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How does Natural Selection shape Genetic Variation?
Background
Importance of the additive genetic variance
As stated here, the fundamental theorem of Natural Selection (NS) by Fisher says:

The rate of increase in the mean fitness of any organism at any time ascribable to NS acting through changes in gene frequencies is exactly equal to its genetic variance in fitness at that time.

NS reduces the additive genetic variance
On the other hand, NS reduces additive genetic variance (discussion about the origin of this knowledge can be found here). The genetic variance of a population for multiple traits is best described by the G-matrix (here is a post on the subject).
What is a G-matrix
A G-matrix is a matrix where additive genetic variance of trait $i$ can be found at position $m_{ii}$. In other words, the diagonal contains the additive genetic variance for all traits. The other positions $m_{ij}$, where $i≠j$ contains the additive genetic covariance between the traits $i$ and $j$.
Question
How can one model how the G-matrix changes over time because of selection (assuming no mutation)?

Great question - I know there is some theory on it, I will do some reading on it but I'm off to a quantitative genetics course tomorrow so maybe I'll have a good answer after that!

You can perhaps ask how can it be modeled instead of "is there a model". In any case the question boils down to - how does a selection operation (random sampling) affect covariance matrix. This is more of a statistical question.

Post edited! Yes, indeed the one who wish to answer this question will probably need some knowledge in statistics.

First of all, here is a program which simulates the evolution of the G-matrix over multiple generations, it's a few years old (they seem to have stopped developing it) and I've only played with it briefly. This could solve how to model the evolution of the G-matrix.
Fisher's fundamental theorem is a great place to start off with the theory of this:

The rate of increase in fitness of any organism at any time is equal to its genetic variance in fitness at that time.

What this means (as I am sure you realise but I will put in so the answer can help others too) is that evolution by selection depends not only on the strength and form of selection, but the genetic variation underlying the selected trait. This is captured in the breeders equation $\Delta \bar z = G \beta$  where $\Delta \bar z$ is the response (in a multivariate space), $G$ is a matrix of the genetic variance within traits covariance between traits (different traits, the same traits in either sex, or the same traits in multiple environments) and $\beta$ is the vector of selection gradients on all of those contexts. It seems reasonable to expect that given enough time selection will erode variation because standing genetic variance is a finite resource and selection removes polymorphism while not adding any new variants (that's for mutation & migration).
This paper discusses the effects of both selection and drift on the G-matrix, they also deal with some modelling to support their results. More specific to simulation, this article by Arnold et al (a number of the big players in the G-matrix circle). It reviews "empirical, analytical, and simulation studies of the G-matrix with a focus on its stability and evolution." It would be a really good read for you on this subject.
This paragraph captures the essence of your question:

Focusing on a longer time scale, we find that the G-matrix evolves in expected ways to the AL [adaptive landscape] and the pattern of mutation. In the absence of correlational selection (rω = 0) and mutational correlation (rμ = 0), the average G-ellipse is nearly circular, although the ellipse fluctuates wildly about this average (first row in Fig. 6). At the opposite extreme, when the leading eigenvectors of the AL and the M-matrix [mutation matrix] are both inclined at an angel of 45°, the leading eigenvector of G is pitched at the same angle (last row in Fig. 6). Between these two extremes, G tends to evolve to a shape and orientation that represents an intermediate compromise between the AL and M. In other words, the simulation results confirm our intuition and theoretical expectations (Lande 1980b) that G should evolve toward alignment with the AL and M.

Simulation studies of the G-matrix:

Bürger R, Wagner GP, Stettinger J. How much heritable variation can be maintained in finite populations by mutation-selection balance. Evolution. 1989;43:1748–1766.
Multivariate mutation-selection balance with constrained pleiotropic effects.
Wagner GP
Genetics. 1989 May; 122(1):223-34.
On the distribution of the mean and variance of a quantitative trait under mutation-selection-drift balance.
Bürger R, Lande R
Genetics. 1994 Nov; 138(3):901-12.
Predicting long-term response to selection.
Reeve JP
Genet Res. 2000 Feb; 75(1):83-94.

The last article there by Reeve is probably the best paper for your question because it describes in some detail the simulation model they use and how it is all set up. Briefly they simulate a population of 4000 diploid individuals with three genetically correlated traits with separate but identical sexes, random mating, and discrete generations. 20000 generations are simulated to allow mutation-selection-drift equilibrium (almost like a burn-in time on an MCMC chain). They then shift the optimum for one trait by 10 standard deviations and simulate 1500 generations in five replicates. There are 100 unlinked loci underlying the traits, with 50 loci affecting each trait (randomly assigned) meaning there is likely some degree of genetic correlation though it is not perfectly correlated (for some reading on genetic correlations and the evolution of differences you can read Bonduriansky & Rowe 2005, Poissant et al 2010, and Griffin et al 2013). The model then assigns phenotypic values to individuals, and fitness is derived. Figure two shows how the mean, skew, and kurtosis of the variance distributions changed for those 1500 generations.

Addition
Roff 2012:

"While the mean trait values change under selection, so also will the
  G matrix, its orientation tending to shift in the direction of
  selection. ... Genetic drift may also play a role in changing the G
  matrix, but in this case the change will be random though on average
  producing a proportional change in the constituent variances and
  covariances."

nice reference.. I got some insight

Yeah I quite like that Reeve paper and the Arnold paper @wysiwyg - quite good papers on the fundamentals of the g matrix

Very sweet @GriffinEvo +1. I will definitely read the articles you cite. I am glad we can ask such a bit advanced questions and get answers that will largely ease my entry into this topic.

I am currently entering the topic too - working on G-matrix and multivariate breeders equations for a research visit! @remi.b

I am presenting a speculative approach since nobody has mentioned about any existent models yet.
Assuming that selection is based on performance in certain tasks; performance is a function of traits which in-turn is a function of genotype. Performance is a non-linear function of genotype and selection imposes a cutoff/bandpass filter on the performance vector. So selection causes some individuals to perish — which genotypes are selected out depends on their relative contribution to the performance function. As you already mentioned in the question, selection would lead to reduction in variance; some of the diagonal terms would reduce. Now if your traits are truly independent (as in case of additive variances) and also uncorrelated then then extradiagonal terms would be very small and their contribution to the eigenvalues would be minimal.
Overall the eigenvalues and hence the determinant of the G-matrix would decrease upon selection.
Addition based on the points mentioned in rg255's answer
The paper mentioned by rg255 talks about the shape of the distribution corresponding to G-matrix.

The eigenvalues correspond to the axes of the ellipse. In the first case eigenvalues are 0.5 and 0.5; in the second case they are 0.05 and 0.95.

Alternatively, assuming a normal (Gaussian) bivariate distribution of
  values, we can represent the cloud with a 95% confidence ellipse whose
  axes represent the principal components or eigenvectors of the
  G-matrix (Fig. 2). The length of each axis is determined by the
  corresponding eigenvalues of the G-matrix.

Selection may reduce the area of the ellipse if the boundary points get selected out, hence causing eigenvalues and determinant to reduce. However, if the central points are removed (some kind of inverse-bandpass filter), then the limits of variation would not change. In other words the shape or size of the ellipse would not change — it would just become sparse.


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Why do moths not die when they fly into a window?
Sometimes at night when I'm inside with a light on, I can hear (I'm sure) moths fly into the window, and it's so loud I can sometimes hear it over the TV from the other side of the room.
Since they're so small, how do they hit the window hard enough to cause such a big noise and not die?

Drop an intact sunflower seed from a tall building. It doesn't crack. Now place it between your teeth and press it. It cracks. A big pressure is needed.

Simply because their body mass is small. It's the same as if an ant falls off from the roof of a building. It will suffer no harm because the speed of its fall will be very slow, but try the same yourself and you will surely die.
More scientifically, it's a question of kinetic energy: $E_{kinetic}=\frac{1}{2}\times mv^2$
You can see from this formula that if mass is small, then kinetic energy will also be small.
The second reason is that although insects are small in size, the materials they are made of are extremely resistant comparatively to their size. Therefore, the bug will survive when it meets the window pane.
An interesting corollary is that the common saying "if an ant was the size of a human, it could carry a locomotive, because it can carry many times its weight" is totally wrong. If an ant the size of a man tried that, it would break its back just like you and me, because material resistance is not proportional to size.

Because of a square-cube relation, an ant the size of a man would be crushed by its own weight in the first place, and because of a similar square-cube relation, it would not be much stronger than a human.

If an ant was the size of a human, it would die of hypoxia.  Arthropod respiratory systems can't scale that big with the Earth's current oxygen levels.

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Microarray probe and target
In a microarray, which one is called a target and which one is the probe? the one that is added later , is that the probe or the one present in the slots of the microarray, that is the probe?
(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if the question seems to silly, forgive me)

The probes are immobilized on the microtitre plate and the labelled targets are hybridized to them.

In an RNA microarray, a hybridization event between a probe and target sequence would indicate a presence of the transcript within the sample. The probes are oligonucleotide sequences found on the microarray chip. The target sequences are representative of the entire transcriptome. The targets are found within your biological sample and have gone through many rounds of amplification in addition to labeling with fluorescent dyes. The fluorescently labeled target when bound to the probe can then be detected using a scanning laser.

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Degenerate Alignment Analysis
Can someone please tell me what is Degenerate alignment analysis? Could not find a good article on the internet that could help me understand what it means?
(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

This would be much easier to answer if you gave us some more context. Presumably you are referring to sequence alignments but where did you read the term? What was it referring to?

