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Which living organisms have antibodies?
I'm wondering if only humans, or only mammals have antibodies and immune system. Obviously humans and dogs have (we vaccinate both) and in my head makes sense since we're so genetically similar to all mammals that we all have antibodies. Do all synapsids, or even amniotes have antibodies as part of their immune system? Do plants have antibodies or insects?

Apparently, cartilagenous fishes are the oldest extant clade that have the true immunoglobulins (antibodies) and the T-cell receptor (Schluter et al., 1997). All extant gnathostomes, incuding cartilagenous fishes, produce antibodies.
However other animals (invertebrates) and even plants have proteins that belong to the immunoglobulin superfamily (to which the classical immunoglobulins/antibodies also belong). Members of this superfamily are structurally related; they are not necessarily involved in immune responses. Hemolin is one immunoglobulin superfamily protein in insects, that is involved in immune function, but not exactly like vertebrate antibodies.

In the animal kingdom adaptive immunity is present in all Gnathostomes.

Agnathostomata (hagfish and lampreys) also have an immune system that is somewhat adaptive, although in many cases it isn't structurally related to the Gnathostome "adaptive immunity".  For example, they have molecules that are analogous to antibodies, including a diversity-generating mechanism, but that are not structurally related to them.  See for example Dual nature of the adaptive immune system in lampreys

@iayork.. I read that too but I as far as I have read they don't produce true antibodies (i.e. immunoglobulins).

@SanjuktaGhosh Yeah I forgot to explicitly state that explicitly but note that adaptive immunity does not really require antibody production as iayork has mentioned.

Definitely not true antibodies (they're structural more like TLRs, as I recall, though I don't recall if they're evolutionarily linked or not) but with surprisingly analogous aspects to them. Lamprey and hagfish immunity is really fascinating, since they share some aspects with Gnathostomes but also have gone in completely different directions in other ways


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What is the name of this yellow / orange fungus?
I've seen this in October 2016 on Corsica (Island of France):

I would guess each one is about 5cm - 15cm in diameter. Obviously, they come in small groups.

It would be nice to see how they look under the hat, and also the stem.

Do you have a picture of the stem or underside??

@theforestecologist No.

Most fungi need to be studied under a microscope to determine a species. I think this belongs to the genus of Pholiota. I couldn't find an English name, if I translate the Dutch name, it would be 'Bundle mushroom'. This name refers to the fact that they always grow in groups, usually on (dead) trees or trunks.
At first look thought this was a Honey fungus, but these are parasitic so usually don't grow on dead wood.

From the article you've linked: 'Because Armillaria is a facultative saprophyte, it also feeds from dead plant material, allowing it to kill its host, unlike parasites that must moderate their growth to avoid host death.'

Pholiota aurivella http://fieldguide.wardial.me/Mushroom%20pages/falllog.htm

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Feeling warm and cool breezes - how does it work?
As you travel with your hand sticking out of a car the sensation you have is one of cooling: even though molecules are transferring energy to your hand, you interpret it as being colder. Now, at a certain speed your hand would actually melt down, and I'm assuming you'd be feeling warmth by the time that happened.
I'm wondering how this works: how can your body sense warmth and cold from a phenomenon that, physically speaking, is just about molecular collisions?

You feel cool because of the evapoative cooling of the thin layer of sweat that exists. There must be a tipping point where the sweat evaporates altogether and air friction takes over. Ya, im just guessing. Sure for the first part.

@Polisetty Pretty solid guess in my opinion. As you said, sure for the first part, good guess for the second part.

This is the same principal behind the wind chill factor. Your body makes heat. This heats up the air around your body. If that air is quickly replaced by unheated air, you have to spend energy to reheat that air, which is again quickly replaced; your body is working a lot harder to warm up the air around you, which makes you sense that it's cold.

You have many different types of sensors in your skin; you probably feel the pressure of the air moving past your hand in addition to the temperature.
The temperature increase in your hand due to collisions isn't very significant, you have to be going at really high speeds to encounter that phenomenon (spacecraft reentry would be an extreme example, for example see this wikipedia page).
Temperature changes due to evaporation are probably most significant (this is why even warm air blown from a fan can feel cool, especially if you are perspirating), as well as the temperature of the outside air around your hand compared to the air inside the car.

Does that mean I will not feel the wind as cool if I'm not sweating? Because that doesn't really look obvious to me.

If the air is colder than your body, you feel it as cold because it is actually cooling your hand; this will be enhanced by evaporation, which will be greatest if you are sweating but even if you aren't sweating your skin still contains water that can evaporate.

@QuantumBrick Sweating is a physiological mechanism to cool down anyway, why would the brain want to actively feel water evaporating as much as it wants to actively think about heartbeats.

The few points mentioned in the threads are correct. Physical collision do not transfer that much heat when it comes to air. Multiple temperature sensors can also be activated simultaneously. For example you could be in a cold room and feel conducted cold, and have the sun shine at you through a glass panel with radiated heat. But this almost never happens with friction with air of course.

@Liu Tianyi: I have to disagree.  It's quite normal to feel a breeze as hot, if for instance you're in Las Vegas in the summertime.  Or think of warm air blowing from central heating vents...  Though of course it's not air friction doing the heating, but convection & conduction.

The collisions result in heat loss because the air molecules bounce off your skin with more energy than they impact with. You have to be moving a tremendous speed before the friction heating is greater than the heat loss through transfer. By moving the air (or moving through the air) each molecule is new and at a lower energy state than your hand and there are more collisions. this cools it faster than standing still where the air around you becomes slightly heated by the collisions and have to diffuse away, so many of them get bounced back now at higher energy states when they contact again resulting in less heat loss. your hand is cooled and thermoreceptors in your skin detect the lower temperature. these sensors just detect specific temperature ranges, warm or cool past these ranges and your body can't detect the temperature.

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Most accurate depiction of cortical homunculus?
I was looking at cortical homunculus and I realized there are several different pictures and they don't quite agree.  For instance:
http://wellbeing.media.mit.edu/2014/02/21/mindfulness-neuroimaging-and-neurofeedback/
http://nawrot.psych.ndsu.nodak.edu/Courses/465Projects11/PLS/4Thesomatosensoryandmotorcortices.htm
One area, for instance, are the feet, which I feel should have a fairly large (not as big as hands) area in the brain, mainly from the personal experience of having more sensations in feet, which like the hands has many nerve endings, though obviously much less fine motor ability.  But that's just my speculation, and I like an accurate depiction so I can start from there and make sense of this.  Thank you.

The reason they vary ever-so-slightly is down to a matter of opinion.

Be sure to distinguish exactly what the diagram is showing. Your first reference is sensory cortex mapping. The second reference is motor cortex mapping. The text of the second reference is admittedly confusing about this, a search for "Wilder Penfield motor cortex" verifies.
It seems reasonable the feet would show sensory response similar to the hands. Stepping on a nail is just about as bad as bumping your hand into one. Motor control is different. Muscles are not all innervated the same. In some of the large muscles, say in the legs, one nerve can control hundreds of cells. In other cases, particularily in the face, one neuron might control only six muscle cells. Thus a greater number of neurons, and a larger portion of the brain, is needed for control in these delicately controlled areas. It would make sense a greater part of our brain would be needed for motor control in our hands versus our feet.


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How large is the range of 'same origin' when determining whether two organs are analogous or homologous?
The pectoral fins of a whale and a shark. Are they analogous organs?
I was looking at this question, and I saw that the two answers defined the range of 'same origin' differently. One said that sharks and whales have the same origin as jawed animals, (therefore they are homologous) and the other said that they had different origins, namely cartilaginous fish and mammals(therefore they are analogous). Now here's the question.
How large is the range of 'same origin' when determining whether two organs are analogous or homologous? Is it as large as a Kingdom or a Phylum? Class? Order? Family? Or is there another criterion?

There is no limit: the ribosomes in your cells and the ribosomes in a palm tree are homologous structures, because both you and a palm tree inherited that structure from your last common ancestor, an unicellular eukaryote, more than 1 billion years ago.
That being said, the question in your link (and several other sources) gives an incorrect definition of homology and homoplasy (or analogy). Homology and homoplasy are not defined for "the function of the organ" or anything like that.
First, both terms apply to structures, which have a different meaning in phylogenetic systematics and evolutionary biology. A structure can be:

Morphological
Physiological
Biochemical
Comportamental (ethological)

Thus, we are not necessarily talking about organs or morphology when we define homology and homoplasy.
The difference between homology and homoplasy is very simple:

Homology: a similarity due to common ancestry.
Homoplasy: a similarity not due to common ancestry.

So, in my example using ribosomes, that similarity ("presence of 80S ribosome") regarding you and a palm tree is due to your (ours) common ancestry.
On the other hand, the thermoregulation in mammals and in birds (and probably other dinosaurs, not only birds) is an example of homoplasy, because the common ancestor of mammals and birds, an early amniote, was probably not capable of thermoregulation. Notice that here the structure is not a morphological one, but a physiological one. Another example using physiology is the pH of the blood: the pH of my blood and the pH of your blood is the same (7.4) because we inherited that feature from our common ancestor. Thus, it's a homology.
Sometimes the situation is tricky. Is the wing of a bat and the wing of a pigeon an example of homology or homoplasy? Since the common ancestor of bats and birds didn't have wings, and both bats and birds developed wings independently in their evolutionary histories, it's an case of homoplasy (analogy). What causes confusion here is that, in both cases, the wing is a modified anterior limb, and the presence of an anterior limb in bats and pigeons is an homology. The "limb" is a homology, not the "wing".
And that brings us to the case of sharks and whales. If the pectoral fin of a shark derives from the same structure that formed the anterior limb of the first sarcopterygii, then you can say (as several systematists say) that the pectoral fin of a shark and the anterior limb of a whale are homologous structures.
Summarising: given two organisms, Y and X

X and Y share a given feature;
find the last common ancestor of X and Y (it doesn't matter how long ago in the past)
did that ancestor have the feature? Did it transmit the feature to both its descendants?

If the answer to that last question is "yes", it's an homology. If "no", it's an homoplasy (analogy).


