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Biological implementation of convolutional neural networks
In computer science, 'convolutional neural networks' are used, that are meant to be inspired by biological network structures like found in the human brain visual cortex.
In the computer implementation, the 'convolution' means that any neuron of a certain 'layer' is linked with several spatial adjacent neurons in the previous layer. When those networks are trained, the 'weights', which are analog to synaptic strength, of all neurons of one layer have an equivalent local topology, and thus can be mapped between the neurons, and finally unified. This way, only one 'weight' is trained for all equivalent synapses on all neurons of an layer.
Is there any biological mechanism found that may sport this feature? My guess would be that the vision cortex is partly organised by self structuring not depending on neural activation to achieve low level vision processing. Otherwise, all neurons in one 'layer' would need a way to exchange information to synchronize their synaptic structure.
However, I guess that the human brain would have some mechanism of this kind, as it would provide for example the ability to learn the detection of certain visual patterns or events independent of their retinal position, without learning the detection individually for every image location.
Is any such mechanism known or how could it work?

As you already said, there are several parts of the brain that have this kind of mechanism. I am not clear about what you are asking.

The usual model of neurons and plastic synapses does not explain this feature, as large numbers of physically unconnected synapses would need to have some magic remote communication to equalize their transmission strength. So my question is if there are any mechanisms known in neural tissue which may implement this feature.

I believe CNNs were inspired on the fact that the visual cortex has neurons that have a fairly small "visual field" and they overlap each other. Not necessarily that they are tied together.

The eye might provide alone an example of a convolution neural network (as made popular for image classification tasks).
The cell types and synaptic connections in the retina are even organized in layers (laminae) to make the parallel clearer, as seen here:

source: http://webvision.med.utah.edu/book/part-vi-development-of-cell-types-and-synaptic-connections-in-the-retina/development-of-cell-types-and-synaptic-connections-in-the-retina/
The topology of the network is in a sense self-structured but a relatively slow process as the blueprint is a product of Evolution and the practical implementation (actual cells and connections) takes place during the development of the organ. "Weight tying" can then be seen as a result of having different cells types in the network.

I would agree that this is a data processing convulutional structure. But shared wheights (maybe encoded by cell types) would be a genetical feature then, and they can not be trained in a shared fashion in the living organism. Simply said, if the circuit learns by weight adaption how to detect an eye projectet to part of the retina, that doesn't mean other parts of the visual field would detect this eye as well.
This feature however holds for CNNs by sharing the weights on all convolutional subunits in one layer and speeds up learning by orders of magnitude.
So can brain do this?

I believe it is important to create a distinction in terms of what level of visual system you are referring to; i.e. retina vs higher level cortical visual areas. Also, if I remember correctly, the weights are represented by the strength of synaptic connections, which are modified adaptively during the process of learning and not hard-coded by genetics. You might find it useful to take a look at http://goo.gl/ygP6nF

One could hypothesize that "learning" takes place at two levels: one is evolutionary and one is within an organism's lifespan. Cell (neuron) types are "trained through evolution (may be not the idea you had of speed though but the same advantage, presumably). Regarding the amount of visual "processing" performed down by the retina (not everything is down in the cortex), there is a relatively short read on wikipedia: https://en.wikipedia.org/wiki/Receptive_field


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Why are nitrogenous bases of DNA hydrophobic if they can hydrogen bond?
Why are nitrogenous bases of DNA hydrophobic if they can hydrogen bond?
Is it that they are only relatively hydrophobic?
This forum explains it but does not give an example of the structure.

This is better off at Chemistry.SE and I voted to close.

They are not hydrophobic.. They are quite water soluble. See this data sheet for adenine.

@AliceD This is about biological molecules, I see no reason why it would be off-topic here.

@MadScientist But this is about solubility, so these are physical properties of the molecule. This fits better into chemistry or physics.

@MadScientist - I don't see any clue to any biological compound in the Q. I know, implicitly I can autocomplete this question with amino acids etc etc, but I don't see it in the Q. Until placed in a Bio framework, I leave my close-vote where it is :) Plus, the link to a physics forum speaks for itself.

Definitely more of a chemistry question. Short version: In addition to hydrogen bonds between pairs of bases, interactions between stacked aromatic purine and pyrimidine rings of nucleotides stabilize DNA molecules.
https://en.wikipedia.org/wiki/Stacking_(chemistry)

@AliceD Nitrogenous base generally refers to the nucleobases in RNA and DNA, and those are certainly biological molecules. The question about hydrophobicity and hydrogen bonding also have biological implications.

@AliceD The question was asked in the biology section of physicsforums.com ;) I think this is on-topic here. Plus there are plenty of question on DNA and more that chemistry SE doesn't send our way.

The term "nitrogenous bases" was confusing; so I fixed it. This is a question on biochemistry and most biochemists would know the answer. I would not consider this off-topic. Note that questions should be pushed to chemistry SE only if they concern certain advanced concepts that are not generally covered in basic biochemistry.

These two concepts are not mutually exclusive. You have constructed a false dichotomy.  Both of these facts are true:

The electrons in the pi orbitals of the conjugated double bonds in the planar rings are hydrophobic and can "stack" on each other as shown in this drawing of a DNA helix where the bases are shown as planar rectangles:

The nitrogen and oxygen molecules (either in the rings, or as substituents on the rings) can participate in hydrogen bonds (H-bonds):

There are other examples of hydrophobicity and H-bonds co-existing.  For example on the interior of proteins.

I am sorry, I don't understand the answer. Why are both the facts true? I think that is what I want to understand more.

Hydrophobicity and and hydrophilicity aren't yes/no things, they're gradients.

@Whitecat Most detergents are also hydrophobic and hydrophilic at the same time.

I think the confusion here is that no, the DNA bases aren't in themselves completely hydrophobic, but in the region of the planar face of each base is a zone of hydrophobicity. In this way, base stacking becomes favorable where water molecules would otherwise attempt to order themselves to maximize hydrogen bonding with each other.

@Kendall Can you add that to the the answer?

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Can someone tell me the species of this lizard?
It's a green lizard with a silver tail, and it has pretty, bluish eyes. I saw it today, July 26th, trying to get some shade on a hot, sunny day (32 degrees) at around 18:00 in Austin, TX USA. It's been hot and dry here the past few weeks, but it rained a lot a few months back.
Austin has a humid subtropical climate. The city is characterized by hot summers and mild winter days and usually cool to cold winter nights. The geo coordinates are 30.4 (lat), -97.7 (long).
Oh, it was able to jump a good meter.
Thank you.

I know nothing about lizards, but this looks like a Carolina anole (Anolis carolinensis), also known as a green anole. Apparently they can change colour:

Yes , an anole. Very common , more than you see because they prefer to be in trees. Sometime wrongly called chameleons.

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Why does a wound itch while it's healing?
During healing of wound (almost in final stage) it begins to itch a lot around wound.
I wondering what the reason for this is?

While healing your wound the cells in and around it are enhancing their communication via messenger substances to quicken and coordinate the healing process. These messengers irritate the sore nerves which we feel as itching.
Skin tension is another factor to itching.
Scratching is bad for the healing process in any way.

Interesting answer. Could you provide a reference?

@GoodGravy i don't remember the exact source but this i found on a quick search.


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Through which mechanisms did the Drosophila Histone Cluster evolve?
The Drosophila Histone Cluster is a gene cluster that contains more than a hundred copies of a sequence that encodes several histone proteins. These copies are very similar.
My question is what mechanism are known that could have played a role in the genesis of this cluster?
I'm aware of the possibility of recombination, which might expand the cluster on one chromosome, shortening it on the other. Are there any other mechanisms to expand or change the cluster and are there telltale signs left by these mechanisms in the genome sequence?
Given that in most species histone genes aren't clustered, it would be weird to assume that recombination is the only mechanism to duplicate these sequences. Also, at one end of the cluster bits and pieces of histone genes are mixed with other sequences, a bit like all the broken copies got pushed to one end. It would be interesting to have an explanation for this pattern.

Isn't this explained via gene duplication events? Or am I misunderstanding the question?https://en.wikipedia.org/wiki/Gene_cluster#Gene_duplication_and_divergence

Yes, but there are different gene duplication events. I already mentioned recombination. Is retrotransposition a possibility for histones? Can replications slippage account for 5000bp duplication? Or what is the max length for replication slippage? Is recombination the only mechanism that results in back to back copies?

It's an interesting question, though I don't think your claim that histone genes aren't clustered in most organisms is correct. On the contrary, both yeast and humans also have histone clusters. Given the evolutionary distance between these species, it would seem reasonable to expect that this phenomenon is quite ubiquitous.

This is the best review I have seen with a comprehensive discussion on gene duplication and amplification mechanisms (and it is also quite recent). It seems like there may be no definitive answers to your question in the literature--perhaps because of a paucity of viable experimental models that would allow one to test various hypotheses.
Also @canadianer is quite correct. Most metazoans with sequenced genomes have some kind of clustering of their histone genes (as well as multiple copies). In Drosophila embryogenesis the early zygotic cell-cycles are extraordinarily brief, on the order of 20 min as I recall, which means the fertilized egg is essentially a bag of DNA polymerase replication complexes.  Therefore there is a very high demand for histone proteins.  The gene amplification you describe is one way to achieve high concentrations of histones in a short time-frame.
Note that not all metazoans undergo this rapid burst of synchronous nuclear division, and therefore not all species have such a high copy number of core histone clusters.

Thank you, that is an interesting tidbit and what looks like a nice overview.  I upvoted so you should get the bounty if nobody else comes along, even if I forget to accept the answer. But I'll probably do that later today anyway.


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What is the DNA sequence of an apple?
I read that the genome for Malus Domestica was mapped, but I can't find a sequence anywhere.
If this is a stupid question, I would appreciate if you would please tell me where I am wrong in this!