First, degeneracy in a basic sense refers to redundancy of the codons in the genetic code.  For example, the amino acid proline is coded for by one of four codons: CCA, CCC, CCG and CCU. The third codon position (the third letter in each group of three) is called four-fold degenerate because it can change without affecting the coding for proline. Phenylalanine is two-fold degenerate because it is coded for by UUC and UUU.
However, this does not account for the alignment part of your question. Without more specific information (such as a reference you saw), I can't be certain of your intent but this paper by Morin et al. (2008) may be helpful. They had a series of small RNA sequences (each about 24 nucleotides long). They wanted to identify DNA sequences in the genome of Lodgepole pine  (Pinus contorta) and rice (Oryiza sativa). To accomplish this goal, they used degeneracy alignment. Here's the relevant section from their methods:

altered to allow searches against genomic sequence. Alignments were kept if they were no shorter than L − 3, where L is the query sequence length. No more than a total of three mismatches or insertions/deletions were allowed within the aligned region.

Their approach was to find genomic sequences that correspond to the small RNAs. They allowed for some degeneracy, either in the genome or the RNA. The sequences could differ in length by no than three nucleotides or mismatches (an A in the query sequence but a C in the target sequence instead of a T; I'm assuming the query is RNA and the target is the genomic DNA). Their degeneracy alignment allowed for a small amount of freedom in identifying potential matches of conserved RNA clusters (high similarity) in the genomes of distantly related plant species.

Morin, R.D. et al. 2008. Comparative analysis of the small RNA transcriptomes of Pinus contorta and Oryza sativa. Genome Research 18: 571-584.

so basically its like finding common sub sequences even with a few alterations , right??

@user3237995 Yes, basically that is it. Alignments can be found even though some mutations have occurred between the two different species.

Ok Ok, clearly understood!!


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Complementarity Determining Regions (CDRs)
Complementarity determining regions (CDRs) are part of the variable domains in immunoglobulins (antibodies) and T cell receptors, generated by B-cells and T-cells respectively, where these molecules bind to their specific antigen. (source: WIKI, with a minor change)
Now does this mean that this CDR is the paratope? As it has the same functionality as paratope, to bind to epitope of the antigen. So is CDR a type of paratope?
(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

The paratope is the part of an antibody that binds the epitope on the antigen. The CDRs (heavy chain CDRs shown below) are part of the structure of the variable domain, and contain the hypervariable regions that bind to the epitope.

From Wikimedia
The actual paratope is within the hypervariable regions, which are within the CDRs - the paratope is not necessarily made up of the entire CDR region, and in fact may only be composed of amino acids contained within one or two of the three CDRs on each antibody chain (heavy and light).
If you're in the market for a good introductory immunology text, I highly recommend Janeway's Immunobiology. An earlier version is also available on the NCBI Bookshelf.

You should attribute the diagram.

@AMR sorry I missed that originally. Done.


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What does it mean to perform in vitro experiments with mutant bacteria?
I came across the following sentence while reading the paper:
Nanchen, Annik, et al. "Cyclic AMP-dependent catabolite repression is the dominant control mechanism of metabolic fluxes under glucose limitation in Escherichia coli." Journal of bacteriology 190.7 (2008): 2323-2330.

These in vivo flux data are qualitatively corroborated by in vitro
  enzyme activities in the Crp and Cya mutants, which exhibited
  significantly reduced activity of the key glyoxylate shunt key enzyme isocitrate lyase ...

My understanding of in vitro experiments is: those performed in artificial set up , possibly only with part of the cell, where the complete cell is not potentially alive. For, example we can test the inhibition activity of a particular enzyme by a metabolite.
In the paper cited, experiments from which flux are derived (chemostat) are considered in vivo. What would it mean to say the enzyme activity was tested in vitro on the mutant? When we say the response of the a single gene knock out mutant, the cell should be intact except for lacing one gene, which would mean that the response is in vivo.
Please help me if I am misunderstanding some thing.

Answer clarified based on comment by @DurgaDatta

What would it mean to say the enzyme activity was tested in vitro on the mutant? When we say the response of the a single gene knock out mutant, the cell should be intact except for lacing one gene, which would mean that the response is in vivo.

The knockouts were performed inside the E. coli cells and, as you noted, the flux measurements were in vivo (in the cell) inside of the chemostat culture. They identified two mutants, Crp and Cya, that yielded much higher biomass. On page 2326, the authors write,

In the Cya (encoding adenylate cyclase) and Crp mutants that lack the cAMP-CRP complex, in vivo glyoxylate shunt activity was essentially abolished....

I am not familiar with these genes but the implication is that the wild type regulators have the cAMP-CRP complex. Because this complex is missing from the mutants, the enzymes no longer function the same. However, it would be possible that some type of interaction of the mutants with other enzymes caused the observed result in vivo. They therefore verified the result by extracting the Crp and Cya mutant enzymes from the cells and assaying their enzyme activity in isolation from the other enzymes (in vitro). The technique is explained in the answer by @dgg32.
In your comment to that answer, you ask.

what difference does it make whether the enzyme was taken from wild-type or the mutant one, since it is the same enzyme?

It is the same enzyme in name but not in function. The mutant enzyme lacks the cAMP-CRP complex so it cannot perform the same function as the wild type. In vitro, they first showed that mutant enzyme activity was altered relative to the wild type.  They then added the wild type enzyme to the in vitro test and restored normal wild type activities:

To verify that the observed changes were not due to polar effects of the still present marker gene or secondary-site mutations, we complemented the Crp mutant with the plasmid-based Crp gene and cultivated the complemented mutant under the same chemostat conditions. In vitro enzyme activities demonstrated that both the isocitrate lyase and isocitrate dehydrogenase activities were restored to the wild-type level

Yes, this was performed inside the chemostat cultures but only with the enzymes, not the living E. coli cells.

But the flux measurement were also performed in chemostat, which are considered in vivo here.

@DurgaDatta I fixed my answer in response to your comment.

It is possible to conduct an in vitro experiment with cell extracts. Meaning that you break up the cells and put their pieces into a reaction glass and do your experiment. It is assumed that the cell molecules (enzyme, sugar or cofactors) will still carry out their functions even though the cell is no more.
In other words, you used the mutant to produce the enzymes you need (minus the knock-outed one) to set up the desired reaction requirements. Once the products are there, you don't need the producers alive or intact any more.
Check the method part in your paper and see whether it is so.

If we would like to do test the activity of an enzyme (not encoded by the knocked out gene), what difference does it make whether the enzyme was taken from wild-type or the mutant one, since it is the same enzyme?

But based on your article excerpt, the authors seemed to knock-out a gene and see how the metabolism flux is affected, just like a police shuts down a street block to see how the traffic is diverted. Their approach gives them a more systematic view of the pathway rather than a single enzyme's activity. In that case, you need the cell extract.


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Why does a blood test show ethanol when no alcohol was consumed?
Why would ethanol show up in a blood test if a person had not been drinking alcohol in many years. What are other reasons for showing ethanol?

There are some situations when ethanol-like compounds can be present in the blood stream:

[...] exposure to hand sanitizers, after shave lotions, perfumes, medications, hygiene products, cosmetics, foods [...]  Uncontrolled diabetes mellitus can cause false positive alcohol tests.

Source: Dr. Kokil Mathur. Answer on: False-Positives for blood alcohol content. Available from MedHelp forums.
Other causes as pointed on eHow.com:

low calorie diets
gasoline, paints, lacquers
lower hematocrit values
diabetes mellitus

Thank you Dr. Kohl for your answer, but none of the above seems to apply. I was in the Hospital Emergency with H.Pylori, Gastritis, Duodenal inflammation. It showed WBC of 15.4 and Ketones 15. I'm not a diabetic

Convincing answer was given
In Syrups or injections Drugs to dissolve the active ingredients use different types of alcohol use or alcohol is also used in some Toothpaste that maybe cause +alcohol test


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Why do we weigh less in the morning?
At first I thought it may be related to physics.  You know, in one half of the day, the gravity changes, and the scale shows a different weight than the other.  Then at night, gravity intensifies, and you become slightly heavier.
But I'm a bit skeptical about that. Is that true?  That it's somehow related to gravitational fields?

Gravity changes over the course of the day? Why should it?

Gravity (at a given location at a given height) doesn't change.  A simple google search would answer your question: respiration releases carbon and water, you sweat, releasing water, and you spent eight hours not eating to boot.  http://www.businessinsider.com/weight-morning-skinnier-2014-7

Veritasium: Are you lightest in the morning?

There is a related question: Physics SE: Are we slightly lighter during the day and slightly heavier at night, owing to the force of the Sun's gravity?, which might be what you mean by "gravity changes", though the commonly held misconception of why you should loose weight during the night is due to digesting food and burning calories (and debunked in the answers below).

Veritasium created an excellent video just on this topic, which I would recommend watching, but will summarize here.
A common misconception is that we lose weight when we digest food or burn calories. Keep in mind that that broken down food and those calories* aren't "going anywhere", so technically you shouldn't loose any mass (unless you get rid of the molecules by going to the restroom).
However, in the "informal" tests done by Derek Muller, he lost about 250 grams each night. Since during the night you sweat (which evaporates or gets absorbed into the sheets and blankets), he estimated that about 150 grams was lost through perspiration and breathing out water vapor.
The more surprising loss of mass, was 0.012 grams of carbon lost with each breath when breathing in oxygen, and then breathing out carbon dioxide. Although this seems like a tiny loss, assuming you breathe in and out about 7,680 times each night, that tiny mass loss adds up to almost 100 grams of weight loss through breathing alone.
I guess health magazines should start running articles like "Top way to lose more weight? Researchers say breathe more!"

* Technically calorie is a unit of energy and not an item that can be "burned". What we mean when we use the word is the process of molecules being broken apart, which releases energy that can be used by the body; however, the pieces of the "broken up" molecules still weigh the same as the molecule as a whole, so we don't loose weight just from "burning calories".

