that although there are many different species concepts that can be better applied to different situations, they all share the basic tenet of defining a "segment of a population-level lineage". In other words, each concept is attempting to put a continuum into slightly different categorical bins, but they all recognize the existence of the same continuum (the lineage). (Also see his 'Species Concepts and Species Delimitation'.)
I think most species concepts have no trouble dealing with polymorphism because the different morphs are all part of the same lineage, that is, "a series of entities forming a single line of direct ancestry and descent" (de Queiroz 1999).

Issue Two: how does your concept of the individual organism deal with colonialism?
In 'Does Biology Need an Organism Concept?'  Pepper and Herron make a similar point to that of de Queiroz. They argue that multiple definitions (concepts) exist, and that these concepts all attempt to categorically bin what is in fact a continuum. Like de Quieroz, they argue that most definitions recognize the same underlying continuum, and that the difference is in the categorical bins.
In the case of the organism concept, this continuum is based on two criteria: increasing genetic homogeneity, and increasing physiological integration.
So, for instance you could have two organism concepts (in the picture below, lighter yellow and darker yellow) that agree that Physalia falls in the same location along these axes, but disagree on exactly where to draw the boundary between their "multiple organisms / colony" zone (yellow), and their "individual organism" zone (white).

I'll finally get to my point, paraphrasing both de Queiroz and Pepper and Herron. For both concepts of the species and of the organism, arguing about whether one concept is better than another is endless (especially on a site that aims at answers rather than discussion). However, recognizing that there are different concepts, understanding that what these concepts do is to bin the same continuum in different ways, and being clear about which concept you decide to use is very useful.

The easiest way to understand this, in my opinion, is to think in social insects. In the ants, for example, there are polymorphisms, since the workers don't have the same phenotype as the queen or the soldiers. Also, one could argue that the whole colony is a massive metaorganism or superorganism, formed by the summation of all the individual ants.
As in an ant colony, in the case of Physalia, each one of the zooids have a fully formed body (cnidarians have a distinct body plan, consisting of a sac-like digestive system with a mouth crowned by tentacles, two embriologycal layers, etc.) and thus each zooid should be considered to be different individuals. In Physalia, the zooids are physically attached, but that's no different than siamese twins, who aren't usually considered to be only one organism.

While refering to an animal say Physalia, we refer to its massive type colony, containing many zooids. Among the zooids, a large cup shaped float is seen, which is bright blue in color and remains above sea water normally. On the undersurface of float many gastroaooids, gonozooids and dactylozooids are present. The colony thus shows a high degree of polymorphism.
This is all I know and thus the reasoning seems to be absolutely correct...


text:
Eusociality and Natural selection?
Eusociality, particularly focusing on the presence of certain altruistic sterile organisms within the social set-up creates questions as to why would the process of natural selection have favoured the persistence of such genes especially in hymenopteric species. One explanation (provided probably by Hamilton) pertains to very similar genetic constitutions of females of such species (owing to haploid nature of males), which increases genetic similarity between the female members of the social group. Thus it would be more "beneficial" (i.e., favourable for the persistence of similar genetic builds) for a female worker to help the fellow siblings, to which it bears greater genetic similarity, than its own offspring to which it bears a lesser genetic similarity. This might in a deeper way explain altruism in case of hymenopterans where the male is a parthenogenetic haploid and the female is diploid.
But why would the sterile condition of the workers in case of almost all eusocial groups be favoured by natural selection on grounds that it improves the 'fitness' of the 'genetic build' of the workers and ultimately the sterile altruists benefit the persistence of its genetic traits? Moreover the altruistic nature of the haploid males also goes unexplained.

In what way are the haploid males altruistic? In the eusocial insects that I know about (not many) they act only as drones i.e. sperm donors, making no contribution to the success of the colony.