Googled "malus domestica genome sequence". First result was this paper, which includes this genome bank entry (which is also the second search result)

@Luigi Thanks, but I don't know how to make sense of the genome bank entry

If all you want is to download the sequence of all the chromosomes, look at the haplotype assembly. Download the first file (psuedomolecules) and unzip it. Then you'll have the sequence of each chromosome in FASTA format.

https://www.rosaceae.org/species/malus/malus_x_domestica/genome_v1.0
You can see the data in the URL above. The details are described in this article.
As others said, NCBI seems useful.
Go to this site.
Chose chromosome you want to see and click genebank or refsequence corresponding to the chromosome in the table (Assembly Unit: Primary Assembly).
You can see overview of the sequence.
Find FASTA in the page showing the overview and click FASTA. Then the sequence data will be downloaded.

Thank you, I had a look at the above link, but I'm still not seeing the DNA nucleotide sequence.

The sequence data is shown like https://www.rosaceae.org/gb/gbrowse/malus_x_domestica/ You might be able to extract sequences from this. But I have not used this particular site. At least, you can see the conting sequences indicated in red by clicking the red areas like https://www.rosaceae.org/gb/malus_details?id=1311210

Thanks for your help. I used the DNA database at http://www.ncbi.nlm.nih.gov/ to find the answer

Here is the apple genome on NCBI.
http://www.ncbi.nlm.nih.gov/genome/?term=Apple

How many lines of nucleotide sequences are there?

Are all sequence lines necessary?

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Identify ~6-7mm long green creature

Here is the creature I found on the glass lid of my light bulb. I guess they are attracted to light as they all concentrate on the light source. I live in Hong Kong. The brown things aren't moving (those might be eggs). The green creatures are about 0.6-0.7 cm long in body length (excluding appendages and antennae). They are sluggish in movement.
Can you help me to identify these tiny creatures?

Welcome to Biology.SE. Can you please try to add some information. For example: Where do you live? What size are those? Can you tel us more about their behaviour? Are the browns things alive or is food or is it just stain on your light bulb?

I don't have much information about it. My mum fear it will spread and so I clear them away immediately after I take the photo. I live in hong kong. They are about the size in the original photo here (no magnification). And the brown, oval things I suppose are their eggs. They are sluggish in movement and I clear them easily. The eggs are kind of sticky.

I edited your post to include those info and make few other modifications. Feel free to rollback if you don't like my edits. +1

This is the first time I use this platform to post question. Thanks for your kind help.

Yep, I know that feeling! This is all good! Thanks for the extra info. I personally have no idea what it could be but I am not a good naturalist!

I see 14 eggs and 14 individuals They must have just hatched, which will make identification very difficult.  Maybe Miridae ?

Good observation. So one likely possibility is their adult form can fly and it reach the light bulb to lay the eggs. The larvae hatched and it seems it was an unsuitable environment for them and so they appear sluggish.

Based on its morphology, it should be evolutionarily adapted to living in aquatic environment I guess.

I have no idea what they are, but they are fascinating looking and rather beautiful in their way. Thanks for sharing.

This is an insect (6 legs) and a seems like a nymph (hatchlings that are not larval); if they really are hatchlings. There are a few family of insects that hatch this way. You may have a look at them. Seems like green mirid but could be baby crickets too (I am not an expert in this area).

Amazing nature.

Let's take a look at the magnified body of the insect (it is a nymphe btw) - we can see 2 brown dots one above the other along the body line. This pattern is very suggestive to Chelinidea species (the most common is Chelinidea vittiger aequoris):

I stop my search at Coreidae family, because multiple species (a lot of bugs actually) of this family have similar appearance, for example:
Gonocerus acuteangulatus:

But other enthusiasts can start from here (Coreidae family) and trace it down more precisely - I am sure they will succeed.

Thanks for your answer. It is very helpful. I will research on it further to evaluate this possibility.

Thanks a lot for sharing your knowledge. Execellent picture quality of those creatures.


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What is the surface area of the vitreous humour in contact with aqueous humour?
This is a question regarding the anatomy of the human eye, however for my purposes medium sized mammals should do. I am interested in estimating the surface area of the hyaloid membrane of the vitreous humour which has contact with the aqueous humour circulating in the posterior and anterior chamber of a typical human eye.
The surface area in question is highlighted in red in this schematic of the cross section of the human eye.

Area=πr², d≈2cm (less than maximal d) -> r≈1cm,  thus the area in question is roughly
3.14*1cm*1cm≈3.14cm²
UPD by request (ref):
The vitreous body base middle is at ora serrata (+-2mm), so we should calculate the area at this level. Here is the reference of the diameter:

from: Basic and Clinical Science Course, Section 02

Wonderful, thank you very much! I don't suppose you happen to know what the point where the vitreous meets the lens is called?

@Freeman i've already told you - come back to your prev. question

@IIan thank you. Thanks for the reference also, that looks like a great book to keep hold of!


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How does Bernoulli’s Principle apply to the cardiovascular system?
Below are graphs which illustrate the cross-sectional area, velocity, and fluid pressure through each vascular segment of the cardiovascular system.

It makes sense that velocity and cross-sectional area should be inversely related graphically (by the equation of continuity, ($v_1A_1=v_2A_2$). However, Bernoulli’s principle states that where velocity is high, pressure is low, and vice versa. However, in the graph above, clearly pressure is decreasing as you move away from the aorta, regardless of velocity.
I can understand how the pressure in capillaries will be higher than those in venules, since a higher pressure in capillaries would accelerate the blood as it moves into the venules with a lesser total cross-sectional area. This agrees graphically, since, past the purple stripe, the pressure curve decreases as the velocity curve rises. Yet the mean arterial pressure in the aorta and arteries seems to violate the relationship between velocity and pressure stated in Bernoulli’s principle. What is there to make of this?
(Image taken from Campbell Biology, 10th edition)

Bernoulli's principle can be a little tricky when applied to the cardiovascular system, but it still holds true across the entire system. You mention a good point that the relationship doesn't seem quite right at the aorta or arteries, because of the constant fluctuation of pressure between systolic and diastolic without a significant change in diameter of the vessel. Remember that this is due to the pulsatile flow of blood from the heart, and has nothing to do with Bernoulli's principle. If the flow was constant (i.e. not pulsatile) then the pressure would be constant as the diameter of the vessels is constant. As the diameter of the vessels begins to decrease the velocity would increase to maintain a constant value.
As you mention, Bernoulli's principle describes how the product of area and velocity of flow must be constant across a system. When the total surface area of the system increases, the pressure decreases as well as flow. It is important to remember that even though the capillaries are so small and individually high resistance (which you would think according to Bernoulli's principle should increase the velocity), you are effectively adding an innumerable number of these very small resistors in parallel (not in series) and the resistance overall (and subsequently pressure + flow) decreases greatly.
When adding resistance in series the total resistance is additive and it adds up quickly! $$R_{Total} = R_1 + R_2 + R_3$$
While resistance in parallel adds the reciprocal of the resistor, meaning that as more resistors (or capillary pathways) are added the total resistance continues to decrease because of the following relationship: $$\frac{1}{R_{Total}} = \frac{1}{R_1}+\frac{1}{R_2}+\frac{1}{R_3}$$
The parallel resistance stuff was difficult for me to grasp when I was a student, because it never seemed to make sense in my mind that the resistance significantly decreased when you added all these small capillaries. One of my physiology professors described it well when he said, "Think of adding resistance in parallel, in the way that capillary beds and other vessels are in the cardiovascular system, like giving the blood another place to go." If the blood has more places that it can go, then it's easier to see why resistance falls so much when you add a bunch of extra places for the blood to flow.

I think there are several things that keep Bernoulli's principle from being straightforwardly applied.
First, Bernoulli's principle would help us calculate the pressure exerted by the blood on the walls of the vessels, but that's not what blood pressure measures. Blood pressure measures the amount of force that has to be applied to stop the blood from flowing forward. There's some relationship between the two, but it's not clean.
Second, the branching makes the surface area calculations different from a single pipe. The arteries have more cross-sectional area than the aorta, but they have have much, much more surface area-- way more of a difference than a single pipe with those cross-sectional characteristics would have.
So Bernoulli's principle does mean that blood is exerting more pressure on the surface of the arteries and arterioles than it is in the aorta. However, pressure is force per unit area, and there's much more area in the smaller vessels, so the pressure in any single vessel is less.

I love this question, and there is a number of things to unpack.
Exactly where we are measuring a pressure in that circut matters. We usually measure a persons BP in the brachial artery, so relatvely on the left side of your picture.
Here, we can consider the pressure to be part of a simple circut, where Pressure = Resistance * Flow (ohms law).
Vasoconstriction of artieroles further downstream could be considered to be increasing resistance. This results in an increase in pressure at the level of the arteries and specifically, where we measure it at the brachial artery.
(As a side note: it doesnt overly matter at this level that the distal system is in parallel. For simplicity, vasoconstriction will still increase the overall resistance. In a parallel system, increasing all or most of the resistors still increases the overall circuit resistance)
==========================================================
If we were to look at what is happening in the microvasculature, its a very very different kettle of fish, and much more akin to what you are describing with Bernoulli's principle.
In areas subject to vasoconstriction, there is indeed a decrease in pressure. This means there is less perfusion at that area (due to a decrease in hydrostatic pressure, see starling forces).
In areas not subject to vasoconstriction, there is a relative increase in pressure and therefore an increase in perfusion.
This about why this matters - We want to keep perfusion high in places that need blood (the brain, the kidneys), so they will stay relatively dilated. Conversly, if we dont need to perfuse our muscles, we can direct blood away from them and perfuse other organs preferentially by constricting their blood vessels.
Its probably worth noting as well - the resistance happens PRIOR to the capillaries. Capillaries dont change size. The artieroles and meta-arterioles do but the pressure before and after them does change and the pressure will be lower in areas that have undergone constriction.
To make matters more complicated however (read on at your peril);
If we also apply Ohms law at the level of the microvasculature and we consider this to be a parallel circuit, consider that increasing resistance will also lead to a decrease in flow. This is "shunting", where blood will flow preferentially to areas of less resistance. This extra flow 'would' (with an ideal fluid and non-compliant vessel), increase flow and decrease pressure. However, blood does not behave like an ideal fluid, and its viscosity prevents its speed from increasing as you'd expect. Moreover, the blood vessels tend to expand with the increased blood volume, increasing the radius of the vessel which significnatly decreases speed and overall actually probably increases its pressure (since radius is SUPER important in determining speed).
NB: This is STILL a huge oversimplification of a complex physics system - we havnt even touched on the effect of gravity and columns of water (is the perfusion pressure in our feet HUGE??!)
Happy learning!