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Can the dietary fibres as chemical compounds be regarded as polymers?
At the level of molecular structure, can the dietary fibres be regarded as polymers?

About which dietary fibers are you thinking?

Dietary fibers are the indigestible portion of food derived from plants.
Most of these are indeed polymers of sugars (that is, a chain of repeated basic unit of carbohydrate), for example cellulose, alginate or pectin. They have glycosidic bonds that cannot be broken down by enzymes found in humans, and are thus indigestible.
But there are exceptions, for example raffinose, a trisaccharide found in beans & cabbage, is also categorised as a dietary fiber, as it is not breakable by human enzymes.


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How to determine continental ancestry group (race) with transcriptome data obtained with RNA microarray?
Say I have a whole genome expression data (transcriptome) for some sampled human tissue. Is this data sufficient to find out the continental ancestry group of a donor?

If you can call genomic variants from your data, depending on your coverage of the genome, you should be able to map ancestry. For example, if you have sequencing reads, you can align your reads to a reference genome and then call variants using existing pipelines.
Once you have variant calls, you could use ancestry-informative markers to infer the ancestry of your sample directly.
Or you could use existing software to map the ancestry of your sample in relation to other samples of known ancestry, using a program like ADMIXTURE, STRUCTURE, EIGENSOFT, or just principal components analysis. For reference samples, you could use a publicly available data set like HapMap 3 or the Human Genome Diversity Project.

Thank you @leekaiinthesky for answering. Do you mean whole genome sequencing reads or just short reads of protein-coding sequences by "sequencing reads"?

I meant RNA-seq reads. But it was just an example. It depends on what kind of data you're starting with.


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Are there any drawbacks to having immutable DNA during lifetime?
Imagine that there is a way to prevent cell DNA from being changed once zygote has been formed. Would this have any negative effects on the target organism? Does DNA change during the lifetime as part of normal operation, or DNA changes are always due to mutations or malfunction?

Mutations in B lymphocytes are necessary to mount a good immune response. This is called somatic hyper mutation. It is a very controlled process, failure of which can lead to ceetainlymphomas

Are you asking about changes in the DNA primary sequence (ATCG), epigenetic changes like DNA methylation, or both? @Polisetty has already mentioned gene rearrangements and somatic hypermutation in certain immune cells (T and B cells, specifically). DNA methylation (along with histone modification) is absolutely essential for regulating the expression of genes in different cellular contexts - you need a way to keep liver enzymes from being expressed in the skin, for example.

It is interesting... do all cells in the body have the same genome? Leaving apart B-cells, T-cells, mosaicism and other gained mutations.

Semantic of the post
This question could arguably be better on-topic on WorldBuilding.SE. The difficulty with the kind of question that ask What if the world was different, it is unclear how different would it exactly so to understand what consequence to draw from this scenario. The other issue is of course that the answer cannot be drawn from empirical studies but only be inspired from current knowledge and make untestable predictions.
Because definitions of epigenetic vary and some of them might be extraordinary broad, I will assume that by mutation, you are referring to any change in the DNA sequence excluding epigenetic changes.
Related post
Does our DNA change during our lives? is a related post.
What do somatic mutations do?
Adaptive Immunity
For species having some form of adaptive immunity, somatic mutations are used for producing a large diversity of antibody than can be tested on the self before being released in the body searching for antigen to bind to. In absence of somatic mutations, the adaptive immunity is pretty much inexistent. This point is probably the most important and has been raised by @Polisetty in the comments.
Cancer
Somatic mutations cause cancers. More generally speaking, somatic mutations create genetic diversity within the body yielding to opportunity for selfish cells that could proliferate to the expense of the rest of the body. In absence of somatic mutations, there would be no (or at least much fewer) cancer. This will affect selection for increased lifespan.
Somatic mutations on genetic diversity
As a fraction of the mutations that are transmitted to the offspring occur before the separation between the somatic lines and the germline, the absence of any somatic mutation would result in a lower mutation rate. This would result in lower genetic diversity overall. It would also affect selection pressure that depend upon the mutation rate and may have other consequences that are hard to predict.
Also, and more importantly, many species undergo asexual reproduction such as budding in plants. In some species, the entire genetic diversity is caused only by somatic mutations. In absence of such mutation, there would be no evolution possible.
What mutations are inherited
If a parent has a mutation in the lineage giving rise to half the gametes, then this mutation will necessarily be passed to half of the offspring. For this reason, offspring tend to share new mutations even if their parent did not have them. Absence of somatic mutations will remove this effect, which I would predict would have little impact on anything!


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Will a Codon result in same amino acid across organisms
Will all organisms with the same 3 nucleotide sequence in the codon produce the same exact same amino acid. I read that the three nucleotide sequence will code for a particular amino acid. I did not understand if that is the case across organisms. Can someone explain this in simple terms.

Yes. One particular sequence of codon code for only and only one amino acid. However, there could be more than one codons for a single amino acid.

@Beginner Please follow the instructions for comments and do NOT use them to answer questions. In this case you also happen to be wrong as I will explain and reference in an answer.

I think it better to not treat this as a duplicate of the mitochondrial question.  This question is even more basic, and one that can be answered straightforwardly and without the confusing twist of context resulting from using that question.

Are you interested in the different codons used across organsims or the different codons used (based on bias, environment etc.) that code for a specific amino acid?

@mgkrebbs OK. I have relented and added an answer focussed at the non-mitochondrial situation.

Although the answer to this question may be found in Mitochondrial Genetic code, because that answer is primarily about mitochondrial genetic codes, I shall give a more directed answer here.
Because the same genetic code that was elucidated in bacteria was found to apply to higher eukaryotes, it was initially assumed that the genetic code was universal, and was referred to as such. Subsequently it was discovered that mitochondria did not generally employ this ‘universal’ code, which is now usually referred to as the ‘standard’ code — indeed different mitochondrial codes were found in different organisms.
However the question seems to be more concerned with the genetic codes of  bacteria and the nuclear genetic codes of eukaryotes. Here also there are deviations from the standard genetic code, which can be found listed either on this Wikipedia page or at NCBI.
Below are some examples from the NCBI list (where references may be found) with the standard coding in parentheses:
 Mycoplasma
 UGA      Trp          (Ter)

 Ciliates, Dasycladacean and Hexamita
 UAA      Gln          (Ter)
 UAG      Gln          (Ter)

 Euplotidae
 UGA      Cys          (Ter)

 Candidate Division SR1, Gracilibacteria
 UGA      Gly          (Ter)

 Pachysolen tannophilus
 CUG      Ala          (Leu)

Finally, tRNAs for the ‘additional’ amino acids, selenocysteine and pyrrolysine recognize, respectively, the UGA and UAG stop codons in specific contexts.


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In the Lineweaver-Burk Plot, why does the x-intercept = -1/Km?
Taking the reciprocal of both sides of the Michaelis-Menten equation yields the Lineweaver-Burk Equation:
$ \dfrac{1}{V} = \dfrac{K_m}{V_{max}}\dfrac{1}{[S]}+ \dfrac{1}{V_{max}} $
Plotting a $ \dfrac{1}{V}$ vs. $\dfrac{1}{[S]}$ graph, I am told that:
y-int $= \dfrac{1}{V_{max}}$ and
x-int $= -\dfrac{1}{K_m}$
How are these relationships derived from the lineweaver-burk plot?  I can see how the y-intercept can be equal to $\dfrac{1}{V_{max}}$ if $\dfrac{1}{[S]} = 0$, but I don't see how x-int $= -\dfrac{1}{K_m}$ by setting $\dfrac{1}{V} = 0$? Can someone demonstrate how these relationships were derived?

Equation of a line: y=mx+c or y=m(x-d) where c is y-intercept and d is x-intercept. The general equation of a line is y-y₁=m(x-x₁)

Set $ \dfrac{1}{V} = 0$ and solve for $\dfrac{1}{[S]}$:
$ 0 = \dfrac{K_m}{V_{max}}\dfrac{1}{[S]}+ \dfrac{1}{V_{max}} $
$ -\dfrac{1}{V_{max}} = \dfrac{K_m}{V_{max}}\dfrac{1}{[S]}$
$ -1 = {K_m}\dfrac{1}{[S]}$
$ -\dfrac{1}{K_m} = \dfrac{1}{[S]} = $ x-intercept


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What is a typical value of the selection coefficient s?
I am trying to gain an understanding of the real world effects of natural selection from the equations, especially comparing it with drift. However I have been unable to find any examples which give an estimated value of the selection coefficient for a population considering a particular trait. Could anyone link me to some studies that give an actual value for a selection coefficient? Thank you in advance!

Try http://scholar.google.se/scholar?q=estimate+%22selection+coefficient%22

This is a very fundamental and important question! But first, be cautious not to confound the Fitness effect of segregating alleles with the mutational effects.
Fitness effect of segregating alleles vs mutational effects
One must not confond the distribution of fitness effect of segregating alleles in a population with the distribution of mutational effects. The distribution of mutational effects will always be narrower in comparison to the distribution of fitness effects of segregating alleles as very deleterious mutations won't stay long in the population and very beneficial mutation will sweep to high frequency very quickly so that it is unlikely to see them.
I am assuming you are interested in the distribution of mutational effects. Below are some papers and generalities that will be of interest to you. Some data come from the quantitative genetics literature and some from classical empirical population genetics. I also talk about mutation rate as these two subjects are highly related typically at determining mutation load.
Short answer
A typical deleterious mutation has a mutational effect of $s=0.1$ or $s=0.05$. In theoretical studies, authors often used a constant value of $s$ as being equal to one of these two numbers.
Longer answer
Distribution of mutational effect
Generally speaking distribution of mutational effects (on both the deleterious and the beneficial side) are thought to approximatively follow a gamma distribution with an extra bump of probability density around lethal mutations. shape might take values around 0.5 or 0.05 while the scale parameters might be of the order 0.1 to 0.001, with typically an average around 0.05. See Halligan and Keightley 2009. I have seen (see Nemo's documentation for example) that the dominance coefficent $h$ is modelled as $h=-log(2 Exp[h])/Exp[s]$.
Mutation rate
Concerning the mutation rate, a reasonable approximation is to consider a deleterious mutation rate per diploid genome of 1. This is known as Drake's law (see this post). Drake's law appears to be an underestimate for humans (Keightley 2012), about right for Drosophila, (Haag-Liautard et al. 2007), C. elegans (Denver et al. 2004) and possibly non-human endothermic vertebrates (Baer et al. 2007), and probably an overestimate for many other organisms (Baer et al. 2007, Halligan and Keightley 2009).
Quantitative traits
If you are uneasy with basic quantitative genetics and the below notation, you should have a look at this post.
For quantitative trait, there is evidence that $\frac{Vs}{Vp}≈5$ on average (Kingsolver et al. 2001, Johnson and Barton 2005). If heritability is $\frac{1}{3}$ (as it rarely significantly different from), then $Vs=7.5$. Empirical estimates of the mutational heritability $Vm$ suggests that $\frac{Vm}{Ve} = 0.001$ (Houle et al. 1996)

@21joanna12 Please let me know if you think I answered your question or if I am off-topic in your opinion.


