text:
How to retrieve logical expression (KO based) for reactions from KEGG?
Whether a module is complete or not can easily be checked by evaluating the Definition entry associated with the module; e.g. in module M00010, it is given by
Definition  K01647 (K01681,K01682) (K00031,K00030)

which can be translated to
K01647 AND (K01681 OR K01682) AND (K00031 OR K00030)

If this expression evaluates to TRUE, the module is complete.
Now I am wondering whether analogue information exists for a single reaction. So e.g. for R00352, one finds the following information about Orthology:

But how do I now know in which logical relation the KOs are?
So it could be
K01648 AND K15230 AND K15231

or
K01648 OR (K15230 AND K15231)

and so on.
Can this information be retrieved from KEGG and if so, how?
EDIT:
In the above example, the correct expression would be:
K01648 OR (K15230 AND K15231)

One either needs K01648 or the other two subunits together. So, unfortunately, it is not as easy as @aretaon describes it in his answer since just one of the two subunits would not be sufficient. One can therefore not just connect the KOs associated to a reaction using a logical OR.

To rephrase what you already mentioned in your question: For a KEGG Module to be completed (so that an organism can perform a certain function) you need a certain set of functional units or enzymes. So to evaluate the abilities of an organism you would check its genome for the gene sequences related to the module by performing the logical operation you mentioned above.
A Module is composed of chemicals (C) and reactions (R), as you can see in your given example. To explain the differences between modules and reactions best have a look at the last reaction, Isocitrate to 2-Oxoglutarate. There are three boxed reactions (one of them is a combination of two) that all lead to Oxoglutarate. When you look at the Orthology (the enzymes involved) for the reactions in the first box (R01899+R00268) and the second box (R00267) you will see, that it's the same enzyme (K0030) performing different reactions. The third box now contains a reaction (R00709) performed by a second enzyme (K0031), that leads the same way (it differs in using NAD+ instead of NADP+ as electron acceptor). So for the module to be completed you could use either of the two (that’s the reason for the OR-operator in the logical operation).
If you now want to evaluate if a certain type of reaction occurs in a given organism it is sufficient to have one of the possible enzymes catalysing this reaction. So:
K01648 OR K15230 OR K15231

Thanks for your reply. Unfortunately, it is not that simple (see my EDIT), but I wish it was... ;)

I tried to find another way but I think there is none. The logical syntax you describe is defined only for modules - and modules cover only selected parts of all pathways. So to be certain if the enzyme in a reaction is only part of a multi-enzyme complex (as in your example) you even cannot go back to pathways because the required parts aren't defined there either.

Yes. I tried to infer it from the module structure and the reaction list but that doesn't work either since that is inconsistent between modules, unfortunately... Too bad that there is no solution to this issue, it seems.


text:
Why must the alcohol decolorizer be used for 30 seconds or less for Gram staining?
I had today a class in microbiology and my teacher said that the Decolorizer component is the critical one and cannot be more than 30 seconds.
The decolorizer has alcohol in high concentration, my lecturer says 95%.
I know that alcohol dissolves the lipid membrane, more exactly here for RBC which should be a similar situation here, not completely sure however.
What component is the critical one that you cannot keep alcohol on your bacteria samples more than 30 seconds?

My guess is that this is because of its toxicity to the bacteria.

@Bitwise: if you're doing a Gram staining you most probably don't care about killing the bacteria.

@nico I was referring to the cells losing their structural integrity (the cells obviously need to be visible).

The crystal violet stain will be removed if the decolorizer is left on too long.  I'm assuming that the crystal violet complexes that are retained in the gram positive bacteria's peptidoglycan layers end up being washed away (perhaps from overdehydrtation).

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sort: votes


text:
Is secondary follicle or Graafian follicle arrested in the second metaphase of oogenesis?
My note about which I am not sure:

Secondary oocyte is arrested in the metaphase II monthly after puberty until fertilization with sperm.

The following picture also satisfies my sentence: .
So you can see that the secondary oocyte that is arrested seems to be Graafian.
I know that Graafian develops during the second week.
I know that the secondary follicle is developing two days before ovulation.
It seems that the development of the secondary follicle ends and the formation of Graafian follicle occurs just before ovulation.
My lecture material suggests that Graafian follicle is arrested in metaphase II, since Graafian follicle is ovulated once in a month and waits sperm in tuba uterina infundibulum:

The answer to my question is not also clear from my previous thread:

An oocyte completes meiosis I as its follicle matures (during ovulation) resulting in a secondary oocyte and the FIRST polar body. After ovulation, each oocyte continues to metaphase of meiosis II.

Which follicle is arrested in the metaphase II of oogenesis?

Graafian follicle.
The secondary oocyte and thus Graafian follicle are arrested in the second metaphase of oogenesis.
After this the corpus luteum develops from the follicle during the luteal phase of the menstrual cycle.

Three follicular stages are recognised,
1) Primary/Preantral Follicles (with primary oocyte inside)
2) Secondary/Antral Follicles (with primary oocyte inside)
3) Pre Ovulatory Follicles (with secondary oocyte inside)
Pre ovulatory Follicles are formed ~36 hrs before ovulation at time of LH surge. This coincides with completion of Meiosis I and formation of the secondary oocyte. The secondary oocyte immediately enters Meosis II.
Appx. 3 hrs before ovulation, the Pre ovulatory Follicle (with the secondary oocyte inside) is arrested in the metaphase of Meiosis II and is extruded out of the ovary - a process called as Ovulation.
It comes to rest in the ampulla of the fallopian tube and here it is fertilised. As the sperm pronucleus is released into the cytoplasm, the Secondary Oocyte (now called the ovum) completes Meiosis II and releases the second polar body.
Hope this helps.

Hi Akshay. It would be great if you can cite a reference.

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text:
Why are (some) cats attracted by bleach?
(Sorry if this question is only partly biological)
I have noticed that several cats (including the one that keeps sleeping in my house), are fond of the odor of bleach (eau de Javel) and chlorine.

Among examples, chlorine is used in small quantities in tape water and the cat is fond of licking the faucet in acrobatic positions even if there is mineral freshwater nearby.
I was one day not careful enough using a bleach based gel cleaning product and some of it got on my hand. Even after cleaning my hands, they still had a bleach "perfume" and my cat cling to me and even cleaned my hands with his tongue for minutes.

Why is this so ? Are there other animals known to have this taste ?
Might it be in fact acquired through living with humans ?
Is this potentially detrimental to their physiology ?