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How to validate the use of an anti-virus monoclonal antibody in IHC by spiking a fresh organ with infected cultured cells?
I have assessed the specificity of a particular monoclonal antibody against a virus by immunofluorescence. I'd like to further validate it by testing it by IHC. Therefore I'd like to infect cells in culture, and then inject them in a piece of fresh organ, fix in formalin, embed in paraffin and then cut slides before performing IHC. Is there any protocol or references to do so ?

Injecting into a fresh organ seems like a needless complication if you're just validating your antibody and not interested in gathering data about the interaction between the cells and the organ. (In fact, if you're using anything more complex than a flatworm I'd hope your IRB would have problems with needlessly sacrificing animals to get those organs.)
It seems like your purpose would be better fulfilled by making an FFPE cell plug and doing your IHC on that. Here's a protocol for making cell plugs:
Johns Hopkins Tissue Microarray Lab Cell Plug Protocol

Thanks you for your answer. Actually this was a request from a reviewer. Regarding organs I work close to the vet necropsy department therefore getting fresh organs is not an issue.


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Can axons act as receptors?
In all histology books, it is stated that all sensory nerve endings (receptors) consist of dendrites that translate physical stimuli from the environment into neural signals. However, several sensory neurons seem to include axons, such as the merkel and olfactory cells shown below. They act as receptors, but feature axons as well. So is it the pictures, or the texts that are incorrect?

Axon is a kind of dendrite actually..

What exactly is your question? Whether 1) axons are part of sensory neurons, or whether 2) axons can have sensory function (given that dendrites typically act as receptor)? Please clarify.

@AliceD Sort of, technically they both are cytoplasmic processes.

@AliceD I just said axon is a kind of dendrite — a specialized one (both of them are grouped together as neurites, btw). So there is no argument here. Moreover, unlike apples and pears, dendrites and axons are the part of the same biological entity.

I removed the apples and the pears - bad analogy :) But I can't settle for an axon and dendrite being similar - http://biology.stackexchange.com/questions/9026/what-are-the-functions-and-differences-between-axons-and-dendrites there are a host of differences. No problem in having a different opinion here though. We are from different disciplines.

@AliceD When did I say that I do not acknowledge the differences? (Also I don't think I come across as an unreceptive person.) They have both similarity and differences. In bipolar neurons they look quite similar as well. In pseudounipolar neurons axons carry both afferent and efferent signals. Biology has several cases of non-absolute rules. You can always find domains of similarity and differences.

i mean can axons act as afferent nerve fibers (receptors)?

I slightly modified the question based on your comment above to clarify this question to the best of my understanding - I added an answer too. Feel free to roll back my changes if it doesn't reflect your ideas. +1 for this question. Very enlightening.

Short answer
The textbooks are right; the receptor part of sensory neurons is always considered to be the dendrite. Axons are nonetheless an integral part of some receptor types to send the signal to the brain. Other, more specialized sensory cells do not have an axon and therefore rely on secondary neurons to send the signal to the brain.
Background
There are three types of sensory cells, namely those with free nerve endings, those with specialized dendritic structures, and specialized receptor cells that synapse directly onto a secondary neuron (Fig. 1).

Fig. 1. Types of sensory neurons. Source: Premed HQ.

Sensory neurons with free nerve endings have an exposed dendrite that functions as receptor. Examples are nociceptors (pain receptors) and hair follicle receptors.
Other sensory neurons are complex cells that feature a dendritic region specialized for a particular receptor function. Examples are the Pacinian corpuscle and olfactory neurons.
The most common receptor type are specialized receptor neurons that have no axon and need a secondary sensory neuron to send the signal to the brain. Examples are the photoreceptor cells in the retina, the hair cells in the cochlea and Merkel cells.

In all histology books, it is stated that all sensory nerve endings
  (receptors) are made of dendrites which conduct sensation from
  environment to body but it doesn't seem to be true.

The phrase "nerve endings" (or "free nerve endings". See Wiki page) is typically associated with fine hairlike structures throughout the skin and organs that act as (one type of) touch, pain, or heat sensors. These are, yes, extensions of the dendrites of sensory neurons whose cell bodies live in the dorsal root ganglia of the spinal cord and who send the signal on via axons, either locally within the spinal cord or to brain structures.
But this is not the same as saying that all sensory structures of any sense modality are dendrites or extensions of them. Each sense has specialized cells to detect that sensory stimulus. The eye has photoreceptors (rods and cones), the ear has inner hair cells, the nose has olfactory receptor neurons, the tongue has taste cells, and the skin and organs have free nerve endings and specialized mechnoreceptors such as pacinian corpuscles. Most of these do the work of transducing the stimulus in a specialized receptor portion of the cell, such as the rod itself, or the cilia of a hair cell or ORN, etc., and then the signal is sent to the next cell in the sensory chain via a synapse, sometimes via a very short axon or just sort of axon "nub".


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Two different Leucochloridium infected snails - different species?
In the last three days, I have found two snails infected by some species of Leucochloridium. I found them in my garden in the south-west of Sweden. Now I'm wondering if they are the same species or not.
One has broodsacs with green stripes and looks like a typical Leucochloridium paradoxum, and the other has brown stripes, which makes me think it's a Leucochloridium variae, but I've seen it mentioned that their appearance can vary.
Update: I have learned that there is only one (documented) species of Leucochloridium in Sweden, so maybe I should close this question, but I would still like to know if there is a way to tell the difference just by appearance.

And here they are in animated form in case that is helpful:

Those pics and animations are so cool. Just to satisfy my curiosity: How does time scale with your gifs? +1

Thanks! Hmm... I'd say that the gifs might be a little bit faster than real life, but the green one looks pretty close to how I remember it. (More here if you feel a need for it: http://reanimateobjects.tumblr.com/)

This is fascinating! Very very little will creep me out but snails parasitized by these flatworms have since I first learned of them years ago. Great photos and gifts!

I wouldn't close the question yet.  It's possible that there is more than a single species of Leucochloridium in Sweden even if there's only a single documented species. Take a look at https://www.fugleognatur.dk/gallery.asp?mode=ShowLarge&ID=388472 that's from Denmark. I don't have any more info than that to share

@Jude Oh, thanks for that link! Searching for the species L. perturbatum (instead of the synonym L. variae) led me to this article saying you can tell brood sacs apart from colour and banding: https://www.ncbi.nlm.nih.gov/pubmed/23659278 So now I just need to find out exactly how to do that.

Very cool.. +1 for the extra work of creating these GIFs. And I'm glad to hear you were able to get your [initial] question answered.

An intriguing question. Because I have not conducted any formal research into the parasitic family of Leucochloriidae, I shall hazard two options which would not require genomic sequencing.
Principally, as you suggested, observing the banding of the broodsacs is one critical means to distinguish members of this genus. The study entitled 'A
REVISION OF THE FAMILY LEUCOCHLORIDIIDAE POCHE (DIGENEA) AND STUDIES ON THE MORPHOLOGY OF LEUCOCHLORIDIUM PARADOXUM CARUS' describes its broodsacs 'typically' to have green banding with dark brown and black spots. On the grounds that this indicator is liable to being variable, the next procedure may yield greater accuracy.
The secondary host of most Leucochloridium species, including paradoxicum, is an adult bird ranging from crows to finches in which the larval mircidia enter the bird's tract and develop into distomes through consuming the snail's infested tentacle. Moreover, if possible, determining the secondary host of the parasite may assist your taxonomic identification: the Leucochloridium often gives its host's left tentacle the resemblance of a maggot, attracting the American Robin, for example.
Ultimately, analysis of the distomes produced in the secondary host phase could allow you to discriminate at the specific level.
Information regarding Leucochloridium variae, available from: http://eol.org/pages/849160/details
The cruel world of parasites


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Why is the pituitary gland located in the brain?
Why is the pituitary gland located in the brain in humans, instead of elsewhere in the body? Why would this be an evolutionary beneficial adaptation?

The evolutionary pressure on the location of the pituitary is likely not the reason why it resides at the basis of the brain. Instead, its (partly) neural origin makes it anatomically (and functionally) part of the brain. Why would it migrate out of the brain when it doesn't have to? What would the evolutionary pressure be on increasing the length of the axons connecting it to the other parts of the brain? It is part of the brain, hence it is located there. It clashes with the principle of parsimony to have the pituitary evolve to a structure located farther from the brain.
The neuroanatomy of the pituitary is schematically as follows (Fig. 1):

Fig. 1. Pituitary gland. Source: Imagekb.
The posterior lobe of the pituitary gland consists largely of extensions of processes (axons) from the hypothalamus and are part of the neurohypophyseal system. There are neural connections to the brain and other centres of the hypothalamus. Hence, the posterior lobe is neural tissue.
The cells constituting the anterior lobe of the pituitary gland are embryologically derived from an outpouching of the roof of the pharynx, known as Rathke’s pouch.


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What is this flower?
I was in Germany recently, and I saw again a flower that I'd only ever encountered before at Meijer Gardens. It's interesting to me because I'd never seen a flower with color variation in only the 'interior' petals. Try as I might, however, I can't seem to find it anywhere! Can anyone tell me what this is? I'd like to be able to learn more about it.

Are you asking about the violet flower or the white/pink one?

For the violet/purple I would guess it is some variety of petunia. (Sorry, I wanted to edit my comment but that guess came 1 minute too late to do so.)

The white/pink one, I probably should have made that more clear.

It's Verbena hybrida Voss (See here; the page is in French though).