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Is it possible to mathematically model the growth of plants?
Are there mathematical equations that represent/model the growth of plants?
For example, if I have a Bellis perennis and I want to know how it develops in a given environment (Sun is shining, defined amount of water etc).
How can one say if it grows a certain height and leafs and all other organs?
I don't want a generic solution for this like using L-System and stuff, I just want to have a source where I can research growth rules for a given plant, flower or tree.
Background:
I'm making a kind of mini-game for a computer-graphics course at university.
Think of it like a 1st-person shooter where you take a seed and plant it into the earth.
The plant starts to grow and you will see it grow like in real life.
Of course there are some environmental constraints that should be taken into account:
A. Time
B. (Sun)Light
C. Water
D. Other nutrition stuff like fertilizer
Don't bother about the technical aspects, i just want to know about the biological aspects of plant-growth.
Let's assume we have a sunflower plant. As it starts to grow I get a couple of questions:
1. How fast does the plant stem grow according to a well defined amount of luminosity and water?
2. When do the first leaves develop?
3. How much thickness the stem gains per day/hour/minute?
4. What happens when suddenly there is less amount of luminosity and/or water? How the growth-rate will be affected?
These are only a few questions that arise when i think about this topic. Therefore i want to have a mathematical description of plant-growth under the environmental constraints mentioned above. I don't need a generic approach, but it would be nice to see such a formalism for e.g. a sunflower or Bellis Perennis. I also don't care about things that won't be able to see in the scene, like micro-biological-level - i just care about the whole architecture of the plant (stem, branches, leafes, fruits, (root)).
I did a lot of search on this topic including the computer modeling side:
http://algorithmicbotany.org/papers/
https://www.informatik.uni-konstanz.de/en/deussen/publications/
But these sources focus more on techniques on how to generate images instead of the biological aspects.
Another book I've searched too solve my questions is "On Growth and Form" by Darcy Wentworth Thompson, but thats too general for my needs.
So are there any formal descriptions of plant-growth that take luminosity, water etc into account?

not sure if anyone has specifically done this for plants, but I would guess that the answer is 'yes' - however, the detail that you seem to be interested may not be easily obtained from a simplified mathematical model. At least in growth of simple organisms (e.g. bacteria, fungi), models make a lot of assumptions on environment, growth conditions, etc - not sure how useful information is at the level of detail that you've described in your question.

I'll add more detail here: I'm working on a prototype of a interactive computer simulation as a university project where you can place a seed of any kind of flower (lets assume Bellis perennis here because it's "simple" and well known). Now I have a sunlight in my scene and a watering can. After placing the seed I want to apply growth rules for the given kind of plant. So i want to know how the stem grows (height, thickness etc) and when and where leafs come up. So i need a formula for this specific plant which takes into account how much light, water and nutrition is given to the plant.

I don't want to go down to the level of micro organisms like bacteria or cells because I'm aiming for visual representation only. So I'm just looking for a "approximated" mathematical representation of a given kind of plant.

Yes it is possible and it is routinely done. For one example: https://team.inria.fr/virtualplants/

@Did I've also found interesting sources right here: http://algorithmicbotany.org/ - I really don't want to read about technical aspects of how one could implement this in a computer application/software. The thing i need is something like "growth rules of plants for dummies" - I just want to read about the biological thing of how the growth of a specific plant behaves. Then you might say: Okay on an acre where the sun shines everyday the growth-rate per day is for example: 1cm * sunlight strength + randomness factor, after it has a height of x it develops leafs and the phyllotaxis is x+y*z

There may be several models. Have you done a google scholar search?

@WYSIWYG Yes i did, but I'm having a hard time with this since my biology-background is like none...

@jackon can you provide some additional details on what exactly you want and which models that you already searched are close to your expectation. Otherwise this question would tend to be too broad.

@WYSIWYG I've updated my original post with some additional information on what i want to do.


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Has the acronym DNA ever been widely understood to stand for deoxyribose nucleic acid?
I have a friend familiar with evolutionary biology who was recently bragging about how much he knows.  I asked him what DNA stood for, and he answered it stood for 'deoxyribose nucleic acid'.  When I claimed it stood for deoxyribonucleic acid, he said it depends on the source you go by.  I was curious and decided to look into it, but the only source I could find using his answer was the paper "Molecular Structure of Nucleic Acids: A Structure for Deoxyribose Nucleic Acid" published in the 1950s, and no explanation regarding if and when the term was officially changed.  Can anyone shed light on the history of the term and explain if deoxyribose nucleic acid is still acceptable?

DNA is not an acronym. It is an initialism.

First off, that paper is the seminal discovery and publication of the structure of DNA, and is absolutely worth the read.  It's one of the most important pieces of scientific literature.

The short answer is no.  DNA stands for Deoxyribonucleic Acid.
The long answer is... this is really just picking at nits.1  DNA, deoxyribonucleic acid, is a type of nucleic acid, specifically a deoxyribose nucleic acid.  So, if your or your friend wants to be pedantic, you can call DNA a type of deoxyribose nucleic acid that stands for deoxyribonucleic acid.
You probably shouldn't, though, since if you really want to be pedantic, saying "deoxyribose" implies it's a sugar, which once it has formed the DNA backbone, it no longer technically is.  Watson and Crick clearly used the phrase your friend has, but suffice to say that British papers from the 1950s used language differently than most folks today.
As a side note, there are nucleic acid analogues, such as PNA and LNA, which generally use the "Whatever Nucleic Acid" construct for naming, but I suspect that's mostly because "peptide" is a broad category, and "locked" isn't actually a biological word.
Also, "it depends on the source you go by" is just a way of getting out of being wrong.
ETA: WYSIWYG correctly notes in the comments that it used to be called desoxyribonucleic acid, such as in this extremely important paper by Avery, MacLeod, and McCarty.

1: See what I did there?  Most people would say "nitpicking" but "picking at nits" is basically the same thing, even if almost nobody says it.

In the old days, they used to call it desoxyribonucleic acid.

Technically, it's not even an acid: http://chemistry.stackexchange.com/q/61457/7399


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What are the differences between Signaler and Primer pheromones?
I have searched few authentic books and have found the following difference between them.
Signaler pheromone induces fast reaction in the recipient and the Primer induces slow reaction.
But I did not find any book that discriminates their function.
P.S. I have read Wikipedia and I'm not counting on it.

A good example of a primer and a signaler pheromone could be in the recently discovered pheromone system in pennate diatoms (unicellular algae). When diatoms reach a certain size as a result of successive divisions (they get smaller with each vegetative division) both mating types start to produce a first pheromone that provokes cellular responses in their mates: 1) to stop dividing vegetatively and 2) to produce either another pheromone (a cell attractant, by one of the mating types) or to induce a sensing system to locate their mates. So, the 'Primer' pheromone would be the first, and the 'Signaler' the second pheromone, i.e. the attractant. A similar system exists in fungi. The evolutionary explanation is likely that organisms don't need to invest in pheromones and their associated repertoire of sex genes when mates are not present.
References:

Metabolomics Enables the Structure Elucidation of a Diatom Sex
Pheromone
Pheromone signaling during sexual reproduction in algae


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Can you identify this flower?
I have found this plant in my garden. I watered it, and now it is blooming. I have no idea what plant it is. Could someone help me to identify this plant? My geographic location is the Indian subcontinent.

Thanks for your effort to bring it up to flowering-stage.

+1 for making it flower. Would it be possivle to add a picture were we can see the flower more closely? See how many petals it has and maybe the color of the stamens inside.

I would say it's champa (plumeria) from the leaves but the flower hardly resembles it. Besides, plumeria's white species is more common in the indian subcontinent.

I am not sure but I think it is water leaf plant ( called sambar cheera ).If you see other pictures, the leaf and flower color matches but I am not sure as I do not know how the flower looks when it is bloomed ( in your picture).
You can see this site http://papanasini.blogspot.in/2012/02/cylon-spinach-sambar-cheera.html
I got a picture of the above-mentioned plant from my house, unfortunately, it is not having flowers and I will get back when it will have one.

Hope this helps!

Great! Finally.. I think this is the one.. Thank you Sarannya E..


text:
Does covariance and phenotypic variance have to be for the same trait to calculate narrow-sense heritability?
I'm working on a problem where I'm given that the phenotypic variance of the parent, $p$, for trait $A$ is $175.2$ and the phenotypic variance of the offspring, $o$, for trait $A$ is $146.1$. However, I'm also given that the covariance between parent and offspring of a different trait, $B$, is $14.6$.
Can I still calculate the narrow-sense heritability of $A$ using
$$\begin{eqnarray}
\frac{h^2(A)}{2}&=&\frac{\text{Cov}(p,o)}{\text{Var}(p)}=\frac{14.6}{175.2}\approx0.0833 \\
h^2(A)&=&2\times0.0833\approx0.167
\end{eqnarray}
$$
even though they're different traits?
I'm also told that any resemblance between parents and offspring is completely due to genetics, ie. without environmental effects. I've read that if this is the case, then $h^2$ is $0.50$, but I'm a little confused with it.