I can't give a definite answer, and there's nothing in the literature about this specifically, but perhaps some relevant information and a suggested behavioural experiment will help.
Background
Firstly, I assume you are talking about sodium hypochlorite (which is usually what people mean by bleach)? If so, there are several compounds your cat could be reacting to. Chlorine is an obvious candidate, which is released as sodium hypochlorite decomposes in solution. Additionally, bleach can react with various organic materials to release a variety of volatile organic compounds (VOCs), which your cat might be able to smell. In addition to also releasing chlorine gas, the same suite of VOCs are released when the chlorine in chlorinated tap water reacts with organic contaminants (Odabasi, 2008). The VOCs include chloroform and carbon tetrachloride.
Next, cats are known to exhibit modified behaviour in response to a variety of compounds. Some are suspected pheromone components of cat urine, such as felinine (Hendriks et al, 1995) and its breakdown products, such as MMB (Miyazaki et. al, 2006).
Some cats also react to externally-produced compounds with a particular response called the 'catnip response', which involves rubbing the face on the ground or other objects, shaking the head, rolling, etc. (Tucker & Tucker, 1988). Not all cats exhibit the response, around 50-50% do, and susceptibility is genetic and heritable. Some sources eliciting the catnip response include:

nepetalactone released from catnip (Nepeta cataria)
actinidine released from valerian (Valeriana officinalis)
essential oil of Actinidia macrosperma (Zhao et al., 2006)
the compounds epinepetalactone, dihydronepetalactone, isodihydronepetalactone, neonepetalactone, iridomyrmecin, boschnialactone, onikulactone, boschniakine, actinidiolide and dihydroactinidiolide (Tucker & Tucker, 1988)

In general all the catnip response elicitors share a two-ring structure, which is not to my knowledge shared by any of the volatiles given off by bleach.
A possible experiment
So, two obvious possibilities (regarding what type of behavioural response is being elicited) are that either:

your cat is interpreting the volatile as a pheremone and therefore as some sort of sexual or territorial signal, or
it is showing the catnip response

As a first experiment, you could check whether your cat (and any others you can get hold of - in an ethical way) respond to bleach and/or to catnip. If the cats do not exhibit the catnip response to catnip, they aren't exhibiting it in response to bleach, and thus some other explanation is more likely.
As a second experiment, you could make a detailed observation of the precise behaviour shown in response to bleach. Compare it to that exhibited when the cats encounter catnip (depending on the outcome of the first experiment) and when they are oestrous (if female) or encounter an oestrous female (if male). You could also compare to the response to the urine of other (male and female, familiar and unfamiliar) cats.
An experiment you shouldn't do
If you wanted to find out which chemical your cat is responding to, you could allow your cat to sniff pure chlorine which hasn't encountered organic contaminants, as well as chloroform, and carbon tetrachloride. However, all three of those compounds are extremely dangerous and could easily kill you or your cat, so please don't.
I general, I would caution against exposing your cat to bleach, because it can induce serious health effects depending on dose and mode of exposure, ranging from asthma to third-degree burns to carcinogenesis. If they are attracted to it, that is a good reason to keep it away from them to prevent them ingesting it, which is more harmful than inhaling the fumes.
I can't comment on whether the behaviour is acquired as result of domestication, but that too could be tested by comparing the reaction of a large sample of wild cats (!).
References

Hendriks, Wouter H., Paul J. Moughan, Michael F. Tarttelin, and Anthony D. Woolhouse. “Felinine: a Urinary Amino Acid of Felidae.” Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 112, no. 4 (December 1995): 581–588.
Miyazaki, Masao, Tetsuro Yamashita, Yusuke Suzuki, Yoshihiro Saito, Satoshi Soeta, Hideharu Taira, and Akemi Suzuki. “A Major Urinary Protein of the Domestic Cat Regulates the Production of Felinine, a Putative Pheromone Precursor.” Chemistry & Biology 13, no. 10 (October 1, 2006): 1071–1079.
Odabasi, Mustafa. “Halogenated Volatile Organic Compounds from the Use of Chlorine-Bleach-Containing Household Products.” Environ. Sci. Technol. 42, no. 5 (2008): 1445–1451.
Tucker, Arthur, and Sharon Tucker. “Catnip and the Catnip Response.” Economic Botany 42, no. 2 (1988): 214–231.
Zhao, Yun-peng, Xiao-yun Wang, Zhi-can Wang, Yin Lu, Cheng-xin Fu, and Shao-yuan Chen. “Essential Oil of Actinidia Macrosperma, a Catnip Response Kiwi Endemic to China.” Journal of Zhejiang University. Science. B 7, no. 9 (September 2006): 708–712.

Thanks a lot for these references and these suggestions.

In response to your experience proposal, I can already give partial answers:

I have already exposed this cat to various compound known to cause "catnip" behavior in cats such as catnip and valeriane (the first bought, the second naturally occuring in my garden), and he did not, did not show any interest in it whatsoever while another visiting cat did.

(I know we are on biology.SE and not on Pet.SE but) Would a neutered male cat exhibit a change in behavior when crossing the path of a female in oestrus?

I marvel on the international character of scientific research on cats (japanese, american, chinese).

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text:
Is it comfirmed that Alzheimer's is a diabetes of the brain?
I read in this New Scientist report, that the mental decline during diabetes may be an early stage of Alzheimer's.  The hypothesis was based on a study with 20 rats.
Has there been any follow up research? Is Alzheimer's such a slow disease that this is will be remain hypothetical for a while?  Are there any other links between diabetes and Alzheimer's that can point in either way?
Or has research even confirmed (or refuted) another weaker hypothesis true, namely, the mental decline during diabetes and Alzheimer's have a common cause?
Many times newspapers say this or that is being research and we will know one day whether this is true or false; but the same newspapers hardly ever do follow up reporting.  So this is why I am asking this here.

You need to pay more attention to the statements. It is nowhere written (at least in peer-reviewed journals) that diabetes causes AD. They only say (if they did) that diabetes is a factor Correlation and causation are different. Also, dependence may not mean strictly causation. These terms may seem to have subtle differences but they mean different things.

@WYSIWYG I guess I should have used the wording "... that diabetes and Alzheimer's might have a common cause".

Far from being confirmed, the notion that diabetes is a significant factor in Alzheimers is held by at most a tiny, tiny minority of researchers.  New Scientist is notorious for wild-eyed hyping of fringe speculation; this is an example.

Some researchers consider Alzheimer's type 3 diabetes. There are lots of papers on the mechanisms involved.


text:
Amount of molecule at equilibrium
A cell produces molecule A at 10 units per second and the molecule has a half life of 15 seconds. How many units of molecule A are inside the cell at equilibrium? Showing your work would be phenomenal.
Geez, a bit hostile, are we? Regardless,
Here's how I went about doing it. Pardon my terrible formatting skills:
P is the concentration of molecule A.
The half-life formula is 2^-(t/15).
At the moment of equilibrium: P = 10 * dt + 2^-(dt/15) * P
Moving things around, I get P = 10 * dt / 1-2^-(dt/15)
I attempt to take lim dt->0 using l'hopital's: 10 / (1/15 * ln(2)) = 150/ln(2) molecules of A at equilibrium.
However, the correct answer should be 300 units of molecule A at equilibrium. Any suggestions?

No, showing your work would be phenomenal.

this looks a lot like homework.  Homework questions aren't forbidden, but this isn't a "do-your-homework-for-you" service; you have to show what you've tried and where you've gotten stuck.

Phenomenal. Finished editing.

I answered a very similar question from you here. Using the formulas on Wikipedia we can find that the mean lifetime $\tau$ is $T_{1/2}/\ln(2) = 15/\ln(2) \approx 21.6$.  Using Little's Law the steady state concentration is (arrival rate) $\times$ (mean lifetime) $\approx 216$.
You could also use the decay rate $\lambda=\ln(2)/T_{1/2}$ and substitute it into the differential equation given in the previous answer.
This is the same as the answer that you got to by a more complicated route. I don't see how we can get to a steady-state concentration of 300 unless you've misstated the question or left something out.