It belongs to verbena genus in the family Verbenaceae. It's about 10 to 50 centimeters tall with a squarish stem and opposite leaves.The flowers are small with five petals, and borne in dense spikes on the top. Verbena hybrida Voss is always used as ornamental plant. They are drought-sensitive, tolerating full to partial sun, and enjoy well-drained, average soils. It's always plant in warm and dry and sunny environment. About why a flower with two colors in one petal, it's because there are always two kinds of pigment in the petals. The pigments in different temperature and different acid alkaline environment present  different colors. When the flower is open, the acid-base property changed will lead to petals present different colors (K. Yoshida et al., 2009).

What is meant by Voss. Is it a subspecies?

It is the authority of Verbena hybrida. In Linnaean binomial system of nomenclature, authority name adds after plant name. But sometimes, Verbena hybrida is all the same.


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Colormetric assay for a phenol product?
I am working on an assay for phenol products created by a colony of bacteria. I have searched up a paper that involves gibbs reageant but the protocol is kind of unclear.
Does any of you know where I can look for a detailed protocol for a gibbs reagent colormetric assay (preferably one that uses cell medium)
Thanks

I have not used the assay myself, but Bhuiya and Liu "A cost-effective colorimetric assay for phenolic O-methyltransferases and characterization of caffeate 3-O-methyltransferases from Populus trichocarpa." Anal Biochem. 2009 384(1):151-8 [link] seems to have a relatively straightforward protocol.
Roughly, you make a 0.4% (w/v) solution of Gibbs reagent in ethanol, and then add one fifth volume of that to your enzymatic reaction mix. You then observe the solution spectrophotometrically.
The biggest issue I see is that it looks like each phenolic compound has its own absorption maximum, and widely varying extinction coefficients. In their protocol it seems they look at full range scans, rather than single wavelength measurements. You'll definitely need a standard curve for your particular phenolics in order to get quantitative results. (Also, any background phenolics or medium absorption in the 400-600 nm range may throw off measurements - use appropriate blanks.)


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What is the definition of the life biologically ?
I want to know what is the definition of the life biologically , on the other hand ,  what is the definition of the death biologically  ?? However, I think it is a very difficult question to answer .

It is something that has its own metabolism and can reproduce I think.

I'm voting to close this question as off-topic because it is about philosophy.

I am really surprised by the attitude, that the question "what is life" should  belong to philosophy only. It should be at the core of biology! The work of Tibor Ganti comes to mind.

Could not fit in a comment..
The question is off-topic
Biology is the study of life. Without a good definition of life, Biology itself is poorly defined. It appears that there is no universally accepted definition of life and therefore Biology (just like Chemistry and Physics to cite other examples) is a poorly defined field of study. But it is not scientists job to decide whether their work should stand within one category or another, nor whether those categories are natural categories (see prototype theory) or not. It is the job of philosophers and therefore this question is about philosophy and is off-topic here.
Few notes about the definition of life
Most often, philosophers see a continuum from not living to living things and not a clear dichotomy (ref.).
Biologists, most often just assume that bacteria, archea and eukaryotes are living things while viruses, viroids and prions are not living things. This arbitrary dichotomy is based on the concept of metabolism. However, this dichotomy can lead to some limit cases. Typically, considering viruses as not being living things yields to intuitive issues when thinking about macroviruses such as Marseillovirus and Lausanevirus.
There are two questions in your post
Of course, the definition of what is dead is a total different question from the question of what is a living thing. A stone is not dead it is just not a living thing. Even then, the definition of death is of interest to philosophers, not to biologists. You should always try to limit your post to a single question.

Well, that is curious to receive down votes for this comment/answer.

I down voted because I disagree with your opinion. Biology is the study of life; how, then, is a question about its definition off-topic?

because this answer dignifies the question

@canadianer The field of Biology is itself poorly defined. Just like are Physics and Chemistry and it is not the job of scientists to care about whether their work should be considered as being part of one field or another. Typically virology is field that is mostly part of biology although viruses are usually considered as not being living things. This question is definitely about philosophy and there are several philosophy books that discuss this issue as the one I linked in my answer.

@aaaaaa the answer dignifies the question. What do you mean? Is it good or bad?

@Remi.b I mean there are some questions that should not be dignified with an answer because those questions are so low-quality

Oh....that's a good point. I guess I often dignify bad questions with answer (and voting to close in the same time). I feel bad when someone don't get any help. But that's probably not helping them nor the site.

@Remi.b If you can provide an answer, it's good to see! But these answers will attract down-votes because they will of course be fundamentally flawed by the nature of the question - hence the question gets closed.

I am curious what you think about the work of Tibor Ganti. He deals with such questions and such theoretical biology does seem to be a valuable area of research. I don't get the remarks why such questions should not be "dignified" with an answer, or get answers like "it's all up to philosophy" from biologists.

I have never read from Ganthi, so I can't comment unfortunately. What is life? can be rephrased what is the definition of life? and a definition is whatever you want it to be. There is no right or wrong when defining terms. Sometimes, there are commonly used definitions of course but there are no right or wrong definition. You might want to read [this post](Why isn't a virus “alive”?) though.

Note that the question has not been closed for being off-topic but has been closed as a duplicate.


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Can geckos climb a wet surface?
We know geckos can climb vertically or even upside down a surface like glass. But can they do that on wet glass?

Yes , they can! (Obama)

Short answer
Yes they can, but with less efficiency.
Background
Efficiency of sticking to a glass surface decreases about 20-fold when the gecko's feet are wet (Stark et al., 2012). On dry glass, Gekko gecko holds on with about 18 N, which is about 18 times their own body weight. Hence, the gecko attachment system is over-designed (Knight, 2012). Wetted toe pads reduce the adhesive force significantly down to 0.9 N. A wetted glass surface does not significantly affect the grip of Gekko gecko, except after the gecko takes multiple steps. Hence, geckos can cling to wet surfaces, but only when their feet are not getting too wet.
Note that gecko attachment is not based on suction, such as the suction cups seen in octopus. Instead, geckos cling to surfaces with Van der Waals forces. Van-der-Waals-based adhesive systems take advantage of weak intermolecular forces between two surfaces. Upside is that these forces are not surface specific, allowing geckos to climb trees, rocks, walls and even glass windows.
Geckos achieve their strong attractive force to the substrate by utilizing small hair-like structures on their toes called setae, which are made primarily of keratin (Fig. 1). Setae contain flexible spatulae which make intimate contact with rough and even dirty surfaces.

Fig. 1. Left panel: Close-up of the underside of a gecko's foot as it walks on vertical glass. Source: Wikipedia. Right panel: Images of (A) dry and (B) wet setae using the same digit of an individual tokay gecko (Gekko gecko). The image in A was taken prior to exposure to water and the image in B was taken after 30 min of soaking in water. Source: (Stark et al., 2012).
The drawback of using Van-der-Waals forces for grip is that the Van-der-Waals forces only exist across surfaces very close together, and an intimate contact between the spatulae and the substrate is required for van der Waals forces to be effective in the gecko adhesive system (Stark et al., 2012). Wetting of the feet decreases the Van der Waals interaction with the surface.
References
- Knight, J Exp Biol 215, i
- Stark et al., J Exp Biol; 215: 3080-6


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What is the general mechanism behind perfusion PET imaging
I understand how tracer kinetics can be used to determine binding potential but how it can be used to detect perfusion eludes me.

How PET works is more of a physics question? Can you clarify what exactly you are asking?

Alex - do you literally mean "perfusion" - like blood perfusion imaging - - - OR - - - do you mean like PET with 18O-fluorodeoxyglucose uptake imaging?


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Why are the sex chromosomes called X and Y?
Is there a specific reason that the letter Y is used as the symbol for the male chromosome and X is used for the female chromosome?

when Y chromosome being replicated, pair looks like letter Y. When X chromosome being replicated, pair looks like letter X.

Sex Chromosomes and Sex Determination by Ilona Miko

The first inkling that sex chromosomes were unique from all other chromosomes came from experiments conducted by German biologist Hermann Henking in 1891… Henking saw that some wasp sperm cells had 12 chromosomes, while others had only 11. Moreover, while observing the stages of meiosis that formed these sperm cells, Henking noticed that the mysterious twelfth chromosome looked different from all the others. He thus named this chromosome the "X element," to represent its unknown nature.

Wikipedia - Y Chromosome

The Y chromosome was identified as a sex-determining chromosome by Nettie Stevens … during a study of the mealworm Tenebrio molitor … Stevens proposed that chromosomes always existed in pairs and that the Y chromosome was the pair of the X chromosome discovered in 1890 by Hermann Henking … Stevens named the chromosome "Y" simply to follow on from Henking's "X" alphabetically.

I know that this is not the most reputable source, but it does cite a couple of books. Take it as it is. Keep in mind that all human chromosomes, even the Y chromosome, appear as X shaped when replicated and condensed. The Y chromosome is quite acrocentric and so the short arms may appear to be one, but they're not.

During metaphase, all chromosomes look like an X with the exception of the chromosome Y. See below

Why Y then? Well, according to wikipedia, just because the letter Y follows the letter X in the alphabet.
Note that many species don't have sexual chromosomes and note that in many species, the Y-looking chromosome is present in the female but not in the male. In such case we call this Y-looking chromosome W and we call the X-looking chromosome Z. Very likely this post will interest you.


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Is NADPH salt still usable after an hour at room temperature?
I accidentally left a delivery of NADPH Tetrasodium Salt (Santa Cruz Biotechnology) at room temperature for a little over half an hour.
In addition, when I opened up the package, I briefly held the bottle by the body instead of the cap (which would have prevented body heat from contacting it).
It was packed with airbags, but no ice packs, which is why I am asking this: is the powder still stable and usable?

AliceD - I rolled-back part of your edit because I think the original meaning was lost. If you disagree, feel free to go back to your version.

@canadianer - you're the expert on these matters :) I'll go for it :)

@AliceD Well I wouldn't say that ;) Actually, whether the bottle was held by the body for a second instead of the cap hardly seems relevant to the question.

@canadianer - yeah, I reckoned half an hour RT instead of -20C (dT=~45C) is a bigger deal than a second of bodyT-RT= 12C :)

Nothing significant would happen in half an hour (especially for a sealed pack of anhydrous powder). -20 is for a moderate long term storage.