It's not really so surprising. Carbon is converted to Carbon dioxide which is exhaled. A quick back-of-the envelope calculation shows this makes sense: 1kg of fat has about 38000kJ, that's a bit over 3 times the energy used in a day, so if we don't eat, we convert about 300g fat into CO2 in a day, or 100g during sleep (1/3 day).

There is indeed a slight weight variation during the day. About 2 - 4 lbs (approx. 1 - 2 kg) [1, 2].
Some causes are:

water loss through respiration, perspiration or urination [1].
the relative long period without eating and drinking [2].
metabolic processing of food and drinks during sleep.

References:

Cindy Banyai. http://www.livestrong.com/article/483853-how-much-can-weight-fluctuate-from-morning-to-night/
http://www.weightlossforall.com/weighing-less-morning.htm

Not eating or drinking and Metabolic processing does not change your weight/mass, that violates conservation of mass. The only thing that affects body mass are excrements (from urine, sweat, and faeces), respiration, and very small amount of debris from your skin/hair.

Mass can be converted into engergy. Setting something on fire does change the weight/mass of for instance your house, doesn't it? This is what your body does when you "burn" calories. You don't eat (add something), but your body stays 37 degrees -> the energy to keep it that temperature (even ignoring things like heartbeat and other processes like your brain) has to come from somewhere. Apart from that, the law of conseveration of mass deals with closed systems (also closed for energy!) which you body certainly isn't.

@Nanne Mass isn't "converted to energy", at least not in our human body (unless we go thermonuclear, which would be awesome, but just doesn't happen). What we do when we "burn" calories is break the chemical bonds between glucose(?) molecules; the breaking of these bonds releases the small amount of energy stored in them by the plants that spent that same amount of energy in order to produce those bonds. The combined mass of the "broken apart" molecules is still the same as the "complete" C6H12O6 molecule.

(If a biologist or chemist could double-check my comment, I wasn't sure if it was glucose or sucrose that gets broken apart. Moreover, as I only have a basic understanding in the field, I may have other minor flaws in my comment)

@Nanne Setting something on fire does change the weight/mass of for instance your house, doesn't it? > It doesn't; if you measure the increased weight of the air (the smoke particles in it) and the remaining ashes, there is no difference in weight. Technically there is a loss of mass, but it is unmeasurable by any equipment you could buy at a store.

There is only one way to gain weight, consume things. Thus after any period of time not consuming anything (i.e. sleeping) we must necessarily weigh <= what we weighted at the start of that time period. Add in respiration, and that becomes a strict inequality!


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Why is it that bacteria and fungi cannot develop resistance against essential oils?
I wonder why bacteria and fungi cannot develop resistance and mutate agains essential oils?
For example, some fungi get killed by oregano oil.
Being not a biologist, I hope my question is not so stupid..
Thank you!

Can you cite a specific example? For any given fruit or plant, I'm sure there is at least one fungus or bacterium that can colonize it successfully.

Here are my thoughts on this, taking your example, oregano oil.
The active anti-microbial ingredient in this essential oil is carvacrol. The WP article states that it probably acts by disruption of the membrane.
 There appear to be no examples of carvacrol resistance, as suggested by your question. In mammals the compound is detoxified in the liver via esterification to increase solubilty, thus promoting excretion.
Assuming that we can create a situation with a strong selective pressure for the development of resistance in a microbe, what would that resistance look like? If the carvacrol does indeed disrupt the membrane, then it is probably useless to develop intracellular degradation - what is needed is the secretion of an enzyme that is able to inactivate the compound, analogous to the β-lactamases that inactivate antibiotics like penicillin (which also has an extracellular mode of activity).
Furthermore, unlike β-lactams, carvacrol is insoluble in water. This suggests to me that most of the time, in the natural environment, free-living bacteria will not experience significant levels of the compound.
In summary - it may be difficult to evolve a system for the degradation of a lipophilic compound, and because it is lipophilic it may be that it is rarely a problem for bacteria unless they are being subjected to laboratory tests for antimicrobial activity.


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What is the difference between second and third generation sequencing
I am writing the section about history of DNA sequencing in the introduction chapter and after reading quite a few research papers, I am still confused about them. Here I compile some questions to make sure that I understand it correctly.

Is second generation sequencing the same as next generation sequencing?
Is Sanger sequencing the first generation?
As of today, is there any commercial 3rd generation sequencing technology in use (or is it still in development)?

If there is any paper reference that could explain all of the above then it would be really great.

More recent related question: https://biology.stackexchange.com/questions/105101/what-is-the-difference-between-4th-generation-sequencing-and-ngs

I'm assuming you mean DNA sequencing (excluding things like RNA-seq).
Is Sanger sequencing the first generation?
From Metzker 2010:

The automated Sanger method is considered as a "first-generation" technology

Some of the technology that was in development when this review was written is no longer in development, but this is still an excellent review and a great place to start.
Is second generation sequencing the same as next generation sequencing?
Also from Metzker 2010:

and newer methods are referred to as next-generation sequencing (NGS).

The "newer methods" in the review are:

Emulsion PCR based like Roche/454
Solid phase amplification like Illumina/Solexa
Single molecule like Helicos BioSciences and Pacific Biosciences

As of today, is there any commercial 3rd generation sequencing technology in use (or is it still in development)?
The development of single molecule methods (third item in the above list) has historically taken longer than the other two, so sometimes they are referred to as third generation. However, note how Metzker above considers them all "next-gen".
A recent paper from PacBio itself makes the distinction of halting:

Second-generation sequencing (SGS): Sequencing of an ensemble of DNA molecules with wash-and-scan techniques.
Third-generation sequencing (TGS): Sequencing single DNA molecules without the need to halt between read steps (whether enzymatic or otherwise).

Ultimately, I think the "generations" are more useful to make the "Sanger vs. Not Sanger" distinction. Sanger sequencing is very different than next-gen in terms of what kind of experiment you can do and what sort of data you obtain.
Past that, the number of a generation is more of a marketing term. For instance, at the bottom of the PacBio paper:

Conflict of Interest statement. All authors are employees of Pacific Biosciences and own stock in the company.

In practice, PacBio competes with second generation platforms. It is in their interest to say their technology is on "another level" compared to what's available on the market, but in practice, this is debatable.
Anyhow, to answer your question:

There is a technology in use and commercially available which has been referred to as third gen (PacBio)
There was a technology in development that falls under most definitions of third gen (Helicos), which went bankrupt in 2012
There is a technology in development (ON MinION) that is single-molecule based and was introduced after PacBio, so if PacBio is third generations, so is MinION (although the MinION is apparently very different from PacBio)

Oxford Nanopore shipped MinIONs to a some researchers a few weeks ago.

@5heikki I was actually unfamiliar with MinION. Does it count as third-gen? Feel free to edit my answer and add it (or submit your own).

In my opinion referring to Sanger sequencing as 'first generation' is historically incorrect. Maxam-Gilbert sequencing preceded it and produced lots of useful results - see Addendum in my answer here: http://biology.stackexchange.com/questions/17598/how-was-restriction-site-of-ecori-sequenced/17603#17603

Ultimately we, as scientists, shouldn't get hung up on the exact use of this terminology since it is clearly now just part of marketing the latest advance in sequencing technology.

@AlanBoyd Strictly saying, it is not about precedence: the distinction between the first generation and the next generation is in terms of throughput. In this respect both Maxam-Gilbert and Sanger belong to the same class of methods.

@har-wadim thanks, I hadn't thought of it like that. What increase in throughput constitutes a generation?

@AlanBoyd I am regrettably not well informed about the history of sequencing technologies past the last decade. I think you have a good point, edits to my question are welcome.

An increase in throughput to discern between different generations is not true for second vs third generation sequencing (PacBio has the advantage of generating long reads but at a throughput lower than that of the second-generation sequencers: http://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-15-699 )

The sanger sequencing and Maxam-Gilbert sequencing methods are considered the first generation sequencing methods. Next generation sequencing is a term used to refer to the sequencing methods that came after those two methods offering high throughput sequencing. Therefore, second and third generation sequencing are collectively called next generation sequencing.

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text:
What would cause crows to be attracted to a human body?
On another SE site, there was a comment that told me something  about biology that I already know:
"A man left murdered in the fields would soon have a flock of crows mobbing his fragrant corpse."
But I don't quite understand why. Is it the "death" part,the fact that someone was injured/bleeding or just the fact the he was immobilized,that would attract the crows?
That is suppose you tied up someone and left him on the field. Would that attract the crows?
Suppose this person fell down, was bleeding, and immobile, but not seriously injured? Or is it the death part?

I think the key is "his fragrant corpse." When an animal dies and begins to rot, a number of quite smelly chemicals are given off, including putrescine and cadaverine. Crows and other carrion birds like vultures are probably very sensitive to these compounds, rather like sharks are to the smell of blood.

+1 for the etymology of "putrid" and "cadaver." The question came from the English Language site, and your answer took it back there. http://english.stackexchange.com/questions/194919/two-crows-being-an-attempted-murder

Carrion birds, such as crows and vultures, eat dead animals. As a whole, it's possible that they detect carrion by the smell or visually.
Crows specifically are omnivorous and predatory in addition to being carrion scavengers. I suspect that they will try to eat anything that doesn't fight back, especially if they are hungry enough and there is exposed flesh. I don't know if crows prefer dead meat or fresh meat, but they certainly eat both.

Suppose you tied up someone and left him on the field. Would that attract the crows?