A friend just told me the same thing. Perhaps the answer key is faulty.


text:
Understanding Genetic Dynamics of Specific Problem
The following questions comes from International Biology Olympiad 2014, theoretical part B.
It states:

Earlier research suggested that the red flower pigment of plant species was the result of a
  chemical pathway including multiple steps and that all intermediate pigments were white. Three
  pure-bred lines with white flowers (White 1, 2 and 3) of this species were crossed with each other
  and the following ratio of colors were obtained among the progeny:

The question was how many genes control flower color. I completely botched it. Here are my thoughts:
Looking at F2 generation, there are 9 reds + 7 whites = 16 total. (I know it's a ratio.) Generally, having 16 suggests at 2 genes controlling the phenotypes. For example, cross AaBb x AaBb, you'll get 16 phenotypes.
Turns out 2 is incorrect, and I have no clue as to how colors are inherited in this problem. Any suggestions?

First of all, since two is incorrect, and one is not possible, three is the most probable answer. It is also supported by the format of question that three different types of white purelines are given. Let the genes be A, B, C. Now, there are three possible ways:-
1) Each one has two homozygous dominant genes and one homozygous recessive.
2) Each has one homo dominant and two homo recessive.
3) Any one has all homozygous recessive and the rest two can have any of the above two.
The problem with (2) & (3) is that they do not explain the red F1. Red will require a dominant allele of each gene. But in crosses of (2) or (3), at least one gene will be left out.   For example, AAbbcc x aaBBcc will give all progeny with cc. So none can be red. Same problem with aabbcc x aaBBcc or AABBcc
So lets go with (1). Let
W1 AABBcc
W2 AAbbCC
W3 aaBBCC
W1 x W2. => all AA Bb Cc (Red F1 of cross 1)
F1 x F1 will be like a cross of BbCc with AA in front of all the genotypes. This will give you exactly 9:7 phenotypic ratio as mentioned in question.
Now, lets solve the question.
A) Three genes. So false
B) F1 were homozygous for one gene and heterozygous for other two. So false
C) F1 of cross 1 = AABbCc and W3 aaBBCC
Since it is evident that it is possible to inherit dominant alleles of each gene (eg. AaBbCc or AaBbCC) so red colour can come. So false
D) F1 cross 1 = AABbCc
F1 cross 3 = AaBBCc
It is evident that one segregation of gene alleles of “a” and “b” will have a dominant allele no matter what. So for a white colour, only chances are from cc. So in cross Cc x Cc there is 1/4 probability for cc. So all in all, 1/4 probability for white (since aa and bb genotypes are not possible here).
So D is True.


text:
Reducing the Proportion of Phenotype in Hardy Weinberg Population through Selection
I was given the following question:
You travel to an unknown island and find a population of strangely colored
slugs! Upon close investigation, you notice that 16% of the slugs have a
shriveled tails, a most terrible condition you decide to name Yilunemia. The condition makes the affected slugs have a 50% chance of surviving to
reproduce. This is a autonomic recessive condition caused by a single gene,
and heterozygotes are not affected.
Assuming Yilunemia confers no discernible evolutionary advantage, how
many generations should it take for the proportion of slugs with the Yilunemia disease to fall below 5%?
Possible answers:

5
6
7
8
9

I've tried to apply usual formula for frequency after selection:
0.36 + 0.48 + 0.16 = 1
0.36 + 0.48 + 0.5 * 0.16 = 0.92
Divide by 0.92 gives:
0.39 + 0.52 + 0.087 = 1
If I keep doing this, after the 3rd generation, the frequency of Yilunemia condition is 0.045, which is less than 5%. However, this isn't an answer choice, therefore I must be doing something wrong.
Any suggestions?

The theory
You have to use the diploid selection equation (see here). Let $p$ be the the frequency of the recessive allele of interest, you get
$$p' = \frac{p^2 W_{aa} + p(1-p)W_{aA}}{\bar W}$$
, where
$$\bar W = p^2 W_{aa} + 2p(1-p)W_{aA} + (1-p)^2W_{AA}$$
You can simply iterate over with this equation. Do no forget to recompute $\bar W$ at each generation as the allele frequency changes, so does the mean fitness $\bar W$. Also, do not forget that we are looking for the generation where the frequency of sick individuals is lower than $0.05$, that is the generation where $p<\sqrt{0.05}$.
I don't think this recursion equation has any general solution unfortunately. This would mean that iteration is the only way to got.
The practice
I am a bit too lazy to compute everything by hand so here a short R code that will do the calculations for us.
frequencySickIndividuals = 0.16
p = sqrt(frequencyHomozygoteRecessiveMutants)
waa = 0.5
waA = 1
wAA = 1
for (generation in 0:10)
{
    frequencySickIndividuals = p^2
    cat(paste0("Generation ", generation, " frequency sick individuals = ", frequencySickIndividuals, "\n"))
    p = (p^2 * waa + p*(1-p)*waA) / (p^2*waa + 2*p*(1-p)*waA + (1-p)^2*wAA)
}

It outputs
Generation 0 frequency sick individuals = 0.16
Generation 1 frequency sick individuals = 0.120982986767486
Generation 2 frequency sick individuals = 0.0935350533786218
Generation 3 frequency sick individuals = 0.0738632061510922
Generation 4 frequency sick individuals = 0.0594638505565122
Generation 5 frequency sick individuals = 0.0487003101360286
Generation 6 frequency sick individuals = 0.0404940467744661
Generation 7 frequency sick individuals = 0.034123112395776
Generation 8 frequency sick individuals = 0.0290951856295452
Generation 9 frequency sick individuals = 0.0250680151553009
Generation 10 frequency sick individuals = 0.0217991643532054

So, it actually takes 5 generations to reach an allele frequency lower than $\sqrt{0.05}$.
Source of information on hardy-Weinberg problems
Note by the way, you might be interested in having a look at a tutorial on how to solve Hardy-Weinberg problems on the post Solving Hardy Weinberg problems.

I understand how to do it this way. I was thinking, given that I have no shouldn't take more than 1.5 minutes or so to (according to problem guidelines), if this is the fastest way to solving the problem.

Please see edit.


text:
Homework - Genetics linkage problem

A farmer purchases f1 hybrid seeds. These seeds contain four heterozygous loci that give a significant increase in crop yield when compared to either homozygote. Two of these loci are on the same chromosome and show partial linkage. If the farmer allows the f1 plants to self-fertilize, what is the probability that a seed from the resulting f2 generation has all four heterozygous loci?

a) at least 1/2
b) between 1/2 and 1/4
c) between 1/4 and 1/8
d) between 1/8 and 1/16
e) less than 1/16
I think it's either d or e. For the first two genes (unlinked), there is 1/2 chance to get heterozygote. So, 1/2 * 1/2 = 1/4. For the next two linked genes, if they were unlinked, it would be 1/2*1/2 = 1/4 for a total of 1/16. But since they are linked, I'm thinking that the chance for heterozygote might be reduced, so maybe the answer is e) less than 1/16?? Not sure where to end, though...

Try to draw a Punnet square! If you have tried already, what difficulties have you encountered? What brought you to think the answer is either 'd' or 'e'?

I agree with your reasoning! If the two genes are perfectly linked, then the answer is $\frac{1}{8}$. If they are perfectly unlinked, then the answer is $\frac{1}{16}$. The answer therefore must be somewhere between $\frac{1}{8}$ and $\frac{1}{16}$.  Good job!
Of course the answer e) is pretty silly as any other answer ('a','b','c' and 'd') would yield to 'e' being necessarily true. So, if you have to choose only one, I would just go with 'd' and highlight that the answer 'e' is silly.

I still don’t understand how if the two are completely linked, the answer would be 1/8.