Since the delivery wasn't temperature controlled, the contents will have been at ambient temperature for essentially as long as it took to get from their warehouse to your site, which could be hours or even days. Is an extra half-hour likely to be significant?

In my experience, half an hour at room temperature will make absolutely no difference.  Boehringer Mannheim (now part of Roche), who at one time supplied the best NADPH, used to recommend storage at 4o C.
By A340 callibration, NAD(P)H is typically about 85% 'pure' based on dry weight measurements, and Sigma will try to tell you that the remainder is mainly water.  That is, if you calculate a concentration based on the dry weight, the A340 will be about 85% what you expect.
Even if some water is absorbed from the atmosphere, this will make little difference as you are probably going to calculate the concentration based on
the A340.
As User 243 has pointed out, if you are concerned that the NAD(P)H is degraded or oxidized, then an A340
measurement will probably set things right.
If you are concerned that all the A340  absorbing material is not NAD(P)H, or that a significant proportion is in the α-form (Oppenheimer & Kaplan, 1975) or is otherwise enzymically inactive, the best thing is an enzymic calibration.
This is done by adding limiting amounts of NAD(P)H to an assay system containing excess substrate and calibrating enzyme, and measuring the total decrease in absorbance (Racker, 1957).
A popular calibrating enzyme for NADH is aldehyde dehydrogenase (EC 1.2.1.3), as the reaction is practically irreversible, and it makes it easy to 'drive' the calibrating reaction to completing (and you don't have to worry about equilibria).
As I said in a previous post, NAD(P)H is UNSTABLE IN ACID (Oppenheimer and Kaplan, 1974). To put it crudely, 'the head (nicotinamide moiety) falls off', causing a bleaching of the absorbance at 340nm.  Making 100mM acetate, pH 5, 100 micromolar in NAD(P)H produces a very significant decrease in A340 absorbance with time (which may be very easily monitored in a spectrophotometer).
Just because all the A340 material is due to NAD(P)H, this does not necessarily mean that the commercial preparation is pure.  In fact, far from it.  Dalziel (1963) showed that commercial preparations of NADH then available contained a competitive inhibitor of many dehydrogenases, most probably adenosine diphosphate ribose.
Accepting Dalziel's value of 17 600 M-1cm-1 for the extinction coefficient for NADH at 260nm, and assuming that NADPH has an identical value, then highly purified samples of NAD(P)H should have an A260/A340 ratio of about 2.83, and values higher than this may indicate the presence of impurities that absorb at 260nm, but not at 340nm. ADP-ribose is a prime example, but NAD(P)+ is another possibility.
I notice that in one of the links given by AliceD, Sigma quote a A260/A340 ratio of 2.32. So is the higher value due to the presence of residual NAD(P)+, or something else (a breakdown product?), or both?
You may need to use chromatography, typically on an anion-exchange resin, to obtain NAD(P)H free of impurities.
References
Dalziel, K. (1963). The purification of nicotinamide adenine dinucleotide and the kinetic effects of nucleotide impurities.  J. Biol. Chem. 238, 1538 - 1543.  [pdf]
Oppenheimer, N. J. & Kaplan, N. O. (1974). Structure of the primary acid rearrangement product of reduced nicotinamide adenine dinucleotide (NADH). Biochemistry 13, 4675 - 4685.[pubmed]
Oppenheimer, N. J. & Kaplan, N. O. (1975). The alpha, beta-epimerization of reduced nicotinamide adenine dinucleotide.  Arch. Biochem. Biophys.166,  526 - 535.
Racker, E. (1949). Aldehyde dehydrogenase, a diphosphopyridine nucleotide-linked enzyme.  J. Biol. Chem. 177, 883 - 892. [pdf]
Racker, E. (1957). Spectrophotometric enzymatic methods for the determination of aldehydes and ketoaldehydes.  Methods Enzymol. III, 293 - 296.
Other References
Ciotti, M. M. & Kaplan, N. O. (1957). Procedures for determination of pyridine nucleotides.  Methods Enzymol. III, 890 - 899
Horecker, B. L. & Kornberg, A. (1948). The extinction coefficients of the reduced band of pyridine nucleotides.  J. Biol. Chem. 175, 385 - 390. [The definitive determination of the extinction coefficient at 340nm] [pdf]
Kornberg, A. & Pricer, W. E. (1950). On the structure of triphosphopyridine nucleotide.  J. Biol. Chem. 186, 557 - 567.
[This paper shows that the 'extra' phosphate in NADP(H) is attached to the  2' position of a ribose.  In Coenzyme A, of course, the phosphate attached to the ribose is on the 3' position. [pdf]
Pullman, M. E., San Pietro, A. & Colowick, S. P. (1954). On the structure of reduced diphosphopyridine nucleotide.  J. Biol. Chem. 206, 129 - 141 [pdf]

You could measure OD at 340nm. If OD340 is much lower than expected, NADPH is oxidized and does not have much biochemical activity.
http://www.bmglabtech.com/media/35216/1043734.pdf

I think when they sent it to you without dry ice, it is probably OK to store it at room temperature.
Sigma seems to advise on their NADPH to store dehydrated NADPH at room temperature, while they advise to store the hydrated forms at -20oC. Likely the presence or absence of molecular water in the material is crucial for its storage.
disclaimer: I am not an organic chemist and when you are doing crucial experiments with your material and you doubt its quality, I'd recommend to chuck this batch away and order new. Likely, a single day of futile experimentation in the lab due to bad reagents is more expensive than the purchase of another jar of NADPH.

@TomD - the water in NADPH-hydrate is not considered part of the molecule. It is part of the crystal. Therefore it doesn't show up in the formulas. The stability difference is because NADPH reacts with water I guess. The dehydrated form is called the anhydrate. I just talked to a chemist about this :) And I linked the question to him too. btw: I +1'd your answer. Great stuff.

@TomD - quite frankly I don't know, and my friend did neither. The only clue I got was the fact that the hydrate salts need storage at -20oC, the anhydrate form not. I'm not a chemist (as posed in the disclaimer :-)


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What are the limiting factors of pathogen population size in human populations?
I understand that one limiting factor in non-human animal populations is that increased pathogen populations decrease animal populations from killing them, which decreases the density of the animals, which makes it harder for pathogens to infect other animals. However, pathogens, at least in developed nations, don't seem to kill a large enough number of people for this to be the main limiting factor. So what else are the limiting factors?

One of the limiting factors is how many uninfected hosts exist. As a pathogen becomes more widespread, the probability of someone infected with it infecting someone else decreases, as it's more likely that the person will spread the disease to someone who already has it instead of someone who doesn't have it, preventing the virus's population size from increasing. See this for more information.
Also the more common a pathogen is, the more likely it is that people will take actions against it, for example by being more sanitary or getting vaccinated against it.


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Can my eyes adjust instantly to my friend's glasses?
My eyesight is pretty much perfect, but I noticed that whenever I try any of my friends glasses, from really thin to extremely thick, my eyes seem to adjust to them within seconds and let me see perfectly fine. Is this weird or abnormal, I was just really curious.

how 'strong' are the glasses? i.e. how many diopters? If they are small correctional glasses the distortion of the image to you may be minimal. Thick glasses expectedly are stronger, but just to verify.

@WYSIWYG the question is understandable. Please, take a look on the answer.

@rg255 the question is understandable. Please, take a look on the answer.

The phenomenon you described as "my eyes seem to adjust" is a particular case of accommodation - adjustment of the dioptric power of the crystalline lens to the object's distance.
When you place a lens before your eye, any object seen through this lens will initially appear at a different distance (and of different size of course) and will be blurred at different degrees (i.e out of focus). Thus, to overcome this discrepancy the eye must accommodate.
Now, the amplitude of accommodation is the maximal power which can be added to the current power of the crystalline lens. The younger the subject, the higher amplitude of accommodation he/she has:

Thus, if one young emmetropic person (person 1) wears some other person's myopic glasses (person 2) with a concave lens with minus power to lessen the actual "overpower" of the optic system, and this power does not have the refractive error of person 1's has (less myopia if they have any "hidden" myopia), the eye must accommodate, i.e. by increasing the convexity of the crystalline lens. If the amplitude of accommodation is much higher than the glasses in question, person 1 will easily adjust to these glasses by elimination of dioptric discrepancy.
Thus, Sherlock Holmes could deduce the following:
You are a young person (under the age of 30) with a high amplitude of accommodation.
You have a lot of "four-eyed" friends suffering from myopia.
From these facts the fiction writer could assume even your nationality (developed country) and level of close work (reading books, using computers) your friends are doing but - let's leave those assumptions to writers! :)


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Driving force for speciation for millions of species today
I would like to know if speciation really occurs (trans-speciation). Have we had enough time for millions of species? A creationist argument is that the slow changes in traits in organisms, taking tens of thousands of years to yield a visible change in variation as evolution suggests, does eventually trap yourself in to a problem of "Time Riddle". You just don't have enormous enough time at hand for all these species to come into being. A quick average time calculation suggests that you should have a new species come into being every 15-20 yrs [just rough average time estimation suggests that in about 1 billion yrs ~50 million distinct species evolved]. Though I believe in evolution, I cant understand this part.

A small note: You don't believe in science. You understand it.

???  this is not my answer

It is not an answer. It is a comment..

Have we had enough time for millions of species? - yes. How do I know? Because there are millions of species. Life has been present on earth for billions of years. Also you seem to have plucked your numbers out of thin air - where is the data to support them?

Also: 3.5 billion years of life, and 10 million species says that one evolves every 350 years. But remember that speciation can occur in parallel (not sequentially), so growth in numbers can be exponential (i.e. 1 becomes 2 species, both of these can then speciate).