Does covariance and phenotypic variance have to be for the same trait to calculate narrow-sense heritability?

Yes. See below for more information.

Can I still calculate the narrow-sense heritability of AA [..] even though they're different traits?

No, you can't. A measure of heritability makes sense only for

a given trait
a given population
at a given time
in a given environment

[I'm also told that if any resemblance between parents and offspring is completely due to genetics, ie. without environmental effects, then $h^2$ is 0.5, but I'm a little confused with it.]

The above is not a exact quote from you but the original sentence made no sense. I rephrase what I suppose you tried to say.
The formulation is inaccurate and could therefore be misleading. It is wrong to say that any covariance between parent and offspring is only due to genetics. In reality, environments between parent and offspring often covary. There might also have covariance due to epigenetic reasons and potentially many other reasons.
You cannot make any claim about what value should $h^2$ takes for the special case where covariance between parent and offspring is solely due to genetic variance (or any other special case considering only genetic variance). You still need to know the relative importance of the genetic variance to the total phenotypic variance. If any of this is unclear, then you should keep on with the recommended reading below.
Reading Recommendation
I recommend that you have a look at Why is a heritability coefficient not an index of “how genetic” something is? for an overview of the concept of heritability and common misconceptions.


text:
How to conduct PSI-BLAST for a given protein sequence against bacterial protein database only?
I have a list of 100+ proteins and I need to conduct psi-blast for each one of them against "bacterial proteins" only.
I went to NCBI's protein blast tool, but couldn't figure out how to select/limit the targeted database.
Here are the 2 configs I tried:

Database: pdb, Organism: bacteria (taxid:2)
Database: landmark, Organism: bacteria (taxid:2)

Can anyone tell me if either of the approaches is correct? If not, please point the right way.

Edit 1 - add more details
All of my data is from "Supplementary Table 10" of paper "Comparative genomics of the neglected human malaria parasite Plasmodium vivax".
About 5% of all my protein sequences are ISS predicted. Remaining sequences are IEA predicted

pdb only contains IDs with deposited structures. I have not heard of landmark, could you provide a link to it? I agree with @Michael_A that Uniprot is the way to go.

Your approach is correct but it is worth considering which database will work best for you. Questions to consider are;

Does the database provide a large search space for the organism(s) you're interested in?
Do its IDs work well for searching other databases?
How does the host database handle identifiers over time?

For protein sequences I would use;

Database; UniProtKB/Swiss-Prot(swissprot)
Organism bacteria (taxid:2) (or a subset)

The reasons for this are that I am comfortable with how Uniprot handles their ID's, they provide a large search space with includes clear delineation between reliable (reviewed) and other (unreviewed) sequences, and finally UniprotKB IDs map well to genes. The latter can be problematic. I also know that I won't have trouble searching PDB with UniprotKB IDs.
Despite using and liking the Protein data bank (PDB) I wouldn't use them for this kind of search as they are a structural database which reduces your search space. PDB has 8292 structures for E.coli compared to 23 017 reviewed and 1,335,860 unreviewed sequences in Uniprot. If you are only interested in structures then the PDB is an ideal fit.
I haven't used landmark.

I am looking for structural homology in bacterial proteins. Since you pointed out that PDB is a structural database, would that make it a better candidate?

I'd still use Uniprot as the uniprot IDs can be used to search PDB. However, you could do both. The only downside to Uniprot is that it will likely return a large list. Taking time to understand the structure of uniprot's holdings will help you to deal with that. If you can get away with reviewed sequences I'd stick with those.


text:
Do humans squint more readily at green light?
I know that humans won't squint their eyes even if exposed to dangerous levels of ultraviolet or infrared light because our eyes simply don't have the capability to detect it. Neither do the irises constrict.
Since the human eye is most sensitive to green light, does this mean that we will squint and/or constrict our irises more readily for green light? Perhaps even when the intensity is safe for our eyes? (Albeit close to dangerous levels)

If it is below danger level, there is no reason for eye to squint even for green light.

As the intensity increases, energy transferred increases, which would cause sensation of heat causing closing of eyes.

Yes.  According to Action spectrum for photophobia Journal of the Optical Society of America A, Vol. 20, pp. 1852-1858 (2003), the most squinting-sensitive wavelength is ~510 nm, which is green.  Squinting sensitivity progressively falls above 510nm, and below 510nm squinting falls to a local minimum at 460 nm, and then rises again below 460nm, but did not reach a higher maximum in the range studied, which ended at 420 nm.

Since this article is behind a paywall, all I have to go off of is the abstract which says "...a trend of increasing sensitivity with decreasing wavelength."

@Myridium if there is something specific you want me to tell you from the full text, let me know, but I can't copy the whole article.

Is there a visual which exhibits the main results? What you tell me in your answer contradicts what I read in the abstract.

@Myridium Yes, there are graphs of sensitivity verse wavelength.  I am telling the actual squinting sensitivity vs. wavelength, whereas the abstract is telling you "After correction for absorption by macular pigment and the ocular media".


text:
Do all multiple sequence alignments employ global alignment algorithms?
Multiple sequence alignments are usually done between sequences of similar length, which resembles best a global alignment. However, I'm not sure at all what the algorithmic background would be in such case. Is it essentially a global or a local alignment when one performs a multiple sequence alignment?

Global or local alignments mean to align parts of the sequence or the whole sequence, whilst multiple alignments is how many sequences to align (one or more than one). They are not mutually exclusive terms. See "what is the difference between local and global sequence alignments?"

It is dangerous to generalize, as different multiple sequence alignment (MSA) programs may well employ different algorithms. However as the objective is to align many sequences along their whole length, and all MSA programs of which I am aware present the results as such, it is difficult to envisage anything other than global alignment being employed.
For the widely used Clustal W and X, this is certainly the case. Clustal employs a progressive alignment algorithm which involves the heuristic assumption that the most closely aligned sequences by pairwise alignment are a valid basis for the order in which progressive multiple alignment is performed. The initial pairwise alignments (which are used to produce a guide tree) use dynamic global alignment, as does each progressive alignment step, although this alignment is to a profile of previously aligned sequences, and uses context-dependent scoring.
There is an extensive Wikipedia article on MSA and one of the original Clustal papers is freely available on-line. The excellent book by Durbin et al., Biological Sequence Analysis, contains a chapter on the topic.

Multiple sequence alignment is a very complex task and there are several approaches depending on what you are looking for.
A global alignment might find the overall closest region. However, it is a well known problem with the lengths. If sequences lengths are very different this can be generate bad alignments.
Local alignment is seeking for the best matching regions along sequences.
It is well known that some genomic regions tend to accumulate more mutations than others. For this the idea of domains is suggested. The main idea behind (and to make it simpler) is like performing several local alignemnts in order to get the optimum alignments for different regions of you sequences.
There are many algorithms that implemented very different methods to do so: from pairwise alignments to HMM profiles.
I would recommend to read this article.

Just as James said these terms are not mutaully exclusive.
you statement is not correct:

Multiple sequence alignments are usually done between sequences of
  similar length

It really depends on what you want to achive with your MSA (multiple seqeunce alignment). First some brief explanation about local and global alignment(the difference between these two is described previously in this question):
 local alingment: trying to match a portion of your sequence of interest with another sequence, this could be done with MSA think about BLAST. Using BLAST you are performing a local sequence alignment with all the sequences in the database. When using this local alignment you are focusing on parts which overlap between your sequence with those in the database --> clue about domains e.g.

global alginemnt: the matching of the whole sequence with another sequence, which DON'T have to be equal in size. When using a global alignment with sequences of different length e.g. what will happen is that depending on the  algorithm that is being used (Needleman–Wunsch), there will be gaps inserted to match those sequences over the whole length.

Some practical examples when to use which alignment:

Making profiles of a group of proteins --> global alignment
Intersted in homologous proteins --> most of the time you use a local sequence alignment especially when you know the homologs are quite distance, so there is not much sequence similarity.
searching proteins which could have simillair function --> local alignment, BLAST will give you the proteins which have same domains e.g. or the same structure when blasting againt the PDB database, which can give you major clues about the function of the protein of interest.

NOTE that these suggestions are just some examples, some people will prefer an other option.

Rick, English may not be your first language, but that doesn't excuse your not using a spell checker. If you can set your browser language to English (Firefox allows me to switch to French etc), most will spell check entered text. Otherwise, copy the text into a word processor such as Word, select it all, set the language to English (British of course ;-) ) and run a spell check.

Thankyou I will try that! , indeed it will spell check my typed words to my browser language(Dutch) So if I type an english word it will change or split it to make it look Dutch so changing my browser setting would fix that problem (I hope) @David


text:
What stops messenger RNA from binding to itself?
Since mRNA is single-stranded, and (mostly) floats freely within the cytosol, what stops it from folding onto itself (like DNA) and preventing transcription?

The premise of this question, that mRNA "(mostly) floats freely", is false. I don't have specific references (hence a comment, not an answer) but recent research on RNA interactions shows that mRNA is in fact rarely unbound. Under physiological conditions it's almost universally in a complex with proteins or (other) RNAs.

Yes @KonradRudolph is right. Approximately 60% of a eukaryotic mRNA is expected to be bound by protein http://biology.stackexchange.com/a/21898/3340.

@Konrad Rudolph Indeed, as mRNA is always bound to RBPs (RNA binding proteins in vivo), many scientists consider that saying messenger RNP (ribonucleotide particle) is more precise. Isolating protein-free RNA in vitro is actually very hard.

It does fold on to itself. There are secondary structures in RNA and some of these secondary structures also have regulatory functions (for example, riboswitches). Some of these structures can also inhibit translation (by different mechanisms such as the masking of the ribosome binding site or analogous eukaryotic sequences, or stalling of ribosome etc). Other non-coding RNAs like tRNAs and rRNAs fold into specific structures that are essential for their function.
Many assays have been developed to study RNA secondary structure in vivo. SHAPE and DMS-seq are some examples.
The translation initiation factor eIF4A has a helicase activity that helps in resolving some secondary structures and facilitate translation (despite this, some structures can impede translation).
Also check out ribosome profiling experiments.