Let's consider that at both loci, we have two alleles A and B. Here is a representation of the first F1 individual
-------A----A-----
-------B----B-----
Here is a representation of the second F1 individual
-------A----A-----
-------B----B-----
Of course, they are the same as the parental lines are pure breed. Now, if the two loci are perfectly linked, then the offspring can have the following possible genotypes
-------A----A-----
-------A----A-----,
-------B----B-----
-------A----A-----,
-------A----A-----
-------B----B-----
or
-------B----B-----
-------B----B-----
, but the offspring cannot be
-------B----A-----
-------B----B-----
or an other combination requiring recombination between the two loci. Therefore the probability to be heterozygote for the F2 at two perfectly linked loci is the same as the probability to be heterozygote at one of these two loci (if we assume the mutation rate is negligible).

Why can't parents be: parent1: -------B----A----- -------A----B----- parent2: -------A----A----- -------B----B-----[?]

Because parental lines are pure lines. When we talk about an F1 generation, we talk about the hybrid between two pure line. By pure line, we mean that we got rid of all genetic variance. So, one parental line is fixed for the A alleles and the other line is fixed for the B alleles.  In other words here are the genotypes of the pure parental lines.
-------A----A-----
-------A----A-----
and
-------B----B-----
-------B----B-----
One parent can therefore only give
-------A----A-----
while the other one can only give
-------B----B-----
so, the F1 generation is therefore necessarily heterozygote at all loci.

I still don’t understand how if the two are completely linked, the answer would be 1/8. It would mean that in order for these two linked genes to produce a heterozygote, they would have a 1/2 chance to do so. Is this necessarily true?

Please see edit.

Why can't parents be: parent1: -------B----A----- -------A----B----- parent2:  -------A----A----- -------B----B-----

@LittleDragon Pleas see edit

Wow, speedy. So you're saying that all f1 parents must have the same alleles in the same order on chromosomes? If so, then I'll mark your response as the answer.

I am not sure why you are talking about ordering. I used the letters A and B at both loci but they are denoting the same alleles of course, they just denote that parental origin. See small edit, maybe it will help you out.


text:
Finding steady state concentration given half life and production rate
Intracellular molecule B is normally synthesized at a constant rate of 1000 molecules/second. The lifetime B = 200 s.
How do I find the concentration of molecule B when it is at a steady state?
I Tried:
For molecule B. P is concentration of molecule B.
2^-(dt/200) * P + 1000 * dt = P
"2^-(dt/200)" is the half life formula. I multiply it by P to give me current concentration of molecule B. Then I add 1000 * dt to give me the amount of molecule B being produced at an exact moment. Rearranging the variables:
P = (1000 * dt) / (1-2^(-dt/200))
Now I limit dt --> 0 to give me P:
lim t->0 (1000 * dt) / (1-2^(-dt/200)) =
l'hopital's rule: lim t->0 1000/ (0.005 * ln2 * 2^(-dt/200))
Plugging in dt = 0, what I get is a steady state concentration of molecule B = 200000 / ln(2).
However, the correct steady state concentration for molecule B is just 200000.
Suggestions?

It's not clear to me how the problem is formulated. It sounds like you have a system at steady state, with synthesis rate = breakdown rate, and you want to relate half-life to concentration, which is fine. But then what do you mean by "reach steady state" -- the sought concentration is a constant? Also, I don't see where your equations derive from. The first equation seems to violate dimensions since 2^(-dt/200) is dimensionless? Somehow, your answer is actually the correct concentration for the steady-state problem. But I don't see how you got there ...

tl;dr besides making this a bit harder than necessary, your main problem is that you have confused the lifetime (average time to removal of a molecule), not the half-life (time until half of the molecules are removed, which is $\ln(2)$ times the lifetime ...) Wikipedia has some formulas ...
You can translate the problem into a differential equation (not as scary as it sounds):
$$
\frac{dB}{dt} = \underbrace{1000\vphantom{\frac{1}{200}}}_{\textrm{production}} - \underbrace{\frac{1}{200} B}_{\textrm{removal}}
$$
The only tricky part here is recognizing that if the lifetime is 200 s, a fraction 1/200 of the existing molecules will be removed per second.
Now we have to solve this at equilibrium: $dB/dt =0$. We get
$$
\begin{split}
1000 - \frac{B}{200} & = 0 \\
1000 & = \frac{B}{200} \\
B = 200000
\end{split}
$$
Or you could memorize Little's Law: steady state = arrival (1000/s) $\times$ lifetime (200 s).

Concentrations are molecules or moles or grams per liter. From molecule numbers alone you cannot calculate concentrations. You need information of the volume it is related to. E.g Substance A has a concentration of 1 mmol/L solved in water.

I understand your point. My question is actually simply referring to the number of molecule Bs the moment it reaches equilibrium.

Then don't use the naming "concentration". It is just the number of molecules at steady-state, nothing else.


text:
Do squids or octopus suffer from myopia(hyperopia)? Do other vertebrates get myopia(hyperopia)?
Both vertebrates and cephalopods evolved very sophisticated camera-type eyes, and both are capable of focus. But it also pose a risk of inability of focusing, such as myopia in human. So is myopia a common problem of vertebrate eyes or just occurred in a few vertebrate species?
Cephalopods also have the ability of focusing, but they focus in a different way. They focus by changing the distance between lens and retina, instead of contracting the lens like human. So are cephalopod eyes more flexible and less prone to get myopia?


text:
Insect identification, UK, 07-19
Can anyone identify this insect found in the North East of the United Kingdom, July 2019. About 3-4cm long.
Could this be a wood wasp?
Thanks.

If by "wood wasp" you mean order Hymenoptera, family Siricidae, the answer is yes; as for which wood wasp, I'm on the wrong side of the Atlantic to go deeper (though I know the genus Sirex is among your possibilities).

It is definitely a Siricidae and looks like a Urocerus gigas (sometimes called Greater horntail), which is also found in the UK.
In the Nordic countries this is one of the more common species of sawflies, and I suspect the same is true for the UK. The picture below and some info on their biology can be found at species.nbnatlas.org:

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


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Why don't we form immunity to some infections?
I read another question, and its answers, about how vaccines work, but I don't see there, and and don't understand, why some infections can, seemingly, not be immunized against at all. For example, someone who gets the flu (or the flu vaccine) is immunized against that particular strain of flu for life (which was relevant, IIRC, when H1N1 came back a few years ago: many people above a certain age had immunity), whereas one person can get group-Α strep throat over and over again. Why is this?

The answer is sort of hidden behind the very first paragraph of your linked question:

Vaccines work by introducing an attenuated strain of the pathogen (or alternatively the antigens that are normally present on the pathogens surface) into the body, whereupon the body mounts an immune response.

The body mounts an immune response based upon a particular epitope (molecule/protein chain) derived from the infection itself.
If the bacteria/virus/parasite evolves so that the molecules/proteins on its surface change significantly, then the version stored in Memory Cells will no longer apply. There's some wiggle room depending on epitope length and specificity of the Immune Response (highly specific MHC proteins will invoke a very strong, very efficient response - while less specific [usually B-cell or early T-cell responses] will invoke a weaker, less effective response), but because pathogens can mutate so quickly it's not uncommon that you'll encounter a descendant of a virus you already encountered that has dramatically different characteristics.
Some pathogens are also just very "clever" at avoiding the immune system. Sometimes they can produce shells which can't be broken down to derive epitopes from, sometimes they live within host cells and simply hide (the most well known example being HIV), other times they can present the same "I'm part of the body!" MHC proteins that tells the immune system not to attack them, and they can even hide in parts of the body where the immune system rarely visits (eyes, brain, other very specialized tissues).
And at times the pathogen can be both very adaptive and very "clever", as in the case for Staphylococcus aureas - which can inactivate antibodies through surface proteins and has the ability to adapt to new antibodies very quickly.
You can think of it like a game of chess. If you play against the same person all the time you're going to learn their moves, their strategy, and be able to beat them very quickly. If you switch partners, or your regular partner learns new moves, you'll spend some time adapting to the new play style you've encountered before being able to win consistently again. Bacteria and virii are simply very, very good at coming up with new play styles.