I'm voting to close this question as off-topic because its flawed, unclear, and poorly researched (seemingly random numbers in the calculations)

I think what the user is asking is how can millions of species have evolved within the earth's given timeline, ergo can you actually explain evolution from a linear model B derives from A, C derives from B. The clear answer is no, you cannot it is much more complicated than that. So maybe the correct question is What forces drive evolution such that we can observe over a million species today?

u have no logic to vote for closing the question & how come its off-topic. U forgot to see that I said- I DO BELIEVE in evolution. I just cant understand this part, WHICH a creationist put before while discussing. I also dont knw what the hell did he get this numbers from? Thats why I want some clarifications.

@KoustavPal thnk u , can u explain What forces drive evolution such that we can observe over a million species today? I ll be grateful, I cant understand this part.

Cool, I'll provide a suitable answer to this question. Maybe you can edit the question and change it to the same?

@rg255 Perhaps you can give a simple example using average mutation rates and timescales. This would basically answer the question of how many DNA changes are possible in a given time. Tanivr: You should understand that mutation and fixation are different phenomena and there are environmental factors that limit the number of "species"; so if some mutations were not selected against, then we would have had many more species.

@Tanivr I suggest to you that you just keep the question specific to the scientific point you are asking. You would agree that your debate with your creationist friend has nothing to do with the actual question. My first comment to you is for telling you that in the process of science we understand things and that is why we know they are true. Belief on the other hand implies that you don't understand something but accept it as true. Try editing your post by making it precise, adding references and removing irrelevant material. I am voting to keep the post open :)

Tanivr. I'm not sure why you're asking this question here, since you asked it on another website just a day earlier. What was wrong with the answers you received there? http://www.rationalskepticism.org/evolution/is-there-enough-time-for-speciation-for-million-species-t50189.html Are you quite sure you "believe in evolution"?

@Shrunk I think it is a reasonable cross post. There is a difference between lay skepticism, which seems to have focused on mathematical possibilities, and a biological justification. I do agree though that the question seems fishy - it approaches the situation with the assumption that there has not been enough time. In reality, there has been enough time because it has happened. The question should be "how much time has it taken" and not "has there been enough time?".

This answer is towards the question, what forces primarily drive evolution such that we can observe a million species today? which is what the user wanted answered.
To answer this question, we can start off at many places. So I wanted to start off at Kimura's neutral theory of evolution which encompasses both Natural selection and genetic drift. I wanted to start here because although it is true, it also brings to light a fundamental trait of phenotype which has been highlighted in this paper which suggests that mutation rate in a species as a whole is not very divergent, but the same rate varies by several magnitudes when comparing genes having lower rates in highly expressed genes and higher in lowly expressed ones.
This brings to light another feature of gene mutation. A very simplistic view is that gene products are perfect for their function, that is not the case (I need to find a proper reference for this, maybe someone can help me with that?). Gene products are never the most thermodynamically stable nor the best at performing their intended function, but rather they are positively selected for once a mutation produces a product that provides increased fitness to the organism.
Till now this answers two things:

Mutation is the governing factor driving evolution.
Unless a new mutation increases fitness of the organism it is considered as a neutral one.
A species as a whole has nearly the same mutation rate.
Depending on their contribution to survival genes have different mutation rates.
A gene will choose to preserve function over improvement because it may result in a loss of function.

So now let us come to the part about millions of species. If you followed me till now, you understood that based on different mutations changes will arise. I would now like to bring in the theory of Punctuated equilibrium which basically states that a species once developed remains nearly the same for it's geological history. Below is an interesting image from the wiki page.

So according to this theory once a species has appeared, until it disappears it will remain largely the same. It will disappear does not mean the entire line will die off. Rather, it means a substantial part of will die off, allowing niche populations to colonise the now empty ecosystem. Or a change in climate may now allow a certain niche species to migrate out of their ecosystem to provide competition to the already existing species in the ecosystem and then to oust them from their place (look at yourself for example), the migratory pattern exhibited by homo sapiens during the end of the last ice age led to the removal of neanderthals from their ecosystem (this is very traditional and overly simplistic but mostly correct so I will not provide the complicated parts here).
This theory worked on the theory of geographical speciation which goes on to state that geographical changes may lead to population separation, which leads to the different species. This is because, in their own ecosystems they will be privy to very different environmental stresses such as climatic conditions, competition, predation, food availability and disease. So after a million years these two populations which were the same will now be very different.
So I think, I have provided a suitable answer to this question, because your view evolution as something very linear. Which it hardly is. There are many factors which guide it, and this is how today you can see millions of species. Another thing to note is that of the millions and millions of species identified on earth today, multicellular organisms represents a handful of crumbs from the pie. Most of it is actually micro-organisms (Anyone know the source for some exact numbers?)

Your math is wrong.  Assume for simplicity that speciation is binary: that is, a speciation event divides one species into two.  50 million species is between 2^25 and 2^26.  So producing that number of species in 3 billion years would require any lineage to speciate on the order of once per 120 million years.
Remember, as per comments above, that evolution works in parallel!
Another point to remember is that most of the species existing today are insects or microorganisms.  Would we even notice the development of say a new species of beetle, if it happened in the Amazon Basin or New Guinea highlands?


text:
Map gene IDs to Ensembl gene ID
Forgive me if this question is too trivial.
I have the gene IDs of the following type
EOG6STSR2
EOG60ZRJB
EOG6SBFJ2
EOG6P5KX3
EOG6B5PRW

from the first supplementary file in Comparative validation of the D. melanogaster modENCODE transcriptome annotation .
I'm not sure as to the type of the IDs. I learned that IDs beginning with EOG are Eukaryotic Orthologous Group IDs but I couldn't find these particular ones in any of the databases.
Is it possible to map them to Ensembl IDs or any of the other commonly used ones?

These are not gene ids, but groups of orthologous genes -- try to search for the ids on Google, I can find this page http://cegg.unige.ch/orthodb6/fasta.fasta?ogs=EOG6STSR2&swaptree= and thus you should be able to download the sequences and ids from OrthoDB.
Note that, strictly speaking, the are no Ensembl ids for Drosophila, only FlyBase ids that are also used by Ensembl.


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How does a smoker's finger or mustache get yellowish by nicotine?
Tobacco use is the leading cause of preventable death around the world.$\ce{^1}$

The stain is considered as a "tell-tale" sign for identifying smokers. Multiple materials stated that it's due to tar (nicotine) disposition. The colouring fades away after the smoker quits. There are also number of search results that point to "removing" these smoking stains in the skin. If it can be removed using chemicals then I wonder what sort of a chemical it utilized there as well.
Is it only nicotine that causes the yellow stains on the skin? What is the role of oxygen deprivation in this scenario? Can this be categorized under smoker's melanosis? What tissues/cells are being "transformed" in this case? What's the biochemical explanation behind the colouring of skin?
How is this staining differe from a ink stain in the skin which lasts for about about 3-4 days?

Please do not change the question significantly, especially after answers have been submitted. Instead, ask a new question.

@MattDMo I am not sure if this is a rule within Biology.SE, because there are ample of times where the original post was edited with closely related info/queries. This one from Chemistry.SE is a big example for that. Someone with moderator reps would be able to view its edit history. The answers were editted without any complain. The colouring of skin by smoking (nicotine, tar) and colouring of skin by inks are two common encounters we see day today life. So, they are related and I see it's fair enough to ask these two questions together.

This is general practice for all Stack Exchange sites, and is referred to as "moving the goalposts." Yes, of course questions may be edited to be clarified, or to add new information requested in comments, etc. However, it is bad form to add new, only tangentially-related questions to the original question, especially after answers have been submitted. Those answers may be downvoted later by users who see the expanded question, and an answer that apparently only addresses part of it. (...)

(...) Additionally, a question should be just that - a single question. Asking multiple different things in the same question makes it more broad, and makes it less likely that a single, concise answer can address all of the points.

Pure nicotine is a yellow colored liquid (although some sources say it's a clear liquid.) "Tar" is a complex sludge that is also yellow-brown. So it's difficult to distinguish 'nicotine stain' from a 'tar stain' based on visual inspection. Let's go to other considerations.
The concept of a 'stain' implies that simple hand washing doesn't remove the coloration. Since nicotine is water miscible, one would expect it's easily removed with soap and water. That implies that either a) a smoker's stain is not primarily nicotine, or b) the nicotine reacts with the skin to create the stain.
Nicotine is sufficiently functionalized that it could conceivably undergo some interesting chemical reactions with proteins, but I don't think that's what's happening. A simple observation is that transdermal nicotine patches do not contain a colored agent, and do not stain the skin. Score one point for the "mostly tar" explanation. Cigarette smoke contains far more tar than nicotine, and tar will deposit on most-any surface (at ambient temperatures), so it's parsimonious to proceed with the "mostly tar" explanation.
The picture shows that the stain occurs on both fingernails and skin. The most abundant protein that's common to those two tissues is keratin. Like other examples of protein staining, the mechanism is complicated and poorly understood, but the basic outline is that parts of keratin are greasy (the non-polar amino acids) that associate with other greasy things.  (EDIT: AliceD's answer also depicts the well-known staining of teeth, which are not keratinized, showing that the staining mechanism is likely a nonspecific adsorption of greasy things onto surfaces.)
The stain can be fixed through the involvement of free radicals and other reactive species in cigarette smoke, like formaldehyde. In this sense, reactive oxygen species are active participants. I don't think oxygen deprivation plays a role here. I don't think this can be described as a melanosis, as the skin isn't producing melanin in response to smoking but is simply being coated in tar.
Even if the stain was completely fixed, the coloring would fade away as the exterior skin cells are sloughed off, consistent with normal skin physiology. This is the explanation for the fading of any stained epidermis. The persistence of tar stains on teeth (which do not exfoliate) further evinces that the stain is removed through the replacement of skin cells.

Parsimonious does not mean what you think it means.

Nicotine is generally yellow to dark brown. While the pure chemical may be colorless, it oxidizes upon exposure to air, changing its color to brown. I added a "citation needed" template to the section of the wiki page you linked, as far more sources I checked said something along the yellow-brown spectrum than colorless.

BTW, I think you meant perspicuous. At any rate, I wouldn't use it here (maybe on [english.se]) as not many native English speakers know what it means, let alone those for whom English is a non-native language.