The crows would probably be attracted because they are curious and want to check out the new, unfamiliar object. They would certainly be able to tell that you are alive by body temperature and sounds of breathing or heartbeats.
I think they will be hesitant to eat you because live humans are unfamiliar to them. They will probably find other carrion nearby and eat that instead. If you stayed unconscious for several days, the crows would get used to you, lose their fear, and eventually one would go for a taste. Once the first gets a bite or two, and you fail to retaliate, I think the others will quickly join in.

Suppose this person fell down, was bleeding, and immobile, but not seriously injured? Or is it the death part?

The fact that they can see and smell the meat, and don't have to bother piercing the skin, would make you more attractive to the crows (supposedly, they like to go for things like eyeballs even on live prey).
However, even if immobile, a conscious human could struggle (shake their head, yell, roll around) which would startle the crows and keep them at bay for a time. If you can't actually interfere with them pecking you, I'm sure they would eventually get over their fear and attack you. If you can physically swat or shake off the crows, they'd just wait for you to get tired or die, which probably won't take too long given the injuries.
In conclusion, I don't think it's impossible for crows to eat bits of a live human, whether conscious or not. However, for various reasons, it would probably take a few days for them to actually get around to it. If you are not dead by this point, larger animals would show up and attack you, and crows would end up picking at the scraps.


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How does core-conductor model correspond to an actual neuron?

Hi guys, looking at your average neuron, it is very difficult for me to imagine how this could be translated into a core-conductor model

On the neuron above, where would be the intracellular space and where would be the extracellular space? Also, where is this membrane we are talking about?

What may be confusing is that the myelin is wrapped around the membrane of the axon.
The easiest way to see this is in cross-section:

From here.
The axon is indicated by #1 in the diagram and the myelin sheath is #4
The intracellular space (as represented by the horizontal resistors in the case of your model of the axon) is the fluid, replete with ions, that is contained within the membrane of the axons.
At the nodes of Ranvier, there is a break in the myelin sheath, exposing the underlying membrane of the axon.  In membrane in those gaps of the sheath, there are sodium channels (voltage gated) and potassium channels that facilitate the influx and efflux of ions that "refresh" the action potential as it travels down the axon.  The extracellular space is simply the milieu of fluid in the space between the axon and any adjoining cells.  For the purposes of analyzing the currents of the neuron, the sodium and potassium ions (and the conductances of the channels) are all that you really need to be concerned with.
What is confusing about your diagram is that it represents the conductance -- the inverse of the resistance of the channels -- of the channels (inwards and outwards) as a single vertical resistor in between the horizontal resistors of the intracellular membrane. This oversimplification is handy when doing the cable theory-type analysis, but it betrays the actual physiology of the neuron.
From a model standpoint, I'm breaking all the rules here, but you can think of things like this:

where one "rung" of your resistor ladder has $r_m$ broken out into the 2 components and drawn differently.

That's probably clear as mud, and I've glossed over a lot, so feel free to ask questions and I'll fill in the gaps.

Hi just to clarify. So the membrane is the axon membrane, the intracellular space is lies within the axon (so the cytoplasm within the axon) and the extracellular space lies outside of the axon and between the neurons (another type of fluid I guess). The breaks between the myelin sheath is used to refresh the action potential and is not modelled. could you provide a realistic example of core-conductor cable model of a neuron? You said the verticle resistors are not realistic and does not represent a part of the neuron.

@IllegalImmigrant The breaks (nodes of Ranvier) on the myelin sheath are modeled by the electrical nodes between the horizontal resistors in your model.  These are the only places between the hillock of the axon (the pointy part at the end of the cell body) and the terminal where ions are being exchanged.  At the other points along the axon, the receptors are covered over by the myelin, so no current leaks out with the movement of the ions.  The vertical resistors are realistic, they just betray the complexity of the actual voltage-gated influx through sodium channels

and the potassium efflux.  There are different subtypes of these potassium channels as well (so Rm take a lot of information about conductances/resistances and jams it down into one component).  My "grounds" in my circuit are a bit exaggerated, since the currents leaving and entering the axon can propagate through the ions in the extracellular milieu.  I just wanted to illustrate that the conductances could be split off into the different components, but it was still justifiable to combine them.

The core conductor model is very limited in scope.  It may be helpful for you to take a look at Hodgkin and Huxley's work with the compartmental models as a way of exploring the limitations of cable theory.


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What good is the MinION?
This year, Oxford Nanopore MinION has been shipped to some researchers for testing.
The advantage of a table-top sequencer for diagnostics and personalized medicine is obvious. Similarly, research "in the field" and forensic science could be aided greatly by this device. My question is about the applications in the research lab.
What does MinION do that a well-equipped lab with access to Sanger and next-gen sequencing cannot already do?
How well does the MinION work? How powerful is it?
What important scientific discoveries are being made using the MinION?
While the website of Oxford Nanopore has a list of publications, the most recent one is from 2013. This is before the early access program began - I am particularly interested in developments since February 2014.

I don't know a lot about it, but basically there is an electrically resistant membrane into which protein pores are inserted. An electric field is applied across the membrane which creates a current through the pore as ions flow through. As DNA passes through the pore, it blocks the flow of ions and thus reduces the current. Each base causes a characteristic current reduction. Its big advantage is that it is fast: it reduces amplification and assembly and can sequence something like 100 000 nts/s. However, it only has (last I heard) ~95% accuracy and so multiple passes are required.

This blog post may be useful https://biomickwatson.wordpress.com/2014/09/07/thoughts-on-oxford-nanopores-minion-mobile-dna-sequencer/

Also http://omicsomics.blogspot.co.uk/2014/09/oxford-takes-some-flak-fires-back.html?spref=tw


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Is there a medical condition in which you can't cut your hair?
Just curious, does there exist a medical condition in which a patient is advised not to or simply cannot cut their (head) hair?

Hair is not alive, so there shouldn't be any problems with that.

Patients on blood thinners are advised to avoid cutting risks, which would suggest "no shaving", but presumably depilation by other means would not have that risk.

What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

An phobia or OCD released to appearance might lead someone to face dire situations when their hair is cut even death if the fear leads to a heart attack.

I like this one

Alopecia and balding, these individual experience hair loss, thus nothing to cut


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Can you change your gut microbiota by changing your diet? Would that affect calorie uptake?
I have seen peer-reviewed papers mentioning the daily changes in gut microbiota composition according to dietary changes. See for example this paper:
http://genomebiology.com/2014/15/7/R89
My question is related to this one:
Relationship between our microbiome and personalized nutrition
If, according to these recently published scientific results, it takes a day to change the gut microbiota to adjust to the dietary change, and the presence of certain microbes makes food assimilation more effective,
Does this mean that alternating a protein-rich meat and dairy diet with a carbs-rich diet every day would make our microbiota switch daily and not have time to increase calorie uptake?

Firstly, it should be noted that a stable, healthy microbiome is generally thought to be a marker of health; actively disrupting it through diet in an attempt to fight with it over nutrients is therefore not necessarily a good idea, as it can affect the health of not only your gut but also your immune system, etc.
Dysfunctional microbiomes are for example associated with behavioral problems in eating disorders.
Nonetheless, diet shifts have been used as a tool to attempt to control the microbiome and put it in a "healthy state". You can indeed use consumption of some foods to shift microbiome composition. Presumably if you did this in a sufficiently disjointed way, you could throw your microbiome into a sort of ecological chaos.
However, it would be much simpler to just constantly take antibiotics to ensure that your gut load of microbes was generally low. This still isn't a good idea, as it can lead to Clostridium difficile or E. coli infections or other bad things, but it would be a much more straightforward way of getting to the desired end state.


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Chromatids in metaphase?
Please see the following picture:

In my book, the author claims that these chromosomes are in metaphase (a metaphase stopped by cholchicin).
I don't understand why they don't have two chromatids...A chromosome looks, by everything I've learned, like TWO chromatids (http://i60.photobucket.com/albums/h1/GameMaster57/Chromosomestructure.jpg) and should be together in metaphase. These chromosomes only look like chromatids to me (1 of 2 pairs).
Have they been separated?
I am also asked to specify which chromosomes are from the father and which are from the mother. How would I go by doing that?
Thank you.

I would have guessed it's metaphase of Meiosis II but there should be only 23 chromosomes in that case.

The chromosomes in your picture do have sister chromatids, they are just very close together. A chromosome needs to pass through replication before it can compact into the typical metaphase chromosome shape depicted above. When I prepare metaphase chromosomes, I usually see a mixture of chromosome sets where the chromatids are close together (like above) and clearly separated. I think this is related to the time each metaphase has spent in the colcemid block-the longer the cell has been blocked at metaphase for, the longer the enzymes that work to separate the two chromatids have acted on it. Also chromosomes keep getting more and more compacted during the colcemid block-if you leave them for too long, they become a lot smaller.  This paper has very cool pictures showing the links between the sister chromatids:
http://www.ncbi.nlm.nih.gov/pubmed/18461479

There are two important terms to note:
Sister chromatids
Homologous  chromosomes.
Sister chromatids are visible during most phases of mitosis, but not rest of cell cycle.
colchasine is an inhibitor of micro tubules so it prevents the chromosomes from 'liningstrong text up" during metaphase hence it arrests  at metaphase and the chromosomes are scattered all
Over the cell.
The spindle also helps withpairing up sister chromatids (for each homolog) so that each new daughter cell gets a complete genome. Since the spindle is not intact the chromatids are not localized.

is it "liming up" or "lining up"? I have never hear the word "lime" before, but it exists, so it may be just my ignorance (both English and chromatid processes).


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Definition of "Effective population size"
Could you explain to me, what is the meaning of "Effective population size ($N_e$)"?
I would appreciate an example as well.

This is potentially a good question, but too vague in its current form. You should say what context you mean so that a better explanation can be given. What formula did it occur in?