MCM's answer is quite correct. There are quite a few specific ways various pathogens escape "immunity" (long term, often not truly life-long, protection).
To quickly restate what he has said:
First the pathogen can mutate to be different enough that your body won't recognize it (ie different strains of flu or HIV), it can hide in cells or immunoprivileged areas of the body, it can actually shut your immune system down, actively combat your immune system, or prevent an immune response from being mounted.
And just a few more thoughts:
There are certain pathogens we are still trying to figure out how they avoid the immune system (the technical quality is immunogenicity).  A good example human respiratory syncytial virus (RSV).  Again this is actually an active field of study for a great many pathogens.  When we test many of these "tricky" pathogens in animal models, we find that they often can gain immunity.
+1 @MCM, I was trying to cram this into a comment, but I didn't think I could.
Some interesting areas to read up on if you are interested in the subject are immune avoidance/evasion and forward genetics.  You will more often hear about reverse genetics, but forward genetic experiments can allow us to see how the "chess game" will be played out by the pathogens in new situations.


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Is lemon water an alkalizing agent in the body?
I was recently having a discussion with someone about whether lemon water actually increases the pH of your body (by which I assume they mean the blood); their claim was that once Citric acid was metabolised it results in an increase in pH due to the "anionic properties of citric acid".
I looked around on the internet at it would seem that this is a common claim circulating around health forums: Example 1, Example 2, etc.
Now to me this sounds like something which cannot possibly be true and appears to be a crazy health fad (they seem to spuriously appear and gain popularity now and again), and I cannot find any scientific papers or articles to support or refute their claim.
Can anyone provide a reliable scientific reference or provide a reasonable scientific explanation (preferably accessible to a layman with only A-level (college level) understanding of chemistry and biochemistry) which either supports or refute the claim that drinking lemon water (citric acid) increases the pH of the blood?
I have crossposted this to Chemistry.SE as well, as it is a crossover between chemistry and biochemistry.

The link in Chemistry.SE is unlinked

The blood pH is tightly controlled since variations are quite dangerous for us. Under normal circumstances the pH is 7.4 (with a normal range between 7.35 and 7.45). Below that we are talking about acidosis, above it about alkalosis. If the blood pH goes about 7.8 or below 6.8, death will occur. This pH is maintained by the Bicarbonate-buffering system, for details see here and here.
Food that we take up does not directly influence the blood pH (and there is also no reason for us to do so, since this is tightly controlled and regulated), so this is a health fad. Details that debunk this myth about it can be found here, here and here.

The website to which you linked states that Lemons have a "moderate to strong alkaline-forming effect"? How is it that something acidic can form this "alkaline-ash"?

Food gets metabolized in the body and molecules get modified in this process. If you think of the stomach, this is highly acidiy, while the duodenum is pretty alkalic. This gets often mixed up...

What about giving lemon jucice in someone already having metabolic alkalosis or acidosis?

Short Answer:
There was an interesting paper that dealt with the pH of urine when citric acid was consumed.
The summary was: There was no increase in urinary pH or total nitrogen in 24 hours collection of urine.
What This Means:
The food we take does not affect the blood pH directly. Acidic food will cause increased secretion of alkaline components into the digestive tract to neutralize the excess acid. This will cause a fall in the bicarbonate ions concentration (this being the major alkaline buffer) in the blood. This might cause acidosis (depending on how acidic the food is).
The body compensates the decrease in bicarbonate concentration by excreting H+ ions in the urine. Thus urine becomes more acidic when there is a relative state of metabolic acidity in the body. There is also hyperventilation and excretion of more CO2 as this will cause excretion of H+ ions.

HCO3- + H+ ----> H2O + CO2

Incase of alkaline foods, the stomach acid itself would be partly neutralized by the alkali present in food. Thus the body need spend only minimal bicarbonate ions to neutralize the remaining acid.
If there is severe alkalosis body compensates by decreasing the respiratory drive (conserving more H+ ions) and excreting more bicarbonate ions through kidneys.
Compare this with the data obtained from experiment
If consuming citric acid would lower blood pH levels then the urinary pH should increase. As the data shows this is not so, that would mean the citric acid does not contribute to the acidity of food in any significant way even when consumed in large quantities.

The paper no where mentions Urinary pH, and deals with excess Citric acid consumption. I dont think your answer is valid

The administration of the material to the other subjects caused slight variations in the citric acid excretion, in general paralleling changes in the urinary pH.
Kindly read through before commenting

Ingestion of citric acid in addition to a constant diet did not affect the pH or the total nitrogen of the 24 hour urine collection.  Last line of summary

Before summary they do mention, there was a dip in urinary pH, but nowhere they quantify it or tell how did they measure.

The excellent answers from Chris and One Face have already written about why the claim is wrong, so I'm going to add a hypothesis for how this sort of nonsense could even originate in the first place.
The reason why lemons are acidic is because they contain a lot of citric acid, so in a solution part of this citric acid ionizes to citrate which increases the concentration of H3O+, thus increasing pH. Now imagine some quackjob with poor knowledge of chemistry reading about this, and only picking up the word "citrate".
Citrate is of course a weak base (since 3rd pka of citric acid is 6.40 then pkb of citrate must be 7.60) so if we pour some kind of citrate salt into water we would get a basic solution.
So basically, I think that the originators of this fad forgot about or didn't know about the H3O+ ions, which of course do not magically disappear when we ingest lemon juice.

Also, note that there are a lot of quack treatments that center around supposedly being able to alter the pH of your blood.  I think that quackery is why anyone would be interested in altering one's PH deliberately.

"The reason why lemons are acidic is because they contain a lot of citric acid, so in a solution part of this citric acid ionizes to citrate which increases the concentration of H3O+, thus increasing pH. " - You mean lowering pH?


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Longevity and extent of transfection after SARS-COV-2 vaccination with Janssen
The Johnson vaccine, unlike the RNA vaccines from Pfizer & Moderna, uses a vector containing DNA encoding for the SARS-COV-2 spike protein. This vector DNA needs to enter the cell, allowing for transcription and translation into viral spike proteins to occur (Fig. 1). These spike proteins are then exposed on the cell surface by the host cells, thereby exposing the antigenic epitopes, creating the immune response.
Basically, this turns the immune cells against their own host, because they are expressing foreign proteins on the cell surface. In effect, I presume, those host cells are subsequently destroyed by the immune system.
Now I was wondering if there has been any research done revealing the consequences of this auto-immune response. In particular how long does it take to get rid of all the transfected cells (or 'vaccinated cells' as they tend to be called) and what is the extent (volume/area affected) of transfected cells? Basically you are genetically altering the host's cells  that are subsequently attacked by the immune system. So I am basically interested in the pharmacokinetics of the vaccine I guess.
This safety report from EMA says that in 1 animal (from how many?) there was still genetic material after 180 days to be detected. However, the report says nothing about the extent of transfected cells nor anything about the auto-immune damage after the host attacks its own cells. No references are to be found either; it all seems to be about internal safety studies.
In retrospect I'd rather not have had the Janssen vaccine; I bet mRNA vaccines are a lot more instable, guaranteeing safe removal of the foreign genetic material.
Anyway, I'm drifting... In short, (1) how long does it take to clear all signs of foreign DNA from the host after Janssen, and (2) what is the extent of the cells that are transfected and subsequently attacked and damaged/killed by the host?