Due respects to everything given here so far (protein associations etc) in reply here as being accurate and part of your answer.  There is however the fundamental distinction between RNA and DNA yet to examine: that whole "deoxy-" matter right there in the 'D' of DNA.  That's the main key to why DNA more readily attains a double helix than does RNA.
There are at least two known physico-chemical reasons starting from the presence or absence of that 2' hydroxyl for this:  (1) DNA can more readily inhabit either an A- or B- form, (whereas RNA is more limited to the A-form).  So DNA has more entropic options as a helix former  (2) RNA's 2'-hydroxyl can become deprotonated and thus hydrolyzed more easily.  So less stability in the long run, not as good an information storage form, less likely to form complementary structures.  Not unlikely, just less likely.  Here's a good reference about this.

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text:
How can axons shrink?
I' ve read that some diseases result in the shrinking of neurons in the brain.
Does the axon shrink or the cell body? And what' s the underlying mechanism that shortens the axons, if that' s the case?
And is it possible that axons shrink even without any diseases?

It might be helpful to know which diseases you have in mind, and where you've read about this; personally, I'm curious whether you are referring broadly to degradation of "white matter" or of something more specific and it would help to know what motivated your question.

I've read this about alzheimer's disease, but don't know where I read about this. My actual interest is to find out whether axons can shrink and if there is any biological necessity for axons to shrink.

Demyelinating disorders like multiple sclerosis cause the insulating myelin around axons to shrink, but that isn't the same as the axon itself shrinking. Alzheimers isn't my area of research but I am aware that damage to the "white matter" is part of the disease - white matter consists of axons and their myelin, but my understanding is that white matter degradation in Alzheimers is due to loss of fibers, not shrinking of the individual axons. It's possible this is what you read but without a citation I don't know for sure.


text:
Can neurotransmitter concentrations in the synaptic cleft add up if there are several impulses in quick succession?
When an electric signal reaches a chemical synapse, the signal is transmitted using neurotransmitters. Afterwards, the neurotransmitters are removed from the synaptic cleft. My question is whether it happens in a normally functioning brain that neurotransmitter concentrations in the synaptic cleft add up if there are several impulses in quick succession? If so, does this serve any purpose? Or is the time between two impulses always long enough for all of the neurotransmitter to be removed from the synaptic cleft?
Edit: To further clarify (as the currently only answer does not really adress my issue), I am aware of the principle of summation, however I do not know whether this is actually caused by multiple neurotransmitter emissions "adding up" in the synaptic cleft or whether the postsynaptic membrane can just somehow remember if there was an increased amount of neurotransmitter recently.
To describe it graphically: According to this article, the concentration of serotonin in the synaptic cleft during a single impulse looks somewhat like that. Now when there is a quick series of impulses, does the neurotransmitter always get removed before the next impulse as on the right side of the following image, or can it add up as on the left side? And if it does add up, does this actually serve the purpose of temporal summation or some other purpose?

I think as bpedit said the temporal summation also occurs at the body of the neuron as well as at the synapse, although I do expect that your left hand image will represent the concentrations if the APs follow each other close enough by overloading the transport mechanisms.

The answer by bpedit is a good explanation of temporal/spatial summation, which can be partly a postsynaptic phenomenon (due to membrane time constants or second messenger sytems, for example).
Your specific question is about whether extracellular neurotransmitter levels sum over time. This definitely occurs regularly with "neuromodulatory" neurotransmitters like serotonin (others that behave similarly include dopamine and norepinephrine/epinephrine). "Faster" neurotransmitters like glutamate and GABA are cleared more quickly, though there are complicating factors there as well that are outside the scope of this question.
Although the summation has been shown many times, I looked quickly for an example and found the paper by Bunin and Wightman, 1998. Figures 2-6 all show extracellular serotonin concentrations that are elevated for seconds after release (let me know in the comments if you can't access this paper at your institution), and they show the changes in extracellular concentrations with multiple stimulus pulses (see in particular Figure 3).

Thanks, something like the figures in the quoted paper was just what I was looking for!

The addition of multiple impulses is termed summation and is instrumental in whether an action potential will be induced in the post-synaptic neuron. If the neurotranstitter released by one action potential in the pre-synaptic neuron was enough to cause an action potential in the post-synaptic neuron, the whole idea of neruotransmitters would be a waste of energy and resources. In these circumstances an electrical synapse would suffice, the chemical synapse being "overkill".
Temporal summation happens when several action potentials arrive in quick succession from a particular neuron. Spacial summation occurs when action potentials arrive from multiple neurons, at roughly the same time, to act on a localized area of a post-synaptic neuron. In either case, the effect of a single action potential is not enough to cause a large enough influx of ions to initiate a new action potential, whereas the combined effect of several action potentials is enough to reach the threshhold value necessary.
There can also be inhibitory contributions to this process as well. These typically increase the resting membrane potential making it harder to reach the threshold needed to initiate an action potential. All-in-all it's rather like a voting process that occurs at the synapse (or small region of multiple synapses). This "voting" allows for complex integration of all the inputs neurons receive.
Here's what appears to be a good reference on summation:
https://www.ncbi.nlm.nih.gov/books/NBK11104/
Here's the Wiki link as well:
https://en.wikipedia.org/wiki/Summation_(neurophysiology)#Temporal_summation
Here's an instructive video, I've only watched a couple minutes but it appears a reasonable visual treatment:
http://www.interactive-biology.com/1660/what-is-summation-2-types-episode-19/

Some of the information contained in this post requires additional references. Please [edit] to add citations to reliable sources that support the assertions made here. Unsourced material may be disputed or deleted.

This is all right out of any introductory Biology textbook, stuff I've taught for over 20 years. All easily verifible online, hundreds of thousands of hits. With what particularily do you have an issue?

You may be familiar with the material, but that doesn't mean everyone else is. I'm an immunologist, and I know the difference between T and B cells, but I always include links to Wikipedia when I mention them here because others may not know, or may simply be interested in learning more. I could not cite them with the excuse that "it's all easily verifiable online", but you could say the same about every citation in a primary research paper. I highly recommend reading completely through this Meta discussion regarding citations.

Just to be sure: the summation is not only caused by the fact that the postsynaptic membrane somehow remembers that there was an increased amount of neurotransmitters shortly before the second impulse, but that there actually still is neurotransmitter left from the first impulse in the synaptic cleft?

@vauge I don't know for sure. There is another mechanism at play as well. Gates in the post-synaptic membrane have opened to allow the influx of ions which depolarizes the membrane. It takes a finite time for these gates to close, independently of how they were opened, which contributes to summation. There is also variation in the nature of these gates and the particular neurotransmitter involved in different synapses. So it's possible a slower degradation of neurotransmitter allows summation in some cases but not others.

@vauge - Both, in a way; there can be residual neurotransmitter in the synaptic cleft, and there can be neurotransmitter that remains bound to receptors (you could possibly think of this as 'memory'). Finally, to add to bpedit's comment, your question referred to serotonin, and most serotonin receptors are g-protein coupled receptors; g-protein receptors subsequently affect second messenger systems like cAMP and IP3/DAG whose effects remain over long time scales, seconds and longer.


text:
Why is darker skin a better defense against sun than lighter skin?
We know from physics that the colour of something comes from the light it reflects.
Dark/Black objects absorb most light while light/white objects reflect most light.
Sunburn is the absorbance of too much light and is bad for your skin's health suggesting that absorbance of light is bad for you.
So why is darker skin better than lighter skin for high sun intesity living conditions? Logically darker skin should absorb more light (and so energy) while lighter skin should reflect most light (and energy).

I have realised there is a similiar question to my one already existing. Should I delete my question?

Within stackexchange? please give a link to that possible-duplicate. (To do that; copy the URL and paste in comment). If that is an exact duplicate; then it could be deleted; but please wait for moderator-intervention. If it is NOT an exact-duplicate then point it out what different thing you're looking for.


text:
Has any animal ever had a rotating part?
Outside of microscopic structures (I'm thinking of a flagellum, which I think is a true motor) has any animal evolved a part that continually rotates compared to the rest of its body?

A more universal microscopic example is the ATP synthase in mitochondria. The flagellum example only applies to bacterial flagella. Can't help on macroscopic examples.

Have a look at this: there's a reasonably well-written popular discussion of why the evolution of such a body part is very difficult to imagine. However the page does mention this as the single known macroscopic example (a rod rotated by cilia).

Not a 360 degree rotation but Owls can rotate their heads by 270 degrees without any serous damage.

Duplicate http://biology.stackexchange.com/questions/7932/why-are-there-no-wheeled-animals

@HuguesFontenelle Not really a dupe, admitedly, if there were animals with wheels then that would answer this question but the lact of animals with wheels doesn't mean the lack of any rotational body part.

@SanjuktaGhosh Thanks, I had considered that though.  The thing is it can rotate, it is a wind then unwind mechanism where the rotation creates increasing torque.


text:
Why do SRIs help in serotonergic neurotransmission?
Serotonin reuptake inhibitors (SRIs) block the action of the serotonin transporter (SERT) which, according to Wikipedia, leads to an increase in serotonergic neurotransmission.
Now this book summarizes serotonergic neurotransmission as follows:

[The neurotransmitter] binds to specific receptors on the postsynaptic cell, thereby
  generating a postsynaptic electrical signal [...]. The transmitter must then be removed rapidly to
  enable the postsynaptic cell to engage in another cycle of
  neurotransmitter release, binding, and signal generation. [Neurotransmitters are removed by] reuptake into nerve terminals [...].

So my question is the following: If, as stated in the quote, the transmitter must be removed rapidly, shouldn't an increased amount / binding potential of SERT actually be a good thing because if there are more transporters, the process of removing the neurotransmitter is much faster? And consequently, why would blocking the SERTs help in serotonergic neurotransmission? Is it because the neurotransmitter must remain in the synaptic cleft for a certain amount of time? Is it because the reuptake takes place before the neurotransmitter could bind to the receptors of the postsynaptic cell? Or ist there yet another reason?