The female workers are altruists in the true sense. The drones, though not altruists by definition, follow or rather hold a social position wherein they take a part only in the societies' development through mating with the queen and do not improve their personal 'fitness' directly. Moreover, a number of drones might not even mate with the queen but still their presence has not been eliminated by natural selection.

I might be misunderstanding, but it seems as though "mating with the queen" is best possible thing you could do to improve 'fitness'! Remember, fitness is number of children, or grandchildren, or great-grandchildren, and in that sense while it applies to an individual, it doesn't manifest except through mating.

A related post: http://biology.stackexchange.com/questions/13693/empirical-evidence-for-group-selection

I hope I've interpreted your question properly... It's an interesting question, but I think it's important to remember that evolution doesn't act on the two sexes separately. Sterile males might evolve and be maintained simply because they're good for their sisters or mothers. Sometimes genes that are advantageous for one sex are linked with genes that are disadvantageous for the other sex, leading to maladaptative traits in one sex. And of course, individuals don't necessarily forego opportunities willingly. If subordinates that attempt to mate are killed by the dominant individuals, then that trait is not advantageous. They'd be better advised to be altruistic and help their relatives, rather than be selfish and be killed (thereby depriving their colony of a worker). This would lead to selection for sterility.
It's also worth noting that while haploidy makes it easier for kin selection to evolve by increasing relatedness, it's not crucial. It all depends on the relative costs and benefits.
In these eusocial situations, nothing really makes sense until you summed the fitness of the whole lineage, not just one caste or one sex or one individual.

There are also a lot of systems where the "satellite/helper" males do just fine by sneaking in copulations when the dominants aren't looking.

True, but I'm not aware of many examples of sneaking in properly eusocial species?

Fair enough, but maybe that's just the terminology we use. There are, for instance, female cheater worker bees (they call them, I'm not joking, "anarchists") who decide to start reproducing on the sly.

+1 for anarchists. I've heard of this - I believe they get very harshly punished if they're caught!

@Oreotrephes Source on the anarchist bees?

@Alex it must have been one of the sources I ctd in this question http://biology.stackexchange.com/questions/5076/modern-reference-for-kropotkins-lazy-bees but I'm not sure which.

Try the 2001 review "Worker reproduction in honey-bees (Apis) and the anarchic syndrome" by Barron and there are also more recent publications.

Group selection, in the extreme, yields eusociality due to the shared fate of the replicators in the group.  In a multicellular sexual organism, this "shared fate" of the "group" is the shared prospect that all replicators (alleles) have for making it into the next generation via the meotic lottery that produces the gamete.  Since they share this prospective fate they have an evolutionary incentive to cooperate in the construction of specialized cells that are, in effect, "sterile caste" members of the total "hive".  Similarly, if it is possible to subject all members of a group of individuals to a shared fate through multiple generations -- they will tend to evolve highly cooperative social structures.  However, one of the confusing aspects of the eusocial insect colonies is whether they evolved to be that way through shared fate of individual organisms, or some variant on the meotic lottery's shared fate of alleles.  The answer appears to be, primarily, that it is a peculiar form of meotic lottery in which the genes of the parents have extended phenotypes in the children that, in essence, parasitically castrate the vast majority of the children to help rear more offspring for the parents -- in particular the queen.  In this respect, one can view the evolution of eusociality in the social insects as a perverse form of individual selection where the genes of, say, the queen, cooperate in constructing not just the queen's body but, also, the entire hive.  The sterile castes are simply extended phenotypes of the queen (and the  drone with which she mates).
See "The Social Conquest of Earth" by E. O. Wilson for an in-depth treatment of eusociality and its evolution as set forth by Nowak et al in their recent paper "The Evolution of Eusociality".  See also "The Extended Phenotype" by Richard Dawkins -- in particular the chapter "Host Phenotypes of Parasite Genes".


text:
What is the formal terminology for two species that are "close" to each other in a phylogenetic tree?
Take for example the human and the chimpanzee, they are "closely related" species since they are "close" to each other in a phylogenetic tree. However, this terminology seems pretty informal, what would be the formal way to specify that two or more species are "closely related"?