Fig. 1. Schematic depiction of the DNA vaccine from Janssen. source: Livingstone et al. (2021)
References
- European medicines agency, Assessment report COVID-19 Vaccine Janssen
- Livingstone et al., JAMA (2021); 325(15): 1575

In your last sentence, I'm not sure that I'd use the word transformed to talk about the cells, as that implies integration of the vaccine DNA into the host cell's chromosome(s), something that is definitely not supposed to happen.

@MattDMo good point, I meant to say transfected; edited!

Both the AstraZeneca (AZ) and Janssen (J) vaccines against SARS-CoV-2 work by using what is known as a viral vector to generate an immune response. In both cases these vaccines use an Adenovirus as the vector (vector in this case means "carrier").
Adenoviruses are a family of double-stranded DNA viruses, most commonly known for being one of the causes of the illness known as the "common cold". There are about 88 human serotypes (how people's bodies react to the virus, different serotypes may not cross-protect by raising an immune response)  of the virus divided over the seven species: Adenoviruses A-G. Overall there are about 50 species from a wide range of animals. Because of the diversity and the abundance of the "common cold" most people will have some immune response to at least some of the human adenoviruses.
Adenoviruses are good vectors for vaccines and for other therapeutic uses such as oncolytic viral therapy because the genomes are easily modified and can be made replication incompetent very easily. To do this essential replication genes are removed and the viruses are replicated in cells that provide the essential proteins for the virus to complete its life cycle, so that you get a viral particle that no longer contains the full genome. These viruses are also tolerant of additions to the genome so they can be used to produce proteins that are not normally found in an adenovirus.
On the other hand the adenovirus component of these vectors can cause its own immune response, lowering effectiveness of the immune response to subsequent vaccines developed using the same or a similar sero-type virus.
The AZ vaccine is based on a chimpanzee adenovirus. The J vaccine on the other hand is based off serotype 26 (Ad26) of the human adenoviruses. In both cases the adenovirus is rendered replication incompetent by removal of essential replication genes.
For adenoviruses to work as vaccines they need to invade a cell and then insert their DNA into the nucleus (as seen in the diagram from OP), where cellular mechanisms produce lots of mRNA copies of the gene(s) and concomitantly produce proteins from these mRNA. These proteins are then translocated to the surface of the cell (this is a natural process).
However, in the process the viral DNAs and proteins are recognized by the cell as non self and trigger the innate immune system causing antigen presentation and activation of the adaptive immune system. This whole process is a natural response of the body to infection and does not result in "self recognition", so there is no auto-immune response to the cellular proteins.
Both the AZ vaccine and the J vaccine are administered intra-muscularly, which is very typical for vaccines. Intra-muscular injection is a good site for injection because it can tolerate a big volume and has a relatively high blood flow (both compared to sub-cutaneous (sub-skin)). However, once injected the virus doesn't necessarily stay in the muscle, it can travel in the blood and a portion will end up in other locations, particularly the liver and alveoli of the lung (places where there is a big blood supply and lots of small blood vessels). The adenovirus can infect any cell that expresses the cellular receptor called Coxsackievirus and Adenovirus Receptor (CAR) on its surface, which includes immune cells. There's a fairly comprehensive review of all the mechanisms and cell types here, but it is in written for the scientist. Here's a suitable quote about cell types:

The cell types present when vaccine is administered i.m. include myocytes, skeletal muscle cells, fibroblasts and endothelial cells, with APCs such as DCs or macrophages representing a minority when compared with the abundance of murine skeletal muscle cells

How long the viral genome persists depends on the paper, but not many people have looked. The data I could find seem to indicate that most protein expression is lost after about 3 weeks, but it may persist longer. e.g.:

Although Ag expression could no longer be detected 3 wk after immunization, examination of Ag presentation within the draining lymph nodes demonstrated that APCs were loaded with Ag peptide for at least 40 days postimmunization, suggesting that Ag remains available to the system for a prolonged period, although the exact source of this Ag remains to be determined.

However, the genomes seem to persist for a very long time, perhaps as much as a year or more:

By days 30 and 90, vector sequences remained detectable in most animals in these tissues but gradually declined 102 to 103-fold. After 1 year, relative copy numbers in liver and the injected muscles were comparable with those seen on day 90, whereas a further decline was seen in spleens.

Note that both of the quotes above are not about either the Janssen or AZ vaccines, but about adenovirus vaccines in general, and several Ad vectors were tested in both. It is highly likely that the AZ and J vaccines will have similar data.
Edited to add: I don't know why the DNA persists for so long, but it does not integrate into our genome. It seems that most replication deficient adenoviruses lack the E1A gene, which allows induction of the cell cycle and frees up resources for viral replication. However, the genes involved in viral DNA replication are E2A and E2B, so are not included in the deletion.
TLDR: Viral genome can persist for a very long time, but protein expression does not - possibly because the immune system deals with it quickly after a few weeks (effective vaccination...). The vectors can reach and infect many tissues in the body, particularly ones with high blood flow and lots of small blood vessels such as lungs and liver.

Wow +1 I'll have a thorough read through all this material! Sweet.

There's also a concern regarding Sputnik (which also uses adenovirus vector) where in some combination, the gene which was removed to stop replication can get regenerated in host & cause adenovirus to replicate (something vaccines are usually designed to not do).

@RedBaron, yes. This is actually a feature of all adenovirus vaccines, not just Sputnik, and why "good" ones are generated in adenoviruses from other species, which are very unlikely to have a human infection. The function is called complementation - cells expressing the missing protein(s), and actually has to happen in the cells that they use to grow up the vaccine. However occasionally the virus reacquires the missing genetic component and becomes replication competent again, but this is tested for in manufacture.


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In Darwinian evolutionary theory, does the environment has any role?
In Darwinian evolutionary theory, does the environment has any role?
To state it clearly:
Suppose I have an isolated system. First, I place several types of entities (organisms) in an environment. According to Darwin, eventually, the fittest will survive.
Next time, I place Only one organism. Will it survive this time as there's no one else in the system?
If not, did Darwin also consider the whole environment as another entity, so that in the above case, there are two entities, the organism and the environment. The environment is more evolved and it survives, other dies?
Moreover, if the climate is favourable and the organism reproduces sexually results in the same fate as the case if climate is unfavourable, organism reproduces asexually, what conclusion does it leads to?

For a great introduction to modern evolutionary theory, check out Understanding Evolution from the University of California, Berkeley. Darwin (and Wallace) may have originated the first coherent theories of evolution, but things have changed a lot since then. The environment absolutely has a role in evolution, otherwise there would be no stimulus to evolve. Additionally, there's no such thing as a truly isolated system - predators need prey, all depend on plants and/or other organisms that depend on the sun, etc. etc.

I don't think you understand Darwin's argument very well.  Organisms never evolve.   If you place one organism, there's nothing to evolve, so your question is meaningless.  Populations evolve. If the organism produces a population (i.e. through its progeny) then there is room for evolution on the population.