Excellent question.
Different neurotransmitters operate at different temporal scales (and even the same transmitter can operate at different temporal scales). Examples of the fastest-acting neurotransmitters are glutamate, GABA, and acetylcholine (with the caveat that they can also act more slowly). These neurotransmitters (usually) open ion channels in the postsynaptic cell, and are cleared rapidly after release, which allows for a temporally precise code, with each release event individually important.
Other neurotransmitters are also considered neuromodulators, such as dopamine, serotonin, epinephrine/norepinephrine, and others. While the basic machinery for release is the same, these neuromodulators aren't cleared as fast, bind to g-protein coupled receptors, and their concentrations can build in the synaptic space between neurons when the presynaptic cell fires multiple action potentials in sequence. For these neurotransmitters/neuromodulators, the amount of neurotransmitter sitting around outside the cell acts as a time average of release in the recent past.
SRIs/SSRIs/similar drugs slow down the reuptake process, such that the concentration of serotonin reaches higher levels with the same presynaptic activity.
Although reuptake can also be important to "restock" the presynaptic cell with neurotransmitter for release, there is typically enough precursor around that reuptake is not the only limiting step.
Your suggested reasoning that is closest to the truth is both: "...because the neurotransmitter must remain in the synaptic cleft for a certain amount of time? Is it because the reuptake takes place before the neurotransmitter could bind to the receptors of the postsynaptic cell?" but it isn't that the transmitter "must remain" longer or that reuptake takes place "before" it can bind: it is that if the neurotransmitter remains longer it has a larger integrated effect on the postsynaptic cell.
Lastly, "good thing" is relative - of course increasing SERT activity would help with faster transmission, but faster transmission might not be important/necessary/fit the function of the circuit where serotonergic signalling is involved.


text:
What is the distance between the insertion of the distal end of the bicep tendon and the head of the radius?
I was unable to find a source that could provide a measurement for the distance between the insertion of the distal end of the bicep tendon and the head of the radius.
Does anyone know a source that might be able to provide this data for the average adult human?

From {1}:

Abstract
  PURPOSE:
  There is little information in the literature describing the anatomy of the biceps tendon insertion. The purpose of this study was to map the footprint of the biceps tendon insertion on the bicipital tuberosity and to report on the relevant anatomy to assist surgeons with correct tendon orientation during surgical repair.
  METHODS:
  Fifteen fresh-frozen adult upper extremities were used in this study. The relationships between the long head of the biceps tendon, the short head of the biceps tendon, the muscle bellies, and the distal tendon orientation were examined. The length, width, and area of the biceps tendon insertion were measured.
  RESULTS:
  In all specimens examined, the biceps musculotendinous unit rotated 90 degrees externally from origin to insertion. The long head of the distal tendon was inserted onto the proximal aspect of the bicipital tuberosity, while the short head of the distal tendon was inserted onto the distal aspect of the tuberosity. The lacertus fibrosus, in all specimens, originated from the distal short head of the biceps tendon. On average, the biceps tendon insertion started 23 mm distal to the articular margin of the radial head. The average length of the biceps tendon insertion on the tuberosity was 21 mm, and the average width was 7 mm. The average total area of the biceps tendon insertion (footprint) was 108 mm(2). The average area of the long head of the biceps tendon insertion was 48 mm(2), and the average area of the short head of the biceps tendon insertion was 60 mm(2).
  CONCLUSIONS:
  Landmarks have been identified that will allow anatomic orientation of the distal biceps tendon during operative repair. The distal short head of the biceps tendon has a consistent relationship with the lacertus fibrosus and a distinct insertion on the bicipital tuberosity. The dimensions of the distal biceps tendon footprint have been determined to assist with bone tunnel or suture anchor placement during surgical repair.

(bicipital tuberosity = radial tuberosity)
Some figures from the same study:

FYI:

How correlated are the lengths of tendons in different part of a human body?
How can I measure my tendon length?

References:

{1} Athwal, George S., Scott P. Steinmann, and Damian M. Rispoli. "The distal biceps tendon: footprint and relevant clinical anatomy." The Journal of hand surgery 32, no. 8 (2007): 1225-1229. https://www.ncbi.nlm.nih.gov/pubmed/17923307 ; https://scholar.google.com/scholar?cluster=16116840451671820399&hl=en&as_sdt=0,22 ; http://www.sciencedirect.com/science/article/pii/S0363502307005163 ; http://dx.doi.org/10.1016/j.jhsa.2007.05.027 ; http://sci-hub.cc/10.1016/j.jhsa.2007.05.027

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Don't the radioactive labeled molecules of dNTPs or DNA harm themselves or their surroundings?
I'm reading some papers for the first generation sequencing methods and some earlier than them, like Ray's Wu first time DNA sequencing from a λ phage virus cohesive 5' ends. Ray Wu, like Maxam-Gilbert and Sanger, used 32P / 3H to label either dNTPs or DNA molecules.
But what happens if you add such radioactive materials inside a test tube with DNA and other molecules like DNA Pol I? For example,  32P emits electrons at 1.709 MeV. Couldn't these high energy electrons harm the DNA or Pol I molecules (bonding destruction), that are present nearby at the time of reaction?

Experimentalists pretend, or act as if, those effects are negligible, or miniscule.  One could calculate the number of DNA or protein molecules that are affected, by plugging in the specific activity of the dNTPs, the concentration of the potential targets, the volume of the reaction, and the time.
Certainly if you create radiolabeled nucleic acids and store them, then over time those strands will undergo scission as the phosphorous emits it's beta particle.  Some of the neighbouring bases might be hit.
If you pulse label growing bacteria or phage you can then mutagenize and select for mutants in interesting pathways (this was called radiosuicide and was invented by Clarence Fuerst).
It is also possible to label bacteria and feed them to C. elegans such that the progeny of those worms will contain new mendelian mutations induced by the radioactive DNA in their mothers' germline.

Thank you very much. Your answer is very informative. I liked the use of "pretend" verb. Do you have any paper in mind "counting" the destroyed molecules from such chemical agents?

It's worth considering how many high energy electrons are actually released compared to the number of molecules in the tube. For instance, I routinely work with $^{32}P$-labeled DNA, and measure the specific activity of samples by scintillation counting. For me, a very hot stock sample of labeled DNA (~1000x more concentrated than I would use in an experiment) will register on the order of $10^8$ disintegrations per minute (dpm). That means each minute, about $10^8$ beta particles are emitted by decaying phosphorous atoms inside the sample. But the amount of DNA molecules in that same tube is about 50 pmol, or about $3 \times 10^{14}$ molecules.
So if each of those beta particles were absorbed by a DNA molecule in the same sample, thus damaging it, that would be a rate of self-damage of $10^{-6} min^{-1}$. Of course, most of those beta particles actually make it out of the tube, so the actual rate of self-damage is much lower still. Since we're probably interested in measuring processes on much shorter time scales than this self-damage rate, it becomes negligible.

Additionally, in an experiment you are generally not looking at the properties of a single molecule. If you were sequencing this DNA, for example, it is exceedingly unlikely, especially given the calculations in your answer, that the majority of bases at a single position would be mutated and therefore affect the result.


text:
What is the ultimate source of ADP/ATP in humans?
I am teaching myself Cell Biology from the internet. Despite my usually good Googling skills, I'm stuck in a loop with this question.
Q: What is the source of ATP?
A: ADP
Q: What is the source of ADP?
A: ATP
At first I thought that ATP synthase actually created ATP from scratch as intimated here:

ATP synthase is an important enzyme that creates the energy storage
  molecule adenosine triphosphate
  Wikipedia

I then realise that ATP synthase doesn't create ATP so much as convert ADP.
My Question
Can humans synthesise ADP/ATP from scratch. If so, where are these phosphates made and if not what food source provides them and how? Also, where do we get the phosphorus?
Thanks

As the concern expressed by the poster has recurred in an essentially similar question despite the excellent answer by @MattdDMo, I shall provide an additional answer labouring the basic biochemical points.

Inorganic phosphate (the term used to describe the mixture of different phosphate ions present at physiological pH) in animals is derived from the diet.

Biochemical processes exist (substrate-level and oxidative phosphorylation) in which this inorganic phosphate is transferred to adenosine diphosphate (ADP) resulting in adenosine triphosphate (ATP).

This explains how the γ-phosphate (third phosphate) of ATP can derive from inorganic phosphate de novo. It does not explain where the α- and β-phosphates of ADP (and hence ATP) come from.

There is an enzyme, adenylate kinase, that catalyses the formation of ADP from ATP and AMP:
         ATP + AMP ⇔ 2 ADP

This can be regarded as transferring the γ-phosphate of ATP (derived from phosphate) to AMP to provide the β-phosphate of one of the two molecules of ADP produced in the reaction. So that explains how the β-phosphate of ADP can derive from inorganic phosphate, and thus how both β- and γ-phosphates of ATP derive from inorganic phosphate de novo. What about the α-phosphate?

The α-phosphate in the purine monophosphate AMP derives from one of its precursors, ribose 5-phosphate. The relative points of the pathway of purine synthesis that can be found in detail in biochemical texts such as Berg et al.:
ribose-5P →→→→→→ inosine monophosphate →→ AMP

And the phosphate in the ribose 5-phosphate derives from the γ-phosphate of ATP in the phosphorylation of glucose in the hexokinase reaction of glycolysis, followed by the reactions of the pentose phosphate pathway. In outline:
ATP + glucose → ADP + glucose 6-P →→ ribulose 5-P → ribose 5-P

In summary, the incorporation of inorganic phosphate (ultimately maintained by dietary intake) into the γ-phosphate position of ATP enables its incorporation into the α- and β- positions during purine monophosphate synthesis and subsequent reactions.