What do you mean by "formal"?

The way that you would find it written in a scientific journal.

Are you looking for something like "sister lineage" (or "sister taxon" or "sister group")
This term may be more specific than what you're looking for, and to use it correctly you'd want to be a little careful – I guess in this case you might have to say something like:

"the lineage that includes chimpanzees and bonobos is sister to the
  lineage of which humans are the only extant species"

or

"the lineage that includes chimpanzees and bonobos and the lineage of
  which humans are the only extant species are sister lineages"

both referring to this phylogeny.

It's also possible that explaining exactly what you mean by 'close', or what it entails, would be appropriate, be it Ilan's suggestion of % genetic similarity (or maybe genomic similarity?), # of nodes between your two taxa (again, this would have to be in reference to a specific phylogeny), or if you have a dated phylogeny you could refer to the time since divergence, as in "coding DNA divergencies ...place the most recent common ancestor of humans and chimpanzees at between 5 and 6 million years ago."(Wildman et al 2003).

Sister lineages would have been my suggestion..

But of course it depends about context, I mean, e.g. fungi and animals are sister lineages just as much as bonobos and chimps..

Good point 5heikki. It's one of those terms like 'endemic' that is pretty meaningless without context.

As genus comes above species I'd consider using this term for the species which are close genetically ("these two species are from the same genus"). Above genus comes family etc...
On the other hand, the proximity or similarity of species could be probably "measured" by degree of biodiversity, and especially genetic diversity considering two close species having low biodiversity and very different species as having higher biodiversity.
Thirdly, and I feel that this is the most strong term to use, you can "express" the genetic closeness of species as being "genetically similar":
"Some monkeys and humans have 98% genetic similarity" or "are up to 98% genetically similar" or "... DNA similar"...


text:
Does tea have its effect if you have a sleep after drinking it?
If I drink tea, then go to sleep for a while, when I wake up, will the effect of tea still be on me (the refreshing effect)?
Does it depend on the duration of sleep?

Caffeine is the stimulant in tea. It has different effects on different people, but if you can sleep right after drinking it, it probably isn't strong enough to have long term 'refreshing effects', And yes, the duration of your sleep does matter. If you sleep for 12 hours, much more caffeine will filter out of your blood stream than after a 1 hour nap.
Some info on how caffeine works, from here:

Caffeine, a component of tea, coffee and cola, induces wakefulness. It binds to adenosine A1 and A2A receptors as an antagonist, but the receptor subtype mediating caffeine-induced wakefulness remains unclear. Here we report that caffeine at 5, 10 and 15 mg kg-1 increased wakefulness in both wild-type mice and A1 receptor knockout mice, but not in A2A receptor knockout mice. Thus, caffeine-induced wakefulness depends on adenosine A2A receptors.


text:
What are the ecological effects of moderately high and prolonged concentrations of nitrogen deposition on an ecosystem?
There are many sources of nitrogen which eventually get deposited out of the atmosphere and onto the land/surface.  Typically higher levels of nitrogen compounds are emitted near urban and roadway locations, raising the levels of nitrogen deposited on the nearby landscape.  What are the ecological effects of moderately high (at least double background) and prolonged concentrations (10+ years) of nitrogen deposition on an ecosystem?  Please be specific about which type of ecosystem your comments are intended.

Would help to define magnitudes. Prolonged = decades? Moderately high = 5g/m2/y?

Too much nitrogen can run off during rain and collect in ponds, leading to eutriphication, find more here: https://en.wikipedia.org/wiki/Eutrophication
It's probably also responsible for dead zones: https://en.wikipedia.org/wiki/Dead_zone_%28ecology%29
This is an important question because we've more than doubled the amount of bioavailable nitrogen on Earth in the last 100 years simply because of the haber process and man made fertilizers. This amount of nitrogen has never been available before.


text:
Is light required for seed germination?
Is light required for germination of every seed? If not, why don't some plants require it? Is there any difference in the quality and duration of light required ?
It would be interesting if someone could give both  physiological and evolutionary reasons.