I'll add an informal answer to complement @Remi.b's excellent answer. In a very simple sense, you can think of the effective population size as the number of reproducing (breeding) individuals in a population. Nature Education has a very good (and free) Scitable article on Genetic Drift and Effective Population Size. The article makes four points, which I've annotated below.

The population has an equal number of males and females. All
individuals are able to reproduce.

Populations of many species contain individuals that have not yet reached sexual maturity, have passed an age of reproductive capability, or might have a genetic condition that prevents reproduction.  All of these individuals count towards the census population size (actual number of individuals present) but not count towards effective population size because they can't reproduce.

All individuals in the population are equally likely to reproduce.
Mating is random.

Not all indivduals (assuming individuals that meet assumption #1 above) are equally likely to reproduce. For example, the process of sexual selection means that some individuals are much more likely to reproduce than other individuals. Sexual selection is not random, and lowers effective population size.

The number of breeding individuals is constant from one generation to
the next.

Population sizes for some species can fluctuate over many generations. For example, freshwater mussels have declined rapidly in population size due to habitat loss and other factors. Nearly 72% of the species in the United State and Canada are endangered, threatened or of conservation concern (Williams et al. 1993). The population sizes for the majority of mussels species are but a fraction of what they once were. This is the case for many endangered species. This too lowers effective population size.
Here's a simple mathematical treatment to highlight points 1-3. Consider a population of zebras. Zebras like the Plains Zebra (Equus quagga) form harems where one male mates with several females. He prevents other males from mating with the females in his harem. Let's make the following assumptions: 1) the population has 250 males and 250 females, all capable of breeding and 2) each male that is able to form a harem gets five females. If so, then only 50 males will actually get to reproduce. The census size is 500 individuals but the effective population size, as shown in Remi.b's answer, is calculate by
$$N_e = \frac{4N_m N_f}{N_m+N_F}$$
where, $N_e$ is the effective population size, $N_m$ is the number of breeding males and $N_f$ is the number of breeding females. Given assumptions 1 and 2 above, $N_m$ is 50 and $N_f$ is 250 (50 males $\times$ 5 females each). Therefore,
$$N_e = \frac{4\times 50 \times 250}{50 + 250} = 166.67$$
Clearly, the effective population size is much smaller than the census population size.

Short answer: The effective population size of a population is the corresponding population size of a idealized (fisherian) population that would function in the same way with respect to genetic drift and inbreeding as the focal population under interest.

Long answer, below.
Definitions:
Heterogenity: the probability that two randomly sampled alleles in the population are identical (identical by descent).
Census Population Size: The census population size ($N$) is the number of individuals in the population.
Fisherian population
A fisherian population is an idealized population of size $N$, where all individuals mate at random, there is no selection, there is no population structure, there is no mutation and generations are non-overlapping. There probably are no perfectly fisherian populations in nature!
Genetic drift causes a decrease in heterogeneity. As the genetic drift is a function of the population size (see this post) this decrease of heterogeneity is a function of the population size. The heterogeneity at time $t$ is:
$$ H_t = H_{0}\left( 1-\frac{1}{2N} \right)^t$$
, where $H_0$ is the heterogeneity at $t=0$. You can verify by yourself that as $t$ increase , $H_t$ decreases. Also, as $N$ decreases, $H_t$ decreases. In other words, the longer you observe, the more heterogeneity gets lost and the smaller is the population, the higher is the loss of heterogeneity.
Effective Population Size
Let Pop_A be a real population. The effective population size ($Ne$) of Pop_A is the size of an idealized fisherian population that would have the same loss of heterogeneity than Pop_A.
You can read the above sentence twice to make sure you understand it. It basically is the definition of the concept of effective population size.
In other words: Let $N$ be the population size of Pop_A. If Pop_A is a perfect fisherian population, then its loss of heterozygosity through time is given by:
$$ H_t = H_{0}\left( 1-\frac{1}{2N} \right)^t$$
If Pop_A is not a perfect fisherian population, then it's decrease in heterozygosity is greater than the one given by the above formula. The decrease in heterozygosity of Pop_A corresponds to the decrease of heterozygosity of an idealize fisherian population of a different size. This size is called the effective population size $Ne$. So, we can rewrite the loss of heterogosity through time of Pop_A as:
$$ H_t = H_{0}\left( 1-\frac{1}{2Ne} \right)^t$$
(Note $N$ has been replaced by $Ne$)
, where $Ne$ is the effective population size of Pop_A.
Usually $Ne < N$, meaning that a real population undergoes more genetic drift than does a fisherian population of the same census size. There are many reasons that may yield a real population to have a higher drift than it would be expected with the same census size but respecting the assumptions of the fisherian population. Below I discuss three reasons:
Examples
Unequal sex-ratio
Think as a first example of a population where the sex-ratio is extremely biased to the point of having one male for 99 females. In such population, half of the alleles of a given locus at the next generation will come directly from the father. In such situations, the genetic drift is much higher than what would be expected from a fisherian population of size 100. Therefore $Ne<N=100$. To calculate $Ne$ when the sex-ratio in unequal you can use this formula:
$$Ne=\frac{4N_mN_f}{N_m+N_f}$$
, where $N_m$ and $N_f$ are the census populatino size of males and females respectively. You can verify that when $N_f = N_m$, then $N_f + N_m = N = Ne$.
Variation in population size through time
If your population size varies throughout a given time (a year for example) and that at time $t=3$ (a given period of the year) the census population size is given by $N_i$, then the effective population size is:
$$Ne = \frac{1}{\frac{1}{t}\sum_{i=1}^t\frac{1}{N_i}}$$
This is particularly relevant for insects for example which population size varies a lot between seasons.
Selection
Think now of a population where there is a great variance in fitness (there is selection). In such population, maybe all offspring will be produced by only a tenth of the current population. As a result the effective population is ten times smaller than the census population size.

You can probably find all these informations from wikipedia: http://en.wikipedia.org/wiki/Effective_population_size
Let me know if the concept of the effective population makes more sense to you now.

I hope you are ok with my edit suggestions.


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How efficient is the human body at metabolizing food?
My friend and I were having a discussion over how "efficient" human digestion is. If a human ate a 1000 calorie hamburger, how many of those calories (how much energy) does the body process into usable energy (i.e. fat or other stores). I've heard things like "it's better to workout on an empty stomach because you will burn fat instead of energy from the food you just ate" - so from this I presume that storing energy as fat is less efficient than using the energy from digestion immediately (though in all honesty I'm not sure if that even makes sense.)
So, to summarize: how many calories of food does your body turn into usable calories via digestions? Percentages would be nice.
Bonus question: If the body does not process at 100%, does the FDA take this into account when labeling food products on their calorie content? If my Basal Metabolic Rate is 1800 calories a day, do I need to eat more than that since my body won't process all of the calories into usable energy?

The calories listed on nutrition labels are calculated so that they are representative of the amount of "digestible energy" - that is the amount of energy that actually enters the blood stream.

Different foods are diested very differently, too.  Richard Wrangham's "Catching Fire" goes into some of the research on the topic.

Do you have a source for "digestible energy"? I thought they used bomb calorimeters to establish the number of kilocalories in an item, which would figure a raw amount. Do they calibrate the calorimeters for a certain % of utilization for a human? If so, that would be the % I would be looking for for "efficiency."

On nutrition labels, they determine the constituents (protein, fat, etc) by mass in the food and use a standardized factor to convert these masses into energy. They do this to address the concerns you raised in your question: that not all energy in food is available for metabolism.

For example, see this: http://www.legislation.gov.uk/uksi/1996/1499/schedule/7/made

The FDA's base metabolic rate is based on how much food you actually have to eat, it was originally established experimentally not through calculation.

A year and a half later, I stumbled upon this article by Ars Technica.
To summarize, research/experts acknowledge that the calorie system is a poor way to measure human metabolic performance. Gut fauna, calorie measuring device differences, and caloric differences produced by different levels of cooking all contribute to this system being unreliable.
To address the original question specifically: there isn't a clear answer or "rule of thumb", because it depends on far too many variables, many of which are directly attributable to the "calorie" being an inappropriate way to gauge food consumption and weight loss.

I suspect that what you are actually looking for is the following:
- 1 gram of fat = 9 kcal
- 1 gram of protein = 4 kcal
- 1 gram of sugar = 4 kcal
- 1 gram of alcohol = 7 kcal

Those are general and inexact values. They're just often used to give a rough idea of the amount of energy we get from different types of food.

I was under the impression that sorbitol was able to be reduced to fructose through the action of sorbitol dehydrogenase and aldose reductase.  I believe that is part of the reason sugar alcohols are not *great sugar replacements for those who have T2DM.

Also, you might look up enhanced nutrient shuttling in the gut from enterobacteria. Depending on the microbiome that's been developed some bacteria will shuttle more calories from the chyme(found typically in the chronically obese).  The question the OP asks is multifaceted.  A good answer (in my opinion) should touch on host nutritional factors, gut microbiome colonies, impact of nutrient cycling, and type of nutrients being metabolized.

@LittleWhiteLithe Hmmm... actually, my biochem is too far behind for me to confirm or infirm your statement. You are probably right, now that I think about it. So I'll edit in consequence. The first part of the answer still holds, though. It was destined to be extremely simplified, beacause I was under the impression that the OP was looking for such a "rule of thumb". However, if you prefer to go into details, please do. It will be instructive for all of us.

Unfortunately, I was looking for more than a rule of thumb. The details are what interest me. This answer is certainly closer, but to use your example: how many Kcals does 1 gram of fat/protein/sugar/alcohol yield in a blast calorimeter? I can't believe it's the same number as the body produces from absorbing the food (and indeed, the fact that we produce physical waste proves that we do not turn 100% of it into energy). In a blast calorimeter (what I am lead to believe gives us the calorie counts we so rely on), all of the matter is burnt to find this number.