I have editted the question for a comparison to understand the skin staining context better. Can you take that into consideration in your answer?

That added part may be a bit vague - there are many types of ink. Permanent marker ink may stay longer than 3-4 days and washing habits may affect this too. How do you know tar persists longer? Consider asking a new question on this and specify what you wish to know. To me it looks like a different question altogether as the ink part is unrelated to the original question.

@MattDMo He/she did not use the word incorrectly. I'm not going to cite a bunch of dictionaries, but you should look at some other ones.

@MattDMo, you certainly don't know what I think 'parsimonious' means, although I do find it interesting that a dictionary of that caliber has such a limited scope. Webster-Merriam apparently needs more logicians on their usage panel!

"far more nicotine [than tar]" is an overstatement. It's about a factor 10 or so.  And tar may deposit at any surface, but will nicotine not do that? While parsimonious may be aptly used, I am not so convinced with the reasoning. For the rest, great answer +1

@AliceD, you misquote me for some reason, although you did understand my 'overstatement.' And my basic intuition is that tar will deposit at a far greater rate owing to its lower vaporization temperature...I don't have any numbers to support it (you don't provide any either.)

@Ryan - yep - I meant to say "far more tar [than nicotine]". :) I share your intuitions. I don't need any numbers to support my claims.

@AliceD, you share my intuitions but not my reasoning, making you a good person to know! Anyway, the quote is "[c]igarette smoke contains far more tar than nicotine..." so you're still misquoting! ;)

Touche :) in the end our answers are in perfect agreement :)

@Ryan do you care enough to enlighten me with the skin staining with regards to inks (fountain pen) and how it differs or similar to smoking (tar, nicotine) stains?

@Ryan Even if the stain was completely fixed, the coloring would fade away as the exterior skin cells are sloughed off, consistent with normal skin physiology. This is the explanation for the fading of any stained epidermis. Great - done. I was trying to search protein mechanism that you have mentioned but was not succesful.

Short answer
Tar deposition is the cause of the yellow cigarette stains.
Background
Both tar and nicotine cause yellow to brown staining. Although nicotine itself is colorless/white, it turns yellow upon exposure to air.
In a study on cigarette stains, the author speaks of tobacco-tar stains, implicitly acknowledging it is tar and not nicotine (John et al., 2013).
Interestingly, e-cigarettes which contain nicotine, but no tar, are reported to leave no stains, pointing to tar as the culprit, and not nicotine.
As to physiological causes of the stains I can say it is simply a tar stain and it has nothing to do with pigment or anoxic conditions, because the teeth and nails also stain yellow:

Tar stains on skin and nails. Source: John et al., 2013.

Tar staining of the teeth. Source: Identalhub.
Reference
- John et al., BMJ Open (2013); 3:e003304

That added part is a bit vague - there are many inks. Permanent marker ink may stay longer than 3-4 days and washing habits may affect this too. How do you know tar persists longer? Consider asking a new question on this and specify what you wish to know. To me it looks like a different question altogether as the ink part is unrelated to the original question.

Nice answer, @AliceD. The final link to John et al seems to point to an incorrect URL, however.

@Ryan - thanks for the appreciation and thanks for taking the time to click through the link :) I fixed it.

@AliceD see my comment on the other answer regarding the color of nicotine. I checked out a bunch of different chemical resources and vendors, and most seem to indicate that it is generally in the yellow-brown spectrum, as it is most commonly exposed to air (such as in a cigarette). I think it's only clear when freshly prepared and/or maintained in an oxidation-resistant environment, which would be the case in pharmaceutical manufacturing for nicotine replacement therapy patches. (...)

(...) Drugs.com indicates that the nicotine is sandwiched between 2 polyester backings and embedded in a matrix of various polymers, so $O_2$ likely can't interact with it.


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Do any amphibians start their lives on land?
Most amphibians - at least, all the ones I know of - start their lives in the water (at least, after they hatch). They then spend time maturing before venturing onto land, where they can breed. The cycle than begins again.
Are there any cases where the reverse is true, i.e. a young amphibian starts life on land before venturing into the water as an adult?
Wikipedia hints that this may be the case, but fails to provide examples:

Amphibians typically start out as larvae living in water, but some
  species have developed behavioural adaptations to bypass this.

I believe that most amphibians lay their eggs in the water because their food (larvae,fish etc.) lives in water.So their newborn babies will have something to eat.

From wiki:

Most amphibians lay their eggs in water and have aquatic larvae that undergo metamorphosis to become terrestrial adults

This suggests clearly that not all of them do so.
Here are a few interesting cases I could think of:

The common midwife toad carry the eggs on their back. The eggs are not necessarily submerged by water then.
To my knowledge, the Seepage salamander have terrestrial larvae but they don't feed before they reach the adult age.
The lungless salamanders has a larval stage that is within the egg. When the egg hatches, the individual that comes out is already an adult.

Arguably, since this frog spends the entire larval stage inside a pitcher plant on land, it has started its life cycle on land.

A group of zoologists with Conservation International say they found
  the frogs by the side of the road in Borneo, near a national park.
  They were very hard to locate because of their small size, but the
  scientists followed the frog's loud calls (you can listen to some
  here) and discovered them living among pitcher plants. They lay their
  eggs on the inside of the pitchers, and tadpoles grow up swimming in
  the tiny pools of rainwater that collect in the bottom of these
  plants. While most species of pitcher plant are carnivorous, the ones
  preferred by these tiny frogs only eat leaves - in fact, the frogs
  most likely help break down the leaf material and aid in the plant's
  digestion.

The moss froglet is an example of a frog which lays eggs on land and the tadpoles develop over several months in the egg mass amongst moss.

The Moss Froglet is a most unusual frog in that tadpoles develop on land. Breeding occurs from November to February. Four to 16 large eggs are laid in clumps of sphagnum or lichen and the tadpoles develop within the egg. After hatching the tadpoles do not feed, but spend the following 9-10 months of development within a fluid derived from the broken-down egg capsules (a gelatinous mass).

Source: http://www.parks.tas.gov.au/index.aspx?base=5258


text:
Why does the number of mutations per individuals follow a Poisson distribution?
I was reading this review. On page 11, left column, first paragraph, one can read:

[..] there is a Poisson distribution of the equilibrium number of mutations per individual, if fitness effects are multiplicative.

with no further explanations. In other words, let the variable $X$ be the number of (deleterious) mutations found in one individual (irrespectively to whether the mutation occurred in the parents gonads or is older back in the lineage). The variable $X$ is Poisson distributed.
Why is this statement true? I suppose that the statement also assumes that all mutations have the same effect on fitness, is that true?

It might be worth reading the paper that is cited there, Kimura & Matuyama (1966). They seem to justify it via the process of free recombination (see page 2, though the derivation starts at the bottom of page 1).

Oh I missed this part where he first talk about it and accompany the statement with a reference. Ok. I'll read that then. The question still hold though. Thank you

A Poisson process follows these postulates:

$\lim\limits_{h\to0+}\frac{P(N_h=1)}h=\lambda$  i.e. the probability of occurrence one event in a very small interval of time is equal to the macroscopic rate or intensity ($\lambda\,$).
$P(N_h\geqslant2)=o(h)$ i.e. the probability of occurrence of more than one events in an infinitesimal interval is essentially zero.
Events are independent.

If you consider a single individual (for simplicity assume a single cell), then the DNA will undergo mutations at some fixed rate (which we assume to be uniform for all loci). Now each mutation event is independent of the previous event and in a very small interval of time the chance of two or more mutations is negligible. Considering all these facts and assumptions, it can be said that mutation in a single cell would behave like a Poisson process.
From the Poisson postulates you can derive the expression for the Poisson distribution which describes the probability of $k$ number of events in a given time interval, $t$. Hence, the number of mutations in an individual for a fixed time window ($t\,$) follows a Poisson distribution.
$$P(N=k)=\frac{(\lambda t)^k e^{-\lambda t}}{k!}$$
You can find the derivation of Poisson distribution from the postulates from many sources. I referred to this book:
Hogg, Robert V., and Allen T. Craig. Introduction to mathematical statistics. New York: Macmillan, 1978.
EDIT
The effect of deleterious mutations, in the mentioned section of the linked paper talks about Muller's ratchet that describes the accumulation of deleterious mutations and its effect on the population (i.e. extinction). Like any mutation event, accumulation of deleterious mutations will also follow Poisson distribution. Muller's ratchet just says that beyond a tolerance limit, deleterious mutations will cause extinction of asexually reproducing organisms. Perhaps if each deleterious mutation had a strong effect on the fitness, then sampling from the population may lead to non-Poissonian estimates.

Sorry, I think there is a missunderstanding. I was a bit unclear. The question is not why the number of new mutations per reproduction event is a Poisson distribution but why the number of deleterious mutations per individual follows a Poisson distribution. Thank you though for your answer, I'll try to clarify the question.

@Remi.b probability of any mutation will have a Poisson distribution. Not specific to deleterious mutations. In fact for deleterious mutations there can be non Poisson observation when you sample the population because they may be selected out.

I talk about deleterious because they assume multiplicative fitness effects. But what they say is that the number of mutations/segregating loci in any single individual is Poisson distributed. Of course the number of new mutations transmitted to the offspring is also Poisson distributed (and I understand why) but I don't understand why the number of mutations/segregating loci is Poisson distributed. Do I missunderstand something?

Sorry, I will just repeat what I said above. I think you are not answering to my question here. I am NOT asking why does the number of new mutations per reproduction event follows a Poisson distribution. I am asking why does the number of segregating sites per individual follow a Poisson distribution.

@Remi.b I did not say anything about reproduction. I also do not know what is a segregating site. I am just saying how the process of accumulation of mutations in the DNA will have a Poisson distribution.

Ha ha seems like we have some communication issue my friend! A segregating site is a polymorphic site, a site for which more than one allele exists in the population (at a given instant of course).

Let us continue this discussion in chat.


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Within and Between Allelic Class Diversity
I am reading Charlesworth et al. 1997. They talk about diversity within and between allelic classes.