Given that germination often happens underground, the answer seems trivially “no”, doesn’t it?

@konrad My first thoughts were the same ! but then I came across  an experiment in which they had exposed seeds to different wavelenghts of light  and they got difference in no of germinated seedlings.

The riddle can be solved by realising that different plants have different requirements, and that some requirements are “soft” – i.e. not absolutely necessary but nevertheless beneficial. I’ll let somebody else with more knowledge provide a more in-depth answer – my comment wasn’t meant to imply that this is a bad question.

Botany was long ago, but if I remember correct, the germination happens usually underground as the seeds contain enough material to supply the developing plant for a while. When it comes through the surface it usually needs light to do photosynthesis to grow further. Most seedlings orientate towards the light.

The short answer is that many species do require light for germination (either to initiate germination or to break dormancy). Some require light of a specific wavelength, and some don't require light. Still others actually require absolute darkness, or the absence of specific wavelengths.

@KonradRudolph in many species, germination can happen underground but not so far that light doesn't penetrate.

Here's a partial answer, based more on common-sense then in-depth knowledge:
Physiological. One reason light is not required immediately is that many seeds are in essence bundles of stored energy (as carbohydrates, I suppose). This is what makes them attractive food for birds, squirrels, humans, etc. When they're able to escape that predation, the growing plant can use that stored energy, rather than relying only on sunlight.
Evolutionary. Seed dormancy can be a powerful tool for fitness – seeds that can remain dormant and germinate during favorable conditions could have a much higher survival rate. These conditions vary from simple: "spring" to more complex: "after having passed through the digestive system of a certain animal"; "after a forest fire"; "when there's a gap in canopy cover / less competition for solar energy". The cues that seeds "read" in order to try to break dormancy and germinate during these times therefore vary among species. Within species, there are probably often a number of cues, and as @Konrad Rudolph suggests these are probably all relatively "soft", or at least act in complex interaction with one another.


text:
Does a fully-resolved phylogenetic tree have to be dichotomous?
I read that wherever there is polytomy there is an unresolved pattern of divergence. I don't understand why this is so.
When divergence takes place, is it necessary that there will be division into only 2 paths? Can't there be more than 2 paths with all the paths being equally related to each other (that is, no 2 paths being related more to each other than to a third path)?
In other words, does a fully-resolved phylogenetic tree have to be dichotomous?

In theory, yes, every tree has to be dichotomous. You can understand a trichotomy in a tree as the summatory of two dichotomies that had happened so close in time that you cannot know wich was first.
Given a certain population, assume that some individuals colonize a new environment, got reproductively isolated and form a new specie. This is the typical speciation process. In this case, the two species, share a common ancestor. If you go back in time, all the individuals of the new specie will descend of only one individual. The same goes for the original specie. If you go back further, this individuals will share an ancestor, too. This is the conceptual meaning of the dichotomy, but normally it is impossible to determinate wich was exactly the common ancestor.
Now imagine that the original population formed not one, but two new species. And that this process happened about the same time as the one described before. It is conceptually possible that a set of three brothers were the origin of three different species (wich will be a true trichotomy), but not only it's very unlikely, but it's virtually impossible to prove. Since two close dichotomies are far more probable than a trichotomy, it's assumed that every tree has to be dichotomous, and that a trichotomy is in fact due to lack of resolution.


text:
How can I text-mine full-text articles from PubMed?
I want to do a text mining study using full-text versions of articles I find on PubMed. My intended search protocol will be roughly as follows:

Search PubMed using a gene name (and any alternate names) as the query, all matching papers are subjected to Step 2; my understanding is that this will return articles that mention the gene in their abstract
Search full-text for any and all matches from a list of keywords; assign each paper a score based on the number of matching keywords; any papers that match have to be read by a human but the most relevant papers will have a higher score and get read first

The two-step search needs to be repeated many times with different genes in Step1 so an automated approach is probably worth the time it will take to develop.
I know enough about programming that I could write a script to do Step2 if I had the paper as a plain-text document (I program in Perl but I also know a little Python) but I have no idea how I could automate the process of searching for papers, downloading them, converting them to plain-text documents that my program could work on.
I considered posting this in StackOverflow but have opted for this site because I have not ruled out the possibility that this can be done without doing my programming.
UPDATE: I have found one tool that might be very useful for exactly this problem. Unfortunately, I am not in a position to ask for a free trial so I cannot evaluate it. Even if it is an appropriate tool, I will most likely not be able to use it for my study.

Thats interesting. Would be interesting so see if there is a ready solution for it.

Do you mean all papers indexed in PubMed, or only those in PubMedCentral that have free full text available.

All papers, @MadScientist

Note that bulk-downloading papers without permission may violate the terms of use of the repositories or journals where they are hosted.  Journals could revoke your subscription (or your institution's) or threaten legal action.

@NateEldredge, thanks for pointing that out. Do you think I could get around that problem by setting up my pipeline to download then analyze each paper before downloading the next one?

I doubt it.  They would probably look for an excessive total number of downloads in a month; a short delay between downloads wouldn't help.  Worst case scenario: http://en.wikipedia.org/wiki/Aaron_Swartz

I'm voting to close this question as off-topic because this is a question about mining and sifting data not Biology.

I appreciate your point about this question being off-topic. My rationale for posting it here is because of the possibility of finding PubMed-specific solutions; something that could be helpful to biologists with limited computer skills.

Below is a Python script that might help you to get started  (apologies if it fails the Pythonic test - it works!). It uses the Entrez part of the Biopython library. The script sets up a query, in this case yeast AND Saccharomyces against the pmc database. Also note that this script uses the 2 step process that NCBI likes you to use - the first part of the fetchByQuery function gets a set of results then the second part uses those results to actually obtain the data.
The output is an xml file which you get to parse with your favourite tools. In your case you will need to get out the text sections and do your token analysis. If you use Python for that I recommend the Natural Language Toolkit (NLTK).
In your case you could just set up search terms as a Python list and loop through writing each dataset to a file named from the search term.
from Bio import Entrez

import urllib
import urllib2
import sys

def fetchByQuery(query,days):
    Entrez.email = "xxx" # you must give NCBI an email address
    searchHandle=Entrez.esearch(db="pmc", reldate=days, term=query, usehistory="y")
    searchResults=Entrez.read(searchHandle)
    searchHandle.close()
    webEnv=searchResults["WebEnv"]
    queryKey=searchResults["QueryKey"]
    batchSize=10
    try:
        fetchHandle = Entrez.efetch(db="pmc", retmax=100, retmode="xml", webenv=webEnv, query_key=queryKey)
        data=fetchHandle.read()
        fetchHandle.close()
        return data
    except:
        return None

days=100 #looking for papers in the last 100 days
termList=["yeast","Saccharomyces"]

query=" AND ".join(termList)
xml_data=fetchByQuery(query,days)
if xml_data==None:
    print 80*"*"+"\n"
    print "This search returned no hits"

else:
    f=open("pmcXml.txt" ,"w")
    f.write(xml_data)
    f.close()

I think it's possible with Entrez Direct
You'd start with something like:
esearch -db pubmed -query "atp6"

And then pipe that to maybe efetch -format ?? and then continue with gnu coreutils. It might be that only abstracts are available as text, in this case, you'd have to extract e.g. pubmed ids and then come up with a way to batch fetch those somehow..


text:
How are our senses dimmed during sleep?
Our senses are not as sensitive during sleep compared to wake. There is an arousal threshold during sleep that only when it is overcome will it wake a person up. My question is how is this arousal threshold lowered as sleep progresses? And how it is raised again during the latter stages of sleep?