Phosphorus is a very common nutrient, found in high levels in proteins, which are in such foods as milk and milk products, meat, beans, lentils, nuts, and grains, especially whole grains. Phosphorus is found in smaller amounts in vegetables and fruit, as well. Adenosine can be found in many of the same foods, both as free ATP/ADP/AMP, and as part of the DNA found in all animal and plant-based foods (are there any other kinds?).
Adenine (the nucleotide base before the addition of ribose creates adenosine) is synthesized via the purine synthesis pathway, whose ultimate product is IMP, or inosine monophosphate. IMP is then converted to adenylosuccinate, then to AMP, which is then phosphorylated to ATP. It should be noted that, as is the case in most biosynthetic pathways, this one requires ATP to power it along, meaning it takes ATP to make ATP.

Would the downvoter care to comment so I can improve my answer? What's wrong with it?

I can't imagine why this was downvoted (+1 from me). Maybe because a quick look at the wiki link obviously requires ADP/ATP in its own production and someone thought it was a circular answer? That's my best guess.

@anongoodnurse The question isn't "Where did the first molecule of ATP come from?", but I guess that's as good a guess as any. I just wish people would leave comments when there's nothing obviously wrong with an answer, like another answer directly contradicting it or something. Oh well, it's not like the rep is a big deal or anything. I just want to be loved! :)

Not my downvote but the only correction I would make is the phosphorous content of grains. They are very rich in phosphate but most of it is locked up in phytate which most mammals can't digest. If you go on a high grain vegetarian diet your phosphorous intake actually decreases. See: https://www.ncbi.nlm.nih.gov/pubmed/21183586

@mimat Thanks for the feedback. Do you know how much is available from proteins and nucleic acids in whole grains as compared to the other foods I listed? That was kind of what I was getting at, not just the total phosphate levels regardless of bioavailability. Also, is phytate broken down by cooking, such that, for example, whole-grain bread has more bioavailable phosphorus than raw grains?


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DNA replication: How many DNA polymerase molecules work in parallel?
Background research
I am aware that DNA polymerase works in pairs, at least. This is to process both opposite stands of a given chromosome. The 3'-to-5' "leading strand", and 5'-to-3' "lagging strand" simultaneously. This two-DNA-polymerase process is beautifully shown in this TED talk by Drew Berry.
I have not checked any non-online sources but simple Google queries failed to answer my questions below.
Question
Within a single Eukaryotic cell, is the process of DNA-replication carried out by just a single pair of DNA-polymerases? Or do multiple pairs of DNA-polymerases work in parallel?

In the (beautifully rendered) video you linked to, the green molecules are DNA polymerases. So you can already see that there are more than two DNA polymerases at work!
At each replication fork, there is generally one DNA polymerase working on the leading strand, but on the lagging strand, multiple DNA polymerases may be working at the same time (as depicted in the video). Note that different types of polymerase are thought to be primarily responsible for the leading (Pol ε) and lagging (Pol δ) strands in eukaryotes (but not prokaryotes, which use Pol III for both).
Next, note that at every origin of replication, there are two replication forks working simultaneously, one in each direction. So that's double the number of polymerase molecules.
On top of that, a single eukaryotic cell has multiple chromosomes. Each one must have at least one origin of replication of its own, which can operate in parallel. In reality, each eukaryotic chromosome has up to thousands of origins of replication (prokaryotic chromosomes generally only have one). Human cells have on the order of 100,000 origins of replication. So depending on how many origins are active simultaneously, there are likely many thousands of polymerase molecules acting at once to replicate the DNA of a single eukaryotic cell.
You could probably do a rough estimate of the number of polymerase molecules active simultaneously by taking the average duration of S phase in your cell of interest and dividing by the genome size and the speed of polymerase.

Never be too trusting of pretty pictures (/videos), there being multiple DNApol in the video could have been precisely why I asked the question in the first place (to check it's accuracy)

Fair point! But after checking the math, I trust that they did get that detail right in the video.

Having another read of your answer this is awe inspiring, thanks leekainthesky!


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Is there a complete connectome of a cortical minicolumn?
I know that there are projects that try to map brain connectivity. Given that a cortical microcolumn has only around a hundred neurons I wonder whether there is a dataset available with the complete connectivity of just a single minicolumn of the neocortex. Doesn't have to be human.
I posed this question on cognitive science stackexchange already, but it doesn't seem to be happening.

I'm voting to close this question as off-topic because it has cross-posted to cogsci.se and has an answer there: http://cogsci.stackexchange.com/questions/16090/is-there-a-complete-connectome-of-a-minicolumn-of-the-neocortex

Perhaps the first place to look would be the Allen Brain Atlas
 (for mice, this is a paper about it), and also [this paper].(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4169118/)


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How do we know Neanderthals DNA?
According to this article, a small amount of Neanderthal DNA was introduced into the modern human gene pool. How do biologists even know what the Neanderthals' DNA look like?
The article doesn't mention how the science recognize what the Neanderthals' DNA actually is at the first place. So how do we know what the Neanderthals' DNA is if I'm guessing we never tested Neanderthals body cell samples?
If you say "From their bones/skull" but how do you know they are actually Neanderthals and not modern humans with some rare gene mutation or something else?

If you want the full story I highly recommend Svante Pääbo's excellent book, "Neanderthal Man: In Search of Lost Genomes"  https://en.wikipedia.org/wiki/Neanderthal_Man:_In_Search_of_Lost_Genomes.  Here's the amazon link: https://www.amazon.com/Neanderthal-Man-Search-Lost-Genomes/dp/0465054951.

Neandertal DNA has been completely sequenced multiple times now, using DNA from bone and tooth samples found in cool or cold environments.  The first Neanderthal genome sequence was described in 2010:
A Draft Sequence of the Neandertal Genome
Since then, as well as higher-quality sequence, more genomes have been completed; at least 6 individuals have been sequenced (perhaps more; I've lost track a little).  As well, complete genome sequences from several Denisovans -- a Homo species that were approximately contemporary with Neandertals, but a distinct species -- have been recovered.
The science of recovering ancient DNA has advanced very rapidly in the last decade, and while it isn't routine to sequence 50,000-year-old DNA it isn't as magical as it used to be.  The current record for sequencing ancient DNA is 700,000 years, which is earlier than the sapiens/neandertalis split.

but how do they know they were not merely modern humans, deformed by diseases such as rickets, arthritis or syphilis?

For one thing, the genomes are distinct and clearly well outside the range of the human species. For another, Neanderthal skeletons don't show signs of disease -- indeed, far from being diseased, Neanderthal skeletons are vastly more powerful and robust than puny humans.  For a third, Neanderthal skeletons, of which many are known, are consistently the same as each other and consistently different from sapiens skeletons. All lines of evidence showing that they are separate species are extremely strong; taken together they are indisputable.

the mt DNA sequence differences among modern humans range from 1 to 24 substitutions, with an average of eight substitutions, whereas, the mt DNA sequence differences between modern man and the Neanderthal specimen range from 22 to 36 substitutions, placing Neanderthals, at worst, on the fringes of the modern range.

no, I don't understand it. I'm just finding arguments against it in order for me to know more about the subject. Thanks anyway for the answer!

Suggest asking a separate question, then; comments are not a good place to raise a completely new issue

Just in case anyone is taken in: Note that the comment by @Grasper above about mtDNA is copied directly (though without attribution) from the notorious "Institute for Creation Research", and as is typical from them is deliberately obfuscatory (i.e. what we call "a lie"). Genomic DNA, not mtDNA, shows that Neanderthals are a distinct species.  Starting point for reality-based understanding: Strong reproductive isolation between humans and Neanderthals inferred from observed patterns of introgression.

The answers here give you reference to the first draft genome. Take a look at these papers for high-quality sequences: Prufer et al., 2014 for Altai Neandertal, Meyer et al., 2012 for the Denisova individual. A third one, the Vindija Neandertal has been sequenced and the sequence is already available (though not published, yet) here. However, one thing has not been mentioned. The presence of ancient DNA can be confirmed by identifying specific damage patterns in the DNA molecules, i.e. mainly deamination. That is used to ensure that the DNA is old and does not result from contamination of present-day humans. Additionally, modern human contamination levels are estimated by two or three independent methods in the papers given above. These methods exploit the uniqueness of Neandertal mitochondria and Y-chromosomes, i.e. the fact that these variants have never been seen in present-day humans.
This answers the sequence part, but my answer focuses on the second part of your question and the issue your raise in the comment sections:

If you say "From their bones/skull" but how do you know they are actually Neanderthals and not Humans with some rare gene mutation or something else?

This can mainly be answered on two different levels. The first level is a parsimony argument: there are a lot of those skeletons (far more than the ones that have been sequenced) and it would be too unlikely they all suffered from the same disease. Additionally, skeletons of present-day humans with the diseases you mention do not at all look like Neandertal skeletons.
The second level is a bit more scientific: bones from the spanish cave Sima de los Huesos have been sequenced as well (Meyer et al. (2014) for a mitochondrial genome and Meyer et al. (2016) for nuclear sequences - not full genome!). Bones from this cave has been dated to approx 430,000 years ago which means that those bones may not even be Neandertal bones but rather Homo heidelbergensis. This makes a strong point against your suspicion as at that times modern humans did not even exist anywhere on the planet and it took another about 200,000 years until the first anatomically modern humans evolved in Africa (and then another 150,000 years until they set foot to Europe).

The sequence of the neanderthal genome is known because it has been sequenced and could then be compared to the human reference genome. The DNA was extracted from a toe bone found in Siberia, as described in reference 1.
The sequencing was done as described in reference 2. The researchers where sure that the bones came from Neanderthals because of anthropologic differences in the built of the bones they found. They are distinct from homo sapiens bones.
References:

A proximal pedal phalanx of a Paleolithic hominin from denisova
cave, Altai
A Draft Sequence of the Neandertal Genome

but how do they know they were not merely modern humans, deformed by diseases such as rickets, arthritis or syphilis?

You can carbon date such bones - the result is pretty clear.

I thought carbon dating is only reliable up to 5,730 years. Neandertals lived 350,000–600,000 years ago.

@Grasper First: 5730 years is one half-life of C14, dating works for at least 10 half-lifes - with special preparations to exclude contaminations even longer. Then the neanderthal lived from about 230.000 to about 30.000 years, which is at least partly in this range.