Those best adapted to their environment will reproduce. Fitness is a value judgement. Take a human with sickle cell anemia and place them in the Himalayas and they will suffer terribly and likely die before they can reproduce. Place the same person in a jungle type environment, and maybe they are better adapted to survive until they reproduce as they are resistant to malaria, where as a Sherpa might quickly fall ill in the jungle and die from trypanosomiasis before reproducing. Both organisms are "fit" just in different ways that the environment places pressures on.

Fitness has no meaning without the environment. There is no absolute fitness. Fitness is always with respect to a given environment.

"According to Darwin, eventually, the fittest will survive"
Darwin never said this. Fitness and survival are two separate concepts.
In a simplistic version, fitness is measured by reproductive output. Survival is, well, survival. You can have higher output than your brother, but have a lower chance survival. In fact, the very act of producing offspring can negatively affect your ability to survive.
No, the environment is not an other organism, in any context. It is the place (stage, arena, etc) in which the measure of fitness (reproductive output) can be measured. The environment can directly influence and affect fitness, and other organisms (inter and intraspecific) ARE part of that environment.
A single isolated organism does not evolve, but can have offspring. However, you need a more than one organism for fitness to have any meaning in a Darwinian model.

It would have to be a bacterium or "simple" eukaryote that either replicates asexually or through self fertilization in order to have offspring if they are isolated. Mammals, reptiles etc. need certain levels of organisms in a population to allow for successful enough reproduction to maintain the species above extinction.

Yes, but it makes do difference to the central concept of fitness vs survival. I did not qualify the organism in isolation.

Prokaryotes and viruses (even prions) can have fitness. Anything that replicates with information persistence can have Darwinian fitness.

-1: I don't think your answer is particularly clear or well constructed, has no references or supporting material, and generally does a poor job of answering the question.

Fitness is a function of both reproductive success and survival. The answer is wrong.

Sorry, Remi.b, but your understanding of fitness is elementary school, at best. Fitness has never meant survival. Without offspring, your fitness is zero. Period.


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If we add only 1 primer in PCR
What would happen if we add only one primer, say forward primer, to PCR?
(Image Credits: Wikipedia) As it is clear from the image that we need both forward and reverse primers to get it working (Unless we have a sequence such that a single primer can work as both forward and reverse). I have read online here that including a single primer will result in linear amplification but I think there should be no amplification at all. Can you help me resolve my doubt?

Welcome to Biology Stack Exchange. However you need to do a little more research before asking questions like this one. Guesses are not enough. There are many resources on the web which describe PCR, and if you read them carefully — especially the diagrams — it will be obvious why two primers are needed. This is fundamental. Look at the diagram here, for example.

Hi @David! I have researched online before asking the question and also looked at the link you sent. My apologies as I didn't make it clear. I will edit the question to make it clear.

PCR with a single primer is similar to DNA sequencing, except you don't have labeled terminal monomers to stop the reaction.

I'm not sure why it has been put on hold as off-topic. It is not a question I'm getting grades for. I am not a student anymore. I study biology because of my interest. I was wondering what would happen if there is only one primer and I think theoretically there should be no amplification. I find contradictory views online and just wanted to know if I'm missing something.

I think the following should happen:
There would be no amplification but we will get n copies of single stranded DNA after n cycles and the only double stranded DNA with started with but with a new complementary strand.

Using 1 primer will results in amplifying the original sequence in each cycle in a linear fashion: the primer will guide a single run of the polymerase. In opposed to the "chain reaction" in PCR which is exponential. Therefore, with one primer you linear amplification of say x40 times the original number of molecules you started with, whie with two primers you get exponential (~240) amplification. You right that with one primer, the amplification is neglectable, almost invisible.

I don't think there would be no amplification at all. What will be present after 40 cycles are 40 single stranded DNAs and only one DNA of interest. Can you explain how would there be 40 more molecules?


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Is there a genetic reason explaining the difference of the height of male and female?
The male and female height difference seems to be around 1.08 if all cultures are counted from these stats: https://en.wikipedia.org/wiki/Human_height
Can this ratio, 27/25, be explained by genetics and is there any research to explain how genes affect the growth of a man and woman? I assume there are a lot of factors that affect height and it might be very difficult to say if environmental and selective reasons or genetics are behind this factor.
ADDED:
GIANT study reveals a giant number of genes linked to height (October 6th, 2014)

“Height is almost completely determined by genetics, but our earlier studies were only able to explain about 10 percent of this genetic influence.”

https://www.broadinstitute.org/news/6119

The fact that only about 10% of the genetic influence can be accounted for suggests that height is definitely not completely determined by genetics.

Please note that the study, which you cite above,  studies growth variability across human populations. It does not (or at least not explicitly) state whether males tend to be taller because of some Y-chromosome specific genes (or possibly something else; - to expand your very intriguing initial question: e.g: silencing of certain growth genes in XX / female or XY / male ?- or non-genetic property of Y or Barr-bodies (silenced X)? -or specific social factors in nurturing? - ....)

@tsttst: The wood, the trees and the vision ... I forgot the genetic mechanism in my answer, but now added that to my discussion. Thanks for pointing that out!

One could say that the absence/presence of the Y chromosome is the major genetic difference, because males and females share all the genes on the 22 autosomes and the X chromosome.  Females enter puberty later, and their epiphyseal growth plates fuse, or close, earlier https://en.m.wikipedia.org/wiki/Epiphyseal_plate. Bones cannot grow longer after this happens.  Males do not enter puberty until later, and so their bones have more time to grow before the plates close. The Y chromosome regulates testosterone synthesis, and that increases growth hormone levels in males, as well.

@kmm the 10% figure is how well that study predicts. It says nothing about how heritable the trait is, which is determined via other methods. Imaging if you predicted height based on a GWAS with only 50 people; you'd explain 0% of the variance but that does not mean height is 0% genetic. In fact, genetic predictors of height now explain 82% of variation in height (by some estimates, this is near 100% of the genetic influence).

Short answer:
There is strong evidence that height is a heritable trait with a strong genetic component. The genetic mechanism could be higher expression of an X-chromosome gene that, expressed in high levels, inhibits cartilage development, perhaps causing lower height. The increased expression seems to be caused by incomplete X inactivation in females. Furthermore, there is differential selection for height between human males and females likely causing the differences we see in modern human populations.

Long Answer:
Genetic basis of height
The genetic variants analysed by Wood et al. (2014) account for ~29% of the phenotypic variance and 60% of the heritability of height.
Due to this high heritabilty (and the fact that there are still expected to be more unknown variants affecting height) there most likely is a genetic reason explaining the difference of height in human males and females. Thinking about the nature of this difference is a bit difficult. It is good to know that the trait has a high heritability and therefore a strong genetic component as this allows us to have a look at how natural selection affects height.

Selection on height
Height is a polygenic trait that is under recent and strong natural selection (Field et al., 2016 - preprint) leading to height increase in both human males and females (Fig. 3D in Field et al. (2016)):

What does this tell us in terms of the genetics underlying the height differences in human males and females? First, we have to understand that natural selection (at least mainly) affects individuals, not species. Then, we can understand that natural selection can affect males and females of a species differently. And Field et al. (2016) have shown exactly that for height. In their analyses, you can see that male and female height show (mildly) differing signals of natural selection (Fig. 4C in Field et al. (2016)):

But selection needs heritable genetic variation that allows this differentiation between the sexes. So what is the mechanism?