At night several changes occur in the body due to absence of sunlight and other surrounding changes. The biological clock inside the body performs certain function in a healthy body whenever changes are sensed.
There are many receptors in our body located on cell membrane. They are made up of proteins and their function is to receive information from neurotransmitters. This information will be sent to specific part of the brain. If we take sensory information then it is Parietal lobe. This lobe receives the sensory information from all over the body and responds to it when body is active. During sleep, the senses that go through the thalamus, are shut down by gating either in the Nucleus Reticularis Thalami (NRT) or in the Thalamus itself. GABAergic inhibition of the thalamus, most likely deriving from the NRT is probably a part of the reason that sensory stimuli doesn't penetrate during sleep.
This is also influenced by release of hormones in the body whose level when rises in the blood causes certain changes in the concentration at some regions such as receptors which gets blocked temporarily and stops signaling the brain. There is a study on how muscle relaxes when we sleep can be found here Muscle sleep. So it is all the neurotransmitters job at the receptors which stops signals going into brain but internal to the brain it will be active controlling other routine works which it has to do when we are asleep.
The main thing to note here is the 5 different stages of sleep such as non-REM and REM sleep. During those stages several changes take place in the body. The below website gives an excellent insight into different changes happening inside the body when body takes rest at night.
Please refer to "What happens to your body while you are asleep".

Another lead are sleep spindles, closely related to the RTN as mentioned before. Basically the thalamus enters a state of high-frequency firing to a low-frequency synchronous one, thereby taking the cortex with it. Sleep spindles are slow-wave potentials as apparent on the EEG that block out the normal flow of peripheral sensory information from thalamus to cortex. Basically this leads to a loss of consciousness as one is unaware of its environment. A similar thing occurs during absence epileptic seizures, where patients temporarily loose consciousness as marked by paroxysmal slow-wave EEG activity interrupting the high-frequency EEG associated with consciousness Kostopaulus (2000). Hope this helps.

When you're awake; the sensations around you as well as your mental will, keep your mind active. How the air smells and what needs to be done all contribute to your day. In order to sleep your brain must weaken these receptors significantly, though not enough that if we heard something too loud or unfamiliar (such as a predator), we overlap those boundaries that keep us resting and wake. Now of course i am talking about the middle of the night. As morning arrives the amount of stimuli needed to overcome the wall that is sleep is diminished, allowing something such as the crowing of a rooster to wake us up.

That's a common theory, but the question is how? How are these 'receptors' weakened? What it is that controls both these receptors and sleep?


text:
The smell from eating asparagus
I am wondering about one thing. I have read different accounts of this (prior to reading it on Wikipedia), so I am wondering.
Here are the two versions I have read:

asparagus leads in a certain percentage of people to a smell that has to do with a reaction of asparagusic acid. That is: not every human body creates the reactions leading to the "smelly" thiol (sulphuric) compounds.
asparagus leads to the processes of the aforementioned asparagusic acid in everybody but only a part of the population is able to smell those compounds.

Which one is true? Or is perhaps some other version I haven't heard about.
btw: The Wikipedia article on asparagus references both versions, too. So I am hoping for a definite answer with references to the respective scientific papers/studies.

Apparently, both are true.