@Grasper There are also other isotopes besides carbon that you can use to date bones and fossils; you can also use entirely different methods, such as analyzing amino acids. It's just that carbon-dating is the most common for human-age artifacts because its half-life and range tend to cover most modern and immediately prehistoric human artifacts.


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What is the rest state for eyelids - Open or Closed?
If one were to not apply any efforts on the eyelid muscles, will they remain open or closed?
In movies when we see a person die, either case could happen - their eyelids could be open or closed when they pass away. (Not sure if that's the case in real life, as I have been fortunate enough to not witness any deaths).
I started thinking about this when I got into meditation. During meditation one is supposed to relax all their body muscles. I wonder, if I were to reach that perfect stage of relaxing what will happen to my eyelids. Will they automatically open? I feel like I've to make tiny yet finite deliberate effort to keep them closed. Not sure if that's the case with everyone.

This depends to some extent on how you define "resting state" (it matters).
Innervation of the eye occurs in the brainstem and upper spinal column, so is, like most brainstem functions, on autopilot (like breathing.)
If you define resting state as that which the lids would assume without any innervation, then the resting state of the eyelids is semi-open. This is the state of the eyelids of most people who die.
However, that position is not beneficial to the living eye, as it would lead to corneal breakdown. When people lose eyelid innervation, for example, following a stroke, the lids don't close completely. Ointment must be applied several times daily and the eye is often taped in the shut position to protect the cornea.
If you define resting state as that which occurs in sleep and in most comatose states, the eyes close completely, because innervation of eye muscles is intact and a main function is to protect the cornea, i.e. vision. This is done with a completely closed eye.
Comprehensive Review in Clinical Neurology, Cheng-Ching et al.


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Can prawns be classified as fish, or is their position ambiguous?
Today a zoologist told me that prawns and fish are very similar, but zoologists/taxonomists have put them in different categories because their distinction is unclear (like hydrogen in the periodic table). This completely bewildered me, as I know prawn and fish are in different classes because there is no similarity between them. I have no connection with biology now but studied it in high school — but even then, I could not believe it. Can someone please elaborate on this?

In any-2 taxa throughout living-world, there are certain-extent similarities and certain extent dissimilarities. for say you must get certain similarity between an amoeba vs an elephant or a prawn vs an oak tree. all them are made of cells, grows, reproduce, respire and such and such. so they are similar. However couldn't find enough cause to make a short group with fishes and prawns even in basis of present-day similarity. Because in basis of more similarity if I put fish and prawn together; I have to keep many other things together such as human; because we have eyes too.

May be the zoologist was giving  simple example to classify with small-number of specimen that you mistook as a whole-classification   (or  may not be...). If only-similarity used is to live inside water; then put with them the dolphins, the whales, the algae Spirogyra and a human foetus inside amniotic fluid. do you know there are terrestrial crustaceans such as woodlouse

Introduction to phylogeny
What makes that two species being closely related or not has nothing to do with whether they look a like or whether they live in similar environment. It has to do with their evolutionary history. Evolutionary history used to be inferred from phenotypic traits ('phenotype'≈'how an individual looks like') but today it is most often inferred from genetic data.
First you should have a look at this recent answer to get a short introduction to phylogeny.
Phylogeny of animals
Here is a basic tree of all animals

From wikipedia

A fish is any member of a group of organisms that consist of all gill-bearing aquatic craniate animals.

Craniates are Chordates, therefore fishes are chordates. You can have a look at the position of chordates on the above graph. Note that all mammals, birds, reptiles and others are also chordates. Note that fishes do not represent a monophyletic group (if you don't understand the term 'monophyletic', then you need to read the linked post above).
A prawn is a crustacean. Crustacean (incl. prawns, shrimp, crabs, ...) and Hexapoda together form a monophyletic group. Crustaceans are arthropods and are therefore much more closely related to insects, molluscs and spiders than to any lineage that we would call fish. Here is a tree of arthropods (and related clades). See the position of arthropods in the above tree. You can also have a look at the position of crustaceans within arthropods below. Please note that the tree is a bit outdated a present crustaceans as being monophyletic which is wrong (according @har-wradim, see comment below).

Your discussion with your friend
There is no doubt about the phylogenetic position of crustaceans as being part of arthropods and therefore not being very closely related to fishes. I think you misunderstood what your friend tried to tell you.
A note on developmental biology
All multicellular animals, undergo a grastrulation during development during whihc a hole is formed called the blastopore. In all deuterostomia (incl. fishes) the blastopore becomes the anus, while in prostomia (sister clade to deuterosomia which includes arthropods), the blastopore becomes the mouth. This a very major difference in how these different clades develop from a single cell (after fertilization) to a multicellular adult.
Online ressources
If you want to have a look at the tree of life, you can find great ressources on this post.


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Spectrophotometric Values of Individual Nucleotides
All around the net you will find this list giving 260/280 ratios of individual nucleotides:
Guanine: 1.15
Adenine: 4.50
Cytosine: 1.51
Uracil: 4.00
Thymine: 1.47
Yet I cannot find a reliable source for these values. One source cites a 70s version of Leninger's Biochemistry but even though I got hold of a more recent edition, I cannot find that information in there.
Does anyone happen to know a quotable source for this?

I too was unable to find the data in the 3rd Edition of Lehninger's Biochemistry.
A good source of such information usually is

Data for Biochemical Research, by Rex M. C Dawson, Daphne C. Elliott, William H. Elliott and Kenneth M. Jones (3rd Edition, 1986, Clarendon Press Oxford).

The first thing to note is that the ratios may be significantly
pH-dependent, and the source quoted by the OP does not specify what pH the data refer to.
The data in Column 2 below  been taken from the above source, from which the data in Column 3 were calculated.
(pH 7)-------------A280/A260--A260 /A280
Adenine             0.13        ~ 7.7
Cytosine            0.58        ~ 1.7
Guanine             1.04        ~ 0.96
Uracil              0.17        ~ 5.9
Thymine             0.53        ~ 1.9

These data seem to have been substantially taken from an article by K. Burton in the second edition of DFBR.

K. Burton (1969) Spectral Data and pK values for purines, pyrimidines, nucleosides, and nucleotides in Data for Biochemical Research by Rex M. C Dawson, Daphne C. Elliott, William H. Elliott and Kenneth M. Jones (2rd Edition, Clarendon Press Oxford).

If it's so important to you that you need a quotable source for this, I'd measure it myself with the equipment I use for the real experiment.
Otherwise I'd suggest you look at a chemical database such as NIST:
http://webbook.nist.gov/cgi/cbook.cgi?ID=C58617&Mask=400 and use the spectra that can be found there.

@tomd: Yes, to get the "true" values that would be required, and apparently also in the literature they didn't get the same values twice. I'd say if you need them for your own experiments, it might be better to actually measure the purities you have.


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Between Cholera and Polio, which disease cannot be controlled by killing the vectors
Since Cholera affects only humans, and also doesn't have an insect vector or animal reservoir host. And Polio is a disease of the central nervous system, spread from person to person through infected fecal matter entering the mouth. Then which one of them can be controlled by killing the vector, I'm not completely sure if cholera doesn't have a vector, but if they don't, then I'll like to know if and how polio can be controlled by killing the vector.

From you description, none of these disease have vectors. A vector is any agent that carry and transmit a pathogen. So you cannot kill any vector as there are no vector to kill.

Both of these diseases do not have vectors,
Cholera is a foodborne / waterborne disease and Poliomyelitis is spread through fecal-oral or oral-oral contact with an infected person.
They both only infect humans.
Thus, both cannot be controlled through killing any vector.
The best way to prevent Cholera is to avoid potentially contaminated food and water and follow proper sanitation practices.
The best way to prevent polio is through immunisation via vaccines.
For more information:
Cholera
Poliomyelitis


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Mammal size and capillary wall thickness
How does capillary wall thickness vary with the size of the animal?

Background/context of question:

Of the following, Figure 1 is most consistent with the fact that, in general, smaller mammals have:
A] thicker capillary walls than do larger mammals.
B] a more rapid metabolic rate than do larger mammals.
C] smaller surface area/volume ratios than do larger mammals.
D] capillaries of more variable cross-section area than do larger mammal

My working:
Of the following, Figure 1 is most consistent with the fact that, in general, smaller mammals have:
A] thicker capillary walls than do larger mammals.
B] (correct answer) a more rapid metabolic rate than do larger mammals. This is correct because a smaller animal has a higher surface area to volume ratio and hence radiates/loses heat quicker, and so must metabolise food quicker to keep their temperature up.
C] smaller surface area/volume ratios than do larger mammals. This is wrong as a smaller object has a higher surface area per volume
D] capillaries of more variable cross-section area than do larger mammal
My issue: I am trying to work out why A and D are wrong.
I can't find anything on the Internet about how capillary wall thickness (Answer choice A) or capillary cross sectionn (Answer choice D) vary with animal size.
If I was going to have a guess based on the stimulus:
For Answer choice A : From the graph, we know smaller animals have less oxygen partial pressure (as they lie to the right) and less HB saturation (as their curves lie to the bottom). If capillary walls were thicker, I would think this means that the oxygen partial pressure would be GREATER. I.e. if I think of a really thick walled balloon, it would be more difficult to blow up and increase in volume (and hence, have a higher pressure) than a thin walled balloon. However, as I know C is the correct answer, A (and my reasoning above) must both be wrong.
For Answer choice D: I don't really know how variation in cross section would have an effect. Maybe by providing a bottle-neck and increasing pressure in that way?

I believe your problem lies in understanding the oxygen dissociation curve. The higher the need for oxygen (e.g. because of metabolic rate or physical activity), the greater the shift to the right. So generally, increasingly smaller animals, having increasingly higher metabolic rates, have curves that shift progressively to the right. Capillary wall thickness is fairly constant in mammals: about one cell thick.

Thanks @anongoodnurse ! That explains why I couldn't find anything about the capillary wall thickness and animal size relationship ; I assumed as A wasn't the answer that the opposite i.e. that LARGER mammals have thicker capillary walls was true (rather than them being equal).