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Do river sharks (genus Glyphis) have reduced rectal glands for salt removal?
Do river sharks of the genus Glyphis have reduced or absent rectal glands for salt removal?
The rectal gland of marine sharks removes excess salts to maintain osmotic balance (Oguri 1964).  In freshwater stingrays (Potamotrygon spp.), the rectal glands are greatly reduced in size  (Thorson et al. 1978) but are apparently functionless (Goldstein and Forster 1971). This is not surprising because freshwater rays do not experience the regular influx of salt water.
I have been unable to determine whether such degeneracy or loss has been observed for the river sharks of Australia (genus Glyphis). Pillans et al. (2009) suggest that osmoregulation is probably similar to bull shark, which would not be surprising because they are in the same family. However, bull sharks that live in salt water but regularly enter fresh water have rectal glands that are normal size (Oguri 1964). River sharks are obligate freshwater species and thus have no need to maintain a large rectal gland for the same reason as the freshwater rays.  From an evolutionary perspective, I would predict reduction or loss of the rectal gland.

I contacted Richard Pillans, the primary author of the article linked to in the question. He told me that he did not know whether the rectal gland was reduced. Researchers are hesitant to capture and dissect the freshwater sharks because of their endangered status.
He did tell me that they have gathered much more data on the movement of the sharks since the 2009 paper was published.  Apparently, river shark is a bit misleading (my words, not Dr. Pillans). Glyphis does occur in freshwater (no salt) but tends to be found in the middle range of brackish water. Brackish water is considered to be anything that is not purely freshwater nor purely salt water, with typical values between 0.5 and 30 parts per thousand (ppt). Freshwater is 0 ppt and open ocean salt water is 35 ppt, the equivalent of 35 grams of salt in one liter of water.
If Glyphis is found primarily in the mid-range of brackish water, then I would expect the rectal gland not show signs of reduction. Pillans and Franklin (2004) showed that rectal gland mass of brackish water bullsharks (Carcharhinus leucas) in Australia did not differ significantly from either freshwater or saltwater individuals.  So, pending further evidence, I would conclude that Glyphis, which in the same family as bull sharks, probably does not show rectal gland reduction.

Pillans, R.D. and C.E. Franklin, 2004.  Plasma osmolyte concentrations and rectal gland mass of bull sharks Carcharhinus leucas, captured along a salinity gradient.  Comparative Biochemistry and Physiology, Part A 138: 363-371.

Your answers are always impressive and supported by several references! Even better when you make both the question and the answer! It is good to have you on this website $\ddot \smile$.

@Remi.b Thanks, I am happy to be here. I keep trying to get to some of your questions but I keep getting diverted with the other questions that to me have an interesting bit of biological trivia (like the one nostril thing). Besides, your questions take more thought and research! :)


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DNA Fingerprint
I recently came across an article indicating that the half life of DNA in the most ideal situations is 521 years (http://www.nature.com/news/dna-has-a-521-year-half-life-1.11555). However, since human's DNA is 99.9% identical (and 98% identical to chimps), I can't quite understand how DNA evidence is often used in old samples. There has been DNA extracted from 100,000 year old Neanderthals, and DNA evidence has been used in cases over 50 years old.
However, with a 521 year half life, after only  0.75 years, there would only be 99.9% of the DNA left. Surely if 99.9% of a human's DNA is identical after only this short amount of time wouldn't it be impossible to distinguish any sample from any other? After 50 years only 93% would remain the same, meaning it would be much less similar to a human than just any chimp I would think.
And the 100,000 year old Neanderthal would only have 1.6*10^-57 % of the original sample left. How is there possibly any sort of useful information left?
All in all, how can DNA be distinguished from other samples when they are all so similar and the half life is so low?

This question belongs on the biology site - to answer it you have to understand how DNA is compared / identified. It's not about the bits that are different, but about certain (shortish) unique sequences that are the same. Such sequences will continue to exist when much of the DNA has mutated - especially when you recognize there is usually material from multiple cells which will not have degraded in the same way. Still - I suggest you ask a biologist.

The original article cited in your reference is available here for free. After a quick skim, I saw that their study was based on fossils of a single species (Moas) all taken within a 5 km radius. Thus, it's possible the fossils were preserved under relatively similar conditions, despite different preservation ages. So, it's not yet clear how their results would compare to other species and varying preservation conditions (which they address to some extent).
Regardless, DNA does degrade in fossils yet scientists have been able to recover very high quality sequences from fossils, such as Neanderthals.  This is because the samples contain many copies of the DNA. If bonds in one copy of the DNA break in several places it is very unlikely that another copy will break in the exact places.
There are a number of different techniques but in essence scientists simply amplify and sequence a very large number of the DNA fragments. Each fragment is relatively short compared to the total amount of DNA but the large number of fragments ensures (within reason) that the entire genome is covered.  Complex computer algorithms are used to align the different fragments with each other.  You can read about the techniques used in one of the major Neanderthal genome studies by Green et al. (2008).


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Conscious evolution
Does intelligence play a vital role in the evolution of an organism? In other words does an expansion of learning capacity, increase the odds of evolution for the particular biological entity?

Short answer: No, it doesn't. Evolution is a statistical process which is not influenced by any means of intelligence.

Why then is it that those who are intelligent develop skills, skills which would assisst them to adapt to the unfamiliar enviroment?

This will influence the procf selection, but not the evolution itself.

Selection is a crucial part of evolution. I disagree with you, Chris. Intelligence can actually be a favorable trait in some cases. This does not mean that evolution has an inherent drive to produce ever more intelligent organisms.

@Hav0k And it is not the other way round that being intelligent directs evolution in a certain way. Evolution can be seen a a two-step process: First a mutation occurs and then this mutation is selected for or against. We can influence the second step but not the first.

There is a disagreement between Chris and HavOk because of how the question is phrased I think. Yes, high(er) intelligence may be favorable (enhance fitness) and I am sure Chris would agree with that. When the OP is asking "Does intelligence play a vital role in evolution", (s)he dosesn't mean "does it influence fitness", (s)he means some kind of weird intelligent-driven evolution "I (because (s)he probably doesn't know evolution acts (mostly) on population) become what I think is better for me" or something like that. There is no way to answer yes or no as the question is too poorly phrased.

I hoped my long answer could help but I'm not totally sure. The OP should start understanding what is mutation, what is selection before going to the slightly more complicated details of my answer.

To whom it may concern: "Use comments to ask for more information or suggest improvements. Avoid answering questions in comments." Seems a reasonable question to me. If you have an answer, give an answer. If not, don't abuse the SE system.

First Comment
The questions in the OP's post (and his/her comments below the post) are very poorly phrased and let the reader think that the OP has few knowledge about evolution (no offense). This is a reason why I don't directly address my below answer in the terms of the question as it seems that the OP uses a unusual definition of the term "evolution". @Chris comment ("No, it doesn't. Evolution is a statistical process which is not influenced by any means of intelligence") probably sums up what the OP needed to read but I can't stand but giving a more complete answer about why is intelligence just a random trait and in the meantime arguing in a far-fetched text that intelligence still has actually some funny properties as it may yield to social help (social help does not necessarily needs intelligence) and eugenics programs (that might be argued that it doesn't need intelligence as well).
Summary of the answer

Intelligence (as many other traits) influences fitness
Intelligence (as many other traits) influence the environment that individuals are facing influencing then future evolution
Evolution is not dependent on the will of the individuals in the population.
Indirectly, intelligence may be of some particular interest as it yields to knowledge about physiology and evolution allowing Eugenic program and medicine which both influence future evolution.

Long answer
Fitness
Intelligence influence fitness (=reproductive success). So yes it plays a role in evolution just like any other trait that influence fitness.
Environment
Intelligence evolves and by its presence it will change future evolution as it changes the environment the individual faces. For example, if a bird is intelligent enough to bottle milk bottle, it might over the long term (and assuming that humans are not inventing some solutions to prevent birds from opening their bottles) evolve longer beak to seek for milk from the bottle. Also Intelligence shape culture (set of traditions). Theoretically, all traits does the exact same thing, so again there is nothing so exceptional about intelligence.
As a subset of the impact of intelligence on the environment the individual experience: Intelligence allow culture which changes through time and it is some kind of evolution called memetics. Again, culture changes the environment the individual faces and if culture changes often because of high intelligence, then the environment may change quickly as well.
General basic comment on evolution
It is very important to not think that intelligence will allow a population to "better evolve". Being intelligent does not yield to higher probability of adaptable evolution. It is not because you know what issue you're facing that you'll be consciously able to evolve to that. For adaptation to occur you have to select individuals that are more fit in the population. If individuals in the population know who are fit doesn't mean that those fit individuals will be more selected than otherwise.
Social help and eugenic programs
In addition to the previous paragraph I must point to some potential, indirect impacts of intelligence on the evolution of a population. A population of intelligent individuals may as a group decide on which individuals will reproduce. This is called eugenics and this is the kind of process by which intelligence influence future evolution in a particularly interesting and unique way. For example, we may decide that all people that carry a non-expressed disease gene are not allowed to reproduce in order to suppress this gene from the population. In the same order of idea the population learn how to treat people that have a given genetic disease, the selection against the gene variants (alleles) causing the disease will decrease, increasing then the frequency of the disease in the population. Therefore, some medical actions (and other kind of social help) cause less adaptable evolution while some eugenic program cause more adaptable evolution. I am not talking about ethics here and am not saying we SHOULD stop treating people with genetic disease. Note that other things like the evolution of trait architecture will yield to different ability to undergoes adaptive evolution.
Interpreting my answer
It is important for a starter in evolutionary theory to make sure to learn more about evolution before trying to interpret further this answer in an incorrect way. I want to avoid that someone with few knowledge in evolution starts to think that intelligence is some kind of magical trait or that evolution is a process answering to the conscious needs individuals may have. For the moment keep in mind that evolution has no foresight and is not the result of the will of the individuals in the population (except for eugenic program). Behind this answer there are (maybe hidden) slightly advanced topics such as the strength of selection, mutation-selection-drift equilibrium, the genetic load, trait architecture and evolvability.