...Individual differences exist in both odorant production and
  odor perception. The biological basis for the inability to produce the metabolite in detectable quantities is unknown, but the inability to smell the odor is associated with a single nucleotide polymorphism (rs4481887) within a 50-gene cluster of olfactory receptors. Pelchet et al. 2010

It's an open access paper (yay!), but to cut a long story short:

Pelchet et al. asked subjects to provide 'before-eating-asparagus'
and 'after-eating-asparagus' urine.
The subjects then acted as
urine-smellers for their own and others samples, and were asked to
choose between two unlabeled flasks which contained the 'before'
urine and which contained the 'asparagus' urine.
Most subjects produced 'asparagus' urine in which an odor was perceived
significantly more times than expected by chance, and
Most subjects perceived 'asparagus' urine correctly significantly more times than
expected by chance, however
~8% of subjects were non-producers, and
~6% of subjects were non-smellers.
Finally, looking at the actual amount of successes in perception: for
Caucasian subjects, one third of the variation in the amount of
correct odor perception was related to the A allele of rs4481887
(having AA or AG rather than GG). There was no connection between
this allele and production.

Pelchat, ML, C Bykowski, FF Duke, and DR Reed. 2010. Excretion and perception of a characteristic odor in urine after asparagus ingestion; A psychophysical and genetic study. Chemical Senses doi:10.1093/chemse/bjq081

Best sentence ever in a methods section: "The raw asparagus (125 g) was prepared by combining it with 1 teaspoon of extra virgin olive oil (Colavita brand) and 0.8 g kosher salt and broiling it for 8 min."

haha.. seems like a cookery manual :D

@Oreotrephes: guess it's just reproducible this way. Thanks and +1.


text:
Species Identification - small insect: is this a bed bug?
I found this bug in my apartment in Chicago.  We had bed bugs in our house the previous year (but we thought we got rid of them).  This bug was very small - maybe 2 millimeters in length.  These photos are all of the very same bug (just different lighting).

Can you smell almonds? Bud bugs have a distinctive smell usually described as being "like almonds".

No noticeable smell.

See my answer to Insect identification - Is this a bedbug?

This is a really old thread but just in case someone happens upon it, this isn't a bed bug.
I am not an expert but it looks like it's likely a book louse or psocid.
See comparison photos of unfed first instar bed bug nymphs vs. psocids/booklice here: http://bedbugger.com/2008/03/04/booklice/
It's all about the shape of the head and body.

I agree, I've had book lice in my Fly lab before and this looks rather like it!

Thanks for following up with this.  I think you're right, the photo you linked to looks spot on.  Actually, the lady in the apartment above us had lice one or two times during this period - so that must have been what I found.  Actually, I'm relieved, I'd rather fight lice than bed bugs.  Either way, our apartment seems to be bug free now.

This is deifnitely a psocid species. See here for another SE example.

Also book lice are not the same as head lice (and are in fact in totally different orders)

Wow, the internet is weird!  Can't believe that I took a photo of a very tiny bug with my phone and then someone across the world identified it.  Modern society is pretty trippy man.


text:
What is a good source for info on disease frequency distribution among age groups?
I need information on the disease frequency distribution among age groups for an Android app I'm building... Hopefully I've come to the right place. Is there a good data source for this? Like a bioinformatics database?

I'd say this is also a bit vague in its current format, could you expand on what sort of information you are looking for.

As the title says, I'm looking for the frequency distribution among age groups...Something like what percentage of type II diabetes patients are among age 40-50. And it's not just the distribution of one specific disease, but all kinds of diseases.

You may need to study each disease individually or do a literature review.  The Online Mendelian Inheritance in Man website may be a good starting point http://www.omim.org/
The Centers for Disease Control and Prevention lists several diseases with a variety of different statistics here:  http://www.cdc.gov/DiseasesConditions/

I've been to the CDC site. I guess I can use the statistics there, but what makes it less ideal is that ages <18 are not included. I am currently working on other stuff, so please feel free to improve your answer in the next few days :) I'll accept your answer if no other better ones pop up.


text:
What is a good identification key for European mushrooms?
I live in the Netherlands, and I am looking for an identification key for mushrooms.
Are there any keys you could share?

1
2
3

There are various types of Mushroom identification Sites. you can take help from:

Mushroomexpert
Rogersmushrooms
MycoKey 4.0

Source: MycoKey 4.0