Nucleotide diversities ($π$) at each neutral site were estimated from the mean of $2 \sum z_t (1-z_t)$, over replicated introductions at the site of single variants, where zt is the frequency of the neutral variant at time t, and summation is over all times until either fixation or loss occurs.
The total genetic diversity at the neutral sites ($π_T$) was also decomposed into that within and between allelic classes at the polymorphic locus. Diversity within allelic classes, which will be written here as $π_A$, was estimated from the mean of $2 \sum \left( x_t(1-x_t)+y_t)(1-y_t) \right)$ where $x_t$ and $y_t$ are the frequencies of the neutral variant within the first and second allelic classes, respectively. Diversity between allelic classes with respect to the polymorphic locus was calculated as the difference between the total diversity values and $π_A$

Note that the parentheses don't match up but this this is what is written in the paper!
Why am I confused about this text?
I am confused about the term allelic class. I first think there is anything fancy in here and I think we can simply replace the term "allelic class" by "allele". but then when I saw the equation for $\pi_A$ I realize that the frequency of the two allelic classes does not necessarily adds to 1 (even though we consider only two allelic classes).
I also got also a little confused about the difference between $\pi$ and $\pi_T$ but I think that they just used two notations for the same think ($\pi = \pi_T$)
In population genetics's jargon, diversity just mean expected heterozygosity. $\pi_T$ makes sense to me. It is just the average heterozygosity $\left(2 z(1-z)\right)$ calculated over all time steps. Maybe a more intuitive to put it would to integrate rather than summing over time rather than time steps.
Question
I can read the equation for $\pi_A$ but I fail to get any intuition behind what it means. For example, I have no idea why it should be called within-allelic class diversity. Where does $2(x(1-x)+y)(1-y)$ come from? My whole issue might boil down to the definition of allelic class.
EDIT
The term allelic class is defined in Innan and Tajima (1997)

Suppose that there are two nucleotides, say A and T, in a particular site. Then, we can divide DNA sequences into two classes: one class includes sequences with A and the other includes sequences with T in this site. We call such a class an allelic class

(Slatkin 1996 might help as well).
I am still not quite sure what the within allelic class variance. Maybe it is: Take the most common sequence in the considered allelic class. For each, sequence, calculate the number of pairwise differences to the most common sequence and square this value. Sum over all sequence and divide by the number of sequences. In math form it would be: $\frac{1}{2N}\sum_i^{2N} (D_i)^2$, where $N$ is the population size and $D_i$ is the number of pairwise difference between the sequence $i$ and the most common sequence in the considered allelic class. Does it sound right to you?

@AMR I deleted my long list of comments...

From the way I have read what you have written z(1-z) translated into a sentence would be the frequency of the neutral variant (z) times the frequency of all other possible variants (1 - z) at the particular time t.
Nucleotide diversity is then the average of 2 times the sum of all of the frequencies of neutral variants (z) times the the frequency of all other possible variants (1-z) for all of the time periods until either there is no longer a change in the sequence or the allele is lost (which can happen over evolutionary time, especially if the allelic class is a deleterious variant, or the heterozygous allele provides enough expression to mask).
To me, this sounds like the result will be the probability of the neutral variant existing over time, which should be a number between 0 and 1. If z was 1, that would imply that the neutral variant is always the case, so the frequency of other variants is 0 making 2* 1(1-1) = 0 which makes sense to me as that would mean there is no nucleotide diversity. That sequence is always that sequence and so there is no sequence diversity.
As this looks like it is dealing with frequency distributions I think that total genetic diversity is implying the probability of all of the different allelic classes that make up an allele. So if you have class one which has the frequency  of x and a class two with a frequency of y it sounds like the overall diversity would be the probability of the neutral variant of x and the probability of the neutral variant y.
Generally, when you are looking at the probability of multiple events, you would multiply the probability of one event times the probability of the other event. As a result, I am inclined to say that the Nucleotide diversity within classes πA is 2 times the average of the sum of the frequency of x times the frequency of y, or 2∑ x(1-x)(1-y) + y(1-y) or factored 2∑ (x(1-x) + y)(1-y) or in words the Within Class Diversity (πA) is 2 times the average of the frequency of x as the neutral variant times the frequency of all other variants when x is the neutral variant times the frequency of all other variants when y is the neutral variant plus the frequency of y as the neutral variant times the frequency of all other variants when y is the neutral variant.
I think that the reason that this might be done is that, for reasons of selective pressure, x might be favored, so those times that the variant is y, some of those variants (possibly all of them) will be x, so by multiplying the within class diversity of x by the frequency of all of the variants when the class is y implies that there will be less diversity within class than if you just added the frequency probabilities together.
One thing I would do is to do a search to see if there was a correction published to this article, as there was a mistake in the formula. That might help to clarify. Also note, I could be wrong in my assessment as I do not have access to the actual paper you have referenced.
Best of luck in working this out.

when you are looking at the probability of multiple events, you would multiply the probability of one event times the probability of the other event. This is true if the events are independent, so P(X,Y)=P(X)P(Y). Otherwise, P(X,Y)=P(X|Y)P(Y)=P(Y|X)P(X).

@ddiez So which formula makes sense? Stats are not my strong suit and I was trying to work through the equation with Remi.b as it seems that there may have been a typo from the original article. Their formula did not have properly paired parentheses and is was difficult to determine whether it should be x(1-x) + y(1-y) or (x(1-x) + y)(1-y)? Thanks.

My comment is meant just as an extension to your statement, to note that the general formula is the later one (it is true in all situations) whereas the first one is only true under the assumption of independence. But that might be perfectly fine in this context (I haven't read the paper). Lets see the OP opinion on this.

The term allelic class is defined in Innan and Tajima (1997)

Suppose that there are two nucleotides, say A and T, in a particular site.Then, we can divideDNA sequences into two classes: one class includes sequences with A and the other includes sequences with T in this site. We call such a class an allelic class

Two elements that were misleading (for me at least) in the article

Implicitly, in the paper of interest (Charlesworth et al. 1997), they define allelic classes for a site that is known to be under selection (and that can only be bi-allelic). The concept of allelic class is not for a polymorphic neutral site they look at but always for the same site (the one under selection).
The formula has an extra parenthesis. The real formula should be $2 \sum x_t(1-x_t) + y_t(1-y_t)$.

What is $x$ and $y$?
Consider a polymorphic (bi-allelic) locus (that is not under selection) and calculate the frequency of one allele in the first allelic class (defined for the site under selection) (this is $x$) and calculate the frequency of the same allele in the other allelic class this is $y$. In other words, consider the selected has two alleles $A$ and $B$ and the neutral locus has two alleles $a$ and $b$. $x$ is the frequency of sequences containing $A$ that also contain $a$ and $y$ is the frequency of sequences containing $B$ that also contains $a$.
Meaning of the formula
The formula is just the sum of the expected heterozygosity within each allelic class. $$2x(1-x) + 2y(1-y) = 2 (x(1-x)+y(1-y))$$. Then, we just have to sum over all time step during which the neutral locus is polymorphic and we get $$\pi_A = \sum_{i=1}^T 2 (x_t(1-x_t) + y_t(1-y_t)) = 2 \sum x_t(1-x_t) + y_t(1-y_t)$$, where $x$ and $y$ are now function of the instant (time) considered and $T$ is the total number of time steps.
What values can $\pi_A$ take?
This measure takes values between 0 and $T$ as all $x_t$ and $y_t$ take values between $0$ and $1$ (and therefore $x(1-x)$ and $y(1-y)$ take values between 0 and 0.5). Dividing the whole thing by $T$ will result in a measure that is bound between 0 and 1.

I would have not been able to understand without the help of @AMR. Thank you


text:
Tissue grafting in marine invertebrates
I'm trying to source a procedure for a transplanting tissue in regenerating polyps. Would anyone happen to know where I can find a method of adhering to donor to host tissue?
Thanks

I think what @bonCodigo is trying to ask is what kind of polyps you are talking about (their habitat etc).

Colonial anthozoans located in the intertidal region. Truthfully, I can't find a procedure for grafting tissue in any aquatic invertebrate. I'm just looking for a good starting point.


text:
Ancestral Allele and Hapmap
I notice on dbSNP rs6352 has an ancestral allele of G - http://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?rs=rs6352
The hapmap in humans for this allele is very rare, the homozygous version practically not existing at all http://hapmap.ncbi.nlm.nih.gov/cgi-perl/snp_details_phase3?name=rs6352&source=hapmap3r3_B36&tmpl=snp_details_phase3
My understanding has been that the ancestral allele refers to the common gene that an ancestor in all humans once shared. Now, I thought the ancestral allele was usually the most frequent in a population, but I can see this was most likely a wrong assumption.
Was it a wrong assumption, or was this example above just a rare exception? Is deviation from ancestral alleles nearly worthless as a metric to investigate possible mutated alleles that may be leading to disease? I realize the proper answer may be too long, but just a brief summary would be appreciated.
Many thanks.

It is kind of confusing.  Here's the sequence, from the ncbi link
GGACATTTAAMGAGGTACGTG
So M is "A or C"
Its a missense mutation, the amino acid called for is either an N or a K.
GGACATTTAAAGAGGTACGTG = K amino acid
GGACATTTAACGAGGTACGTG = N amino acid
GGACATTTAAGGAGGTACGTG = K amino acid
GGACATTTAATGAGGTACGTG = N amino acid
When you blastx it, the top hits are all the K allele, across a few species.
When you blast the DNA, the non-human hits in nr all have a G, not an A or C.  So I guess that's why they are calling that the ancestral allele.  The human hits to nr all have A, so the K amino acid is conserved.

Typically, the ancestral allele is inferred from the allele chimpanzees as our closest relative (and possibly some primates) have. While for most sites humans and chimps have the same allele, there are many cases where the ancestral allele is even completely absent from humans, and where all humans have a different allele from chimpanzees, which we call a substitution.
A substitution in a critical part of a protein can indeed indicate some biological significance, a classical example is the FOXP2 gene, that is related to speech development. In most cases however, substitutions are merely due to genetic drift occurring over millions of years.