Seems safe to assume that intelligence CAN influence fitness, depending on the selection pressures. As Hav0k mentioned, this won't necessarily be favorable, i.e. lead to more progeny. In the case of modern humans, even if a person got more mating opportunities by being, or just appearing to be very intelligent in some areas, it might not do much to affect the population if he/she chose to have fewer or no offspring. To the extent that intelligence was valued in a population, it could of course become very influential. Whether or not (potential) intelligence is something quantifiable that is vertically transferred is another discussion I guess.

Intelligence can have an impact on selection, but keep in mind that flexible intelligence (like the kind humans possess) is a high-cost/high-reward kind of adaptation.  Brains consume a lot of energy, so the resulting intelligent behavior needs to 'pay for itself' (in terms of survivability and ability to reliably gather the necessary food) if it's going to create a competitive advantage.


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Do bacteria die of old age?
I know that the cells of mammals at least stop dividing when they are old, and then die a programmed cell death. Then other cells have to replace them.
But in a bacterial colony, each cell replicates for itself. Obviously, if a division of a bacterial cell of generation N were to produce two new cells of generation N+1, and all bacteria died of old age at generation M, there would be no bacteria left around.
So how is it regulated in bacteria? Are their divisions simply unlimited? Does a cell never die and just divide forever?

This is yeast, not bacteria, but very related to your question: http://www.pnas.org/content/109/13/4916.full

This is a interesting question and for a long time it was thought that they do not age. In the meantime there are some new papers which say that bacteria do indeed age.
Aging can be defined as the accumulation of non-genetic damages (for example oxidative damage to proteins) over time. If too much of these damages are accumulated, the cell will eventually die.
For bacteria there seems to be an interesting way around this. The second paper cited below found that bacteria do not divide symmetrically into two daughter cells, but seem to split into one cell which receives more damage and one which receives less. The latter one can be called rejuvenated and seems to make sure that the bacteria can seemingly divide forever. Using this strategy limits the non-genetic damage to relatively few cells (if you consider the doubling mechanism) which could eventually die to save the others.
Have a look at the following publications which go into detail (the first is a summary of the second but worth reading):

Do bacteria age? Biologists discover the answer follows simple
economics
Temporal Dynamics of Bacterial Aging and Rejuvenation
Aging and death in an organism that reproduces by morphologically
symmetric division.


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What is meant by drug tolerance?
What is meant by drug tolerance?
This question is in my biology textbook for IGCSE and I have no idea what drug tolerance is. It would be very helpful if someone could clarify. Thank you.

Have you read the article in the Wikipedia about it? http://en.wikipedia.org/wiki/Drug_tolerance Do you have specific questions about it?

Yes I did but I still couldn't get a clear picture of it in my head.

Would you happen to know another site with a clearer definition?

Can you tell us what you find unclear in this definition? This makes writing a meaningful answer easier.

"when a subject's reaction to a specific drug and concentration of the drug is progressively reduced, requiring an increase in concentration to achieve the desired effect."

Does this mean the more the user takes the drug, more of it is needed for him to achieve a high?

It basically means, that the body gets used to certain drugs and that you need to raise the dose to reach an effect. This is for example true for a number of anesthetics or pain medications as morphine.
Permanent application leads to a down-regulation of the drug receptor (for morphin this is the mu-opiod receptor) and the activation of counteracting signaltransduction pathways. To still get an activation you will need a higher drug concentration.
For more details have a look at these articles:

Opiate tolerance and dependence: receptors, G-proteins, and
antiopiates
Cellular neuroadaptations to chronic opioids: tolerance, withdrawal
and addiction


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Importance of knowing GC Content of an organism
I was looking at the GC content percentages of few organisms. I also know calculating the GC content percentage. But, what I want to know is, what information would we get., let us suppose if human genome has 40% of GC in the genome.
Does it help us compare the number of genes between different species, for example, a bacteria has less GC content than human, so does it mean Human produce more genes than bacteria?
or Is it that the 40% of the genome,has coding regions in them and more genes are found in those regions? What is the number "40%" actually indicate us?
Please help me understanding the concept. Would be thankful your answers and suggested reading.
EDIT: My question is what does knowing percentage of GC content help us knowing? If the GC content is 40%, does it correlate to number of genes in the genome?
Regards,
Prakki Rama.

I don't understand your question. Do you want to know the function of the different GC-contents of different genomes?

Hi, Please check my edit.

Interesting question. The GC-content seems to evolve over time and it also seems that the GC-content of coding regions is higher than for the surrounding non-coding regions (see reference 1). If there is a specific function for this higher GC-content or not is (if I understand this right) debated among the groups which do research in this field. Have a look at the references (and probably also their references) to decide on this:

Both selective and neutral processes drive GC content evolution in
the human genome.
Integrating genomics, bioinformatics, and classical genetics to
study the effects of recombination on genome evolution.
Recombination Drives the Evolution of GC-Content in the Human Genome
GC-Content Evolution in Mammalian Genomes: The Biased Gene
Conversion Hypothesis
Contrasting GC-content dynamics across 33 mammalian genomes:
Relationship with life-history traits and chromosome sizes

Thanks for the references. So, is it that the number "40% GC content" is just a statistic to know about the organism and there is not much information associated with the number?

As far as I understand it, yes.


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Why do I see so many handicapped dorbeetles?
Living in southern Germany, I often visit nearby forests and pastures.
From early spring to autumn, I frequently see lots of dorbeetles on my wanderings. An estimated amount of 50% of those bugs seem to be somewhat handicapped or crippled. All of them share the same symptoms:

They stretch their legs away from their body, moving them in a
swimming-like manner, which causes them to be unable to get over the
smallest rocks or plants. It looks very clumsy, almost drunk. Often they draw back one of their rear-end legs, getting caught in parts of plants.
Many of them are lying on their backs, struggling to get back on
their feet. When I turn them around, they will start walking in the
fashion I described above, falling over again almost instantly

Like already pointed out, not all of the dorbeetles behave like this. I see lots of bugs that seem to be perfectly fine, too.
What can possibly cause this?

My first guess would be senescence (i.e. old age after reproduction), since most adult insects are rather short lived (often less than a couple of months). The same type of apparence can be seen in e.g. bumble bees in late summer, when the bumble bee colonies start to break down, and you can se lazy and uncoordinated males and workers barely hanging on to the flowers they visit. However, I do not have any specifics for dor beetles (Geotrupes), and there might be other reasons for this particular taxa. Disease/parasites would seem like another obvious reason.

I do not know for certain but one possibility is an internal parasite.
A number of parasites have been documented to alter the behavior of the hosts to suit the life cycle needs of the parasite.  For example, Toxoplasma is a parasite use rats and cats as hosts. Toxoplasma alters the behavior of the rats so that they no longer respond to the smell of a cat. That makes the rats much more likely to be captured by the cats, which transfers the parasite to the cat from the rat (Berdoy et al. 2000).
This YouTube video shows how a fungal parasite of ants alters the ant behavior to help the fungus reproduce.
My favorite example, which I use in my introductory biology course, is Euhaplorchis californiensis, a parasitic fluke. The parasite lives in marshy habitats, such as Carpinteria Marsh in California, USA. This parasite uses wading birds (herons and egrets), a snail and a fish as it's host.  The adult lives in the gut of the wading birds. Eggs from the adults pass out with the bird feces. Horn snails consume the fecal material and the eggs.  The eggs hatch inside the snail. The larvae actually castrate the snails so that the snails cannot reproduce. Instead, the snails only feed, which provides nutrients for the parasite larvae. The larvae then leave the snail and swim into the marsh, where they are consumed by the California killifish (Fundulus parvipinnis). The parasite works its way from the gut of the fish to the brain, where it releases chemicals that alter the behavior of the killifish. Normally, if a killifish sees a wading bird, it would dive deep. Instead, the parasitized fishes no longer dive. They remain near the surface and swim eratically. This behavior makes it much easier for the wading bird to see and catch the killifish. The parasite is transfered back to the wading bird, and its life cycle begins again. Details of this fascinating life cycle can be found in (Shaw et al. 2010).
Therefore, it is possible that the behavior of the dorbeetles is being influenced by an internal parasite. These dung beetles may consume a parasite when they ingest dung from a certain species. The parasite could alter the behavior of the beetle making them more vulnerable to a particular predator, thereby continuing the next step of the parasite's life cycle.
Your description of the beetle behavior would fit this hypothesis but I stress that I do not know this. I raise the idea as one possibility among many.
A good not technical book on parasites is Parasite Rex by Carl Zimmer. It covers the biology of parasites, the many ways that parasites can affect their hosts, and the creative scientific minds that uncover the complex life histories of many parasites. (I have no connection to the author or the book.)  The book covers the above examples and more in some detail.

Thanks for your thoughts. I am truly amazed by Euhaplorchis californiensis


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what is the function of satellite in a chromosome?
What is the specific function of a satellite in a chromosome ? How are sat-chromosomes different from others ? On molecular basis, what are the functional advantages of it ?

There are at least 2 SAT chromosomes in each diploid nucleus. They
  play a vital role in the formation of the nucleolus after cell
  division is completed.
In humans, chromosomes number 13, 14, 15, 21 and 22 are examples of
  SAT chromosomes.

cuted from http://en.wikipedia.org/wiki/Satellite_chromosome


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SEREX serological analysis of cDNA expression library
What is Serological Analysis of cDNA expression library? I went through this article:http://cancerimmunity.org/serex/introduction/ but could not really make out. Can someone please explain this to me in a simpler manner?(I have not studied biology since last 8 years and now I am going through it because I need it for my research. So if someone can describe it in simple language it would be very helpful)

With this method you want to identify proteins on cancer cells which are immunogenic so you can use them to boost an immune response against the cancer cells.
To do so, you extract the complete mRNA from a cancer. These mRNAs represent all the genes which this cancers expresses (which then also contains the immunogenic proteins). These mRNAs are cloned into bacteriophages (viruses that only infect bacteria) and are then used to infect bacteria. During this infection the virus expresses the protein which has been cloned into his sequence and which originates from the cancer cell. The infection of the bacteria leads to the formation of plaques (wholes) in the bacteria which grow on the surface of a culture plate.
You then use the serum of cancer patients on these expressed proteins to see, if there are antibodies which can recognize these cancer antigens (and could be used to detect and mark them). If there are proteins which only react to the sera of cancer patients but not to controls (to exclude) unspecific reactions, then these proteins are identified and can be used to generate antibodies against this specific cancer type. It works like in the figure below (from this paper):

I hope this is understandable. If there are any questions, let me know.

" mRNAs are cloned into bacteriophages (viruses that only infect bacteria) and are then used to infect bacteria." so basically the bacteria now has the characteristics of the cancer cell? Meaning it becomes a substitute for cancer cell right??

@user3237995 No, the virus expresses (as a part of the genome of the virus) one of the proteins from the cancer cell. The virus causes then the bacteria to lyse (destroys them) which releases this protein.

The bacteria is destroyed?? or is it that the bacteria destroys the virus?

If you look on the image above, then you see these plaques in the bacteria. This is caused by the infection of the bacteria with a virus. The bacteria are used to produce the cancer protein and get subsequently destroyed. This is useful as it releases the protein for further testing.

"If there are proteins which only react to the sera of cancer patients but not to controls (to exclude) unspecific reactions, then these proteins are identified and can be used to generate antibodies against this specific cancer type."
Can you please explain what this line means?

It means that these proteins from the cancer cell cause an immune response. The hope is to mount this immune response against the cancer cell. To be able to do so, you have to be sure, that you are not targeting other cells of the body as well, which would obviously have bad effects.


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Enzyme Assay - pectinase
During assaying an enzyme at high temperature, the substrate (Pectin) is degraded by the high temperature rather than by enzyme, so, how can I minimize degradation of the substrate by the temperature?

Why do you run the assay at high temperatures? The solution sounds easy, run it at lower temperatures, but is there a reason to not do this?

I wanted to check whether the Pectinase (enzyme) is thermo-stable or not

pretreat the enzyme at high temperature before carrying out the assay at the standard temperature

Thats what I would test as well. Incubate the enzyme at different temperatures for the same time. How do you perform your experiment? In small tubes? Is it possible to premix the whole enzymatic reaction without the pectin and the pre-incubate it at higher temperatures?

I perform the the experiment in test tubes, I pre-incubate the enzyme and the substrate for about 5 minutes separately, , then I mix the enzyme and substrate then follow by incubating vfor about 10 minutes,  I tried to draw the graph enzyme activity vs temp. The rexn is good till 65°c , however, in higher temps.the absorbance values are very high

@Oli absorbance values are high even for control?

Pretreat the enzyme at high temperature before carrying out the assay at the standard temperature –  Alan Boyd


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Is this a grackle with an unusually long decurved bill (Phoenix AZ, USA)
Can someone help me identify this bird (sorry only had the iphone)? It looks like a grackle, but the bill is much longer than any I have seen. The bill looks like a Le Conte's thrasher, but it was all black. It looked pretty ratty because he was molting. It was definitely black, and in an area with lots of grackles.
The pictures don't do it justice, it was a really long bill. The pictures were taken in Phoenix, Arizona, US on Greenway bike path near Thomas Rd on 7 Sept 2014.

The picture is not that clear, but it definitely was not something that the bird was holding in his beak. That was my first thought when I saw him, but I watched him awhile, it was very clearly his beak that was long and decurved. Sure wish I had my real camera at the time.

Could it be that the bird was holding something into its beak, which made it look curved?

It could be a crow, a blackbird or a raven for all we know because deformed bills on birds has been a matter of debate (reference) and there is a group on flickr (reference) where you can post such pictures. I have actually noticed few pictures of birds with beaks that resemble the one in your photo.

A crow with a deformed bill (reference)


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Why Hasn't my Cactus Grown Deadly Spines?
I recently purchased a small cactus plant from my local store for about $5.
I've been giving the cactus lots of sunlight and a good watering every week.
I've noticed that since I bought it, the other cactii at the store have sprouted long and deadly looking spikes of at least 2 inches in length. My cactus has extra little clones growing out of it but its spikes are stunted and disappointing.
Why won't my cactus grow spikes?
My cactus is of this variety:
http://www.friendsschoolplantsale.com/sites/default/files/images/colors/a-flat-cactus2-ns.jpg?1364265449

Cross posted and answered on [gardening.se]: http://gardening.stackexchange.com/questions/13989/why-hasnt-my-cactus-grown-deadly-spines

This question has been cross-posted to "Gardening & Landscape" and answered there. The answer can be found here: http://gardening.stackexchange.com/questions/13989/why-hasnt-my-cactus-grown-deadly-spines


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What kind of spider is this? And is it dangerous? (photo)
I found this spider hanging from a web off the side of my house (in Buffalo, NY). It's probably 3-4in total length. Any thoughts on what kind of spider this is? And if it's dangerous?

I would think this is a European garden spider (or cross spider). See here and here.
It can bite humans but it is not dangerous for them.

Indeed, I recognise it from my European garden. It's not dangerous.

i think its a cross spider because it doesnt have hair around its legs

Looks like a variety of the very common and diverse group of "garden" and/or "orb weaver" group(s).  They really pop up everywhere during the spring/summer but die off w cold weather (in southeastern US).  Like mentioned, they'll bite but not poisonous...  They're the guys whose webs you're constantly being freaked out by when u hit it face-first---but then never see the spider, or at least aren't bitten normally.
The ones you gotta watch for around here don't make webs that you'll typically see, and either leave their webs often and/or remain in cracks/crevices (e.g.) brown recluse or black widow...).

If you're in NY- I'm pretty sure you would need be worried only about brown recluse and black widow- if even applicable up there (I'm in GA, so warmer here...).


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Can a single axon propagate multiple simultaneous action potentials?
I have not been able to locate any research that indicates whether a single axon of a neuron or nerve cell can conduct multiple simultaneous (i.e. spatially separate) action potentials. I am aware that in many neurons refractory periods would preclude this possibility, however in some cases delays along axons are large enough.
Is this the case? Can you point me to any citations supporting your answer?

Yes, but there is an upper bound to the maximum amount of energy per axon. There is no empirical evidence of this about what is the exact energy spectrum which each axon can hold. This would also show you which action potentials an axon can propagate or hold. There is no sufficient imaging technology there openly which could be used to do some of the research.

When you say multiple simultaneous action potentials I assume that the stimuli for all of them are temporally overlapping. In such case a neuron can integrate the different stimuli and launch an action potential. Of the multiple stimuli some can be excitatory while others can be inhibitory. The net response would be an integration of all the signals [ref].
However, if there is a gap in the stimuli then the cell may not react as it would be in its refractory period (which results until the ions levels are back to their original state and the membrane potential is restored).
There can be long delays, which depends on various factors such as ion deficiency, ATP deficiency (ATP is needed by Na+/K+ ATPase) or neuropathological conditions. In case of nervous signaling over many neurons then synapses can suffer from synaptic fatigue, which results because of depletion of neurotransmitters.
EDIT:
Maximum AP propagation speed/Nerve conduction velocity = ~120m/s (Can't find original source. From wikipedia)
Longest myelinated axon (sciatic nerve in humans) = ~ 1m
Time required to reach synapse = ~8ms
Time required for repolarization = ~5µs
So multiple action potentials (~160), are possible (lets call it situation-X).
The squid giant axon is ~500µm. I believe it is also non-myelinated. In this case if NCV is less than 100m/s then situation-X can happen. NCV can go as low as 0.5m/s (again the reference is wikipedia as I cannot find the original source).
Having said that, situation-X can also cause synaptic fatigue if the firing rate (AP frequency) goes beyond a certain value. This value would depend on how much neurotransmitter is released per AP, how much is in storage and the uptake rate.

"stimuli for all of them are temporally overlapping" ... this is not the right idea. the question is not about summation of stimuli but production of APs in short succession which are simultaneously propagated in the same cell (obviously with some spatial distance). Also refractory periods are discussed in the question.

@watsonic Ahh. You mean what if in a long axon the first AP has not reached the synapse but the soma/dendritic region is already repolarized?

yes, for example. or one AP on the axon proximal to the soma and one distal.

@watsonic see the edit. I hope it answers your question.

Let us continue this discussion in chat.

I don't see why not, once the sodium and potassium channels along the axon have returned to their resting state. But I am not aware of a hard citation. I would suggest looking in the recent optogenetic literature, where researchers are exciting axons and axonal terminals using channelrhodopsin. People have most likely quantified action potentials for varying illumination durations and intensities, and you might be able to judge by the maximum firing rate how feasible multiple simultaneous spikes would be.
Also, it's most likely possible to trigger an antidromic spike while the neuron is firing an orthodromic spike. Not quite what you asked, but close.

Antidromic electrically evoked potentials plus normal  physiological responses :) - Good thinking !