Genetic mechanism of height differences between human males and females
As pointed out by @tsttst in the comment differences between sexes are usually caused by genes on the X and Y allosomes. There is evidence that the height differences between human males and females are related to the X-chromosome (which also explains some of the missing heritability of the GWAS study by Wood et al. (2014)), reported by Tukiainen et al. (2014). They write

In one of these three associated regions, the region near ITM2A, we observed that there is a sex difference in the genetic effects on height in a manner consistent with a lack of dosage compensation in this locus. Further supporting this observation, ITM2A has been shown to be among those chrX genes where the X chromosome inactivation is incomplete.

They also give a molecular mechanism how this hypothesised increased expression of ITM2A can cause the height difference. They report that the ITM2A gene is
involved in cartilage development (van den Plas et al., 2004) and that the height-associated ITM2A variants change expression of the ITM2A protein. This is interesting as increased ITM2A expression in mesenchymal stem cells of adipose tissue seems to inhibit cartilage development (Boeuf et al., 2009). Tukiainen et al. (2014) conclude:

As the allele associated with shorter stature associated with increased expression of ITM2A (sic), this suggests the allelic effect to height could be mediated through the capacity to generate cartilage and bone.

Finally, how can this be interpreted from an evolutionary point of view?

Evolutionary interpretation of height differences in human males and females
Differences in height (but also other traits) between sexes of a species are refered to as sexual dimorphisms. Sexual dimorphism (at least in primates) in height is strongly related to differences in mating behaviour and a sign of aggression and/or dominance-based mating patterns (Wynn and Coolidge (2011, p.82), sorry for that poor referenc link). The counterpart to this is pair-bonding, or in human terms marriage: a primate example is our pretty close relative, the Gibbon, that is (at least socially) monogamous and as expected does not have a height-related sexual dimorphism. Great apes including humans do have this polymorphism even though pair-bonding in humans is widely spread. Therefore, it was not surprising to find a reduction in height dimorphism from Australopithecus over Homo erectus to Homo sapiens (Wynn and Coolidge, 2011, p. 83, see also this, especially the last paragraph of this chapter).

Update on the main source
One of the papers I mainly used for this answer - to illustrate selection on height - was a preprint. It is now published in Science: Field et al. (2016).


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What is this tiny insect?
I took this picture in central Mexico. The insect is about 1mm in size. I found lots of these dead on a desk, so many that at first I thought they were just dust. I assume they came from a plant that was above the desk.

Does anyone know what it might be?
EDIT:
I found the culprit walking nearby! I guess that verifies what others pointed out: It seems to be the molted cuticle of an aphid. (sorry for the poor quality of the pictures)
Thanks a lot!

Since you suggest they come from a plant, they might be dried aphids. These insects usually feed on plant sap, and I already noticed some tiny, white, and apparently dead ones on plants.
As suggested in the comments, these are actually not dead aphids, but only the cuticle they leave after moulting, or ecdysis.

Aphids shed skin, maybe this is simply an abandoned exoskeleton?

Agree with Alex that this is the shell of an aphid.  A quick search for aphid ecdysis returns this picture: http://footage.framepool.com/shotimg/qf/482460604-moulting-ecdysis-afid-varmint-skin.jpg


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How to get started in bioinformatics
I'm a second year bachelor electrical engineering student and self-taught programmer. I've always had a interest for biology, but never got into it (besides two year biology in secondary school and some basic biochemistry in chemistry class).
I'm especially fascinated by the interplay between computer science and biology, both computer science used for biology and computer science concepts inspired by biology. Think of things like the human genome project, genetic algorithms, deep learning, protein structure prediction etc etc. I think many of this things (the computer science used for biology things) are - as far as I know - part of bioinformatics.
I've done challenges on Rosalind and although they are nice, it feels more like training/reinventing the wheel. Althrough it may be too much to ask, I'm want to do something "real" which could actually be used. Not that I want to start straight away without learning, but I don't have a picture in mind of what I can do after learning some theory.
I'm looking for an overview of the field of bioinformatics and some guide on how to get started. Some examples on what I can work on. Maybe there are some power intensive algorithm I can start designing chips (ASICs) for, in order to speed up the process. This just one example.
I hope you can help me, thanks in advance.

Welcome to Bilogy.SE! I am unsure whether you are more interested in Bioinformatics, Computational Biology or Biological Computation. The distinction between these fields is sometimes unclear and may differ depending who you may ask but I think worth it to take some time to read their definitions.

A first step to Bioinformatics or computational biology is probably to understand the basics of molecular biology (Here is a khan academy link that may help)

Thank you. :) To my knowledge bioinformatics and computational biology are really close to each other. Bioinformatics slightly more focusing on (theoretical) computer science, while computational biology focuses slightly more on the mathematics. (Again, this is my idea of it.) For biological computation I see a bigger difference, cause it's the other way around (computers using biology instead of biology using computers). I have some basic knowledge of molecular biology (or biochemistry, I think that's more or less the same). (continue...)

I know for example how you can translate a string of DNA into RNA into aminoacids or identify (some simple) mutations. But (of course) I really don't know how I would predict the 3D structure of a protein. So it's a little bit hard to me to know where I should begin. If I look at how I got into coding, I wanted to build a website so I looked up a tutorial. When I wanted something new, I searched how to do it and learnt it on the way. For bioinformatics it's harder for me. I don't really have a goal in my mind like making that website, if you understand what I mean. (continue...)

And that's because I don't really know what I will be doing with it (bioinformatics knowledge). Anyway, really appreciating your help.

Good that you have these basis. I would recommend to narrow the post down then. For the moment I don't think it is possible to completely address your question as it is too broad. As an example, I am a computational biologist (computational population geneticist to be more accurate; I study various evolutionary processes using individual based simulations and try to develop statistical methods) but I have no idea how to predict the folding of a protein.

If I may ask the question: Why are you in electrical engineering if you are interested about bioinformatics? I don't see much connection. Of course there is no shame (it is quite the opposite actually) to have when working on a subject different from the one your receive through your university training but I am just curious

I'm interested in computers and electronics, that's why I chose it. I feel like electrical engineering really teaches you how they work. Besides that biology (and bioinformatics) have always interested me, so something combining this two should be great.

@Remi.b Also https://www.newscientist.com/article/2082706-bio-coding-language-makes-it-easier-to-hack-living-cells/ shows a nice (and to me really interesting) example.

I am voting to close as too broad. I agree though as @David said that if you can't narrow down your interest, the best for you is probably to contact someone at your own university which research is of interest to you.

I am voting to close because this is opinion based. I know bioinformaticians who started as physicists, biochemists, biologists, computational scientists, mathematicians, MDs etc. and they work on wildly different projects. There is no single-track "best" pathway, or correct niche to get into. Apply for some bioinformatics projects/positions/internships and see if you get them. Good luck.

@Remi.b Also, EEE will have a lot of systems engineering modules, and include proper programming modules (most bio courses have at best a single module on R or Perl that barely introduce you to the idea of a variable), and a tonne of maths. This degree would put you in good stead for a tool building project: The biology you can pick up later!

You will find various bioinformatics tutorials on: https://www.biostars.org/t/Tutorials/
As a computational biologist I would however strongly suggest to attend biology lectures, and read many textbooks that cover topics outside of the favorite topics of today's bioinformatics (Bruce Albert's "Molecular Biology of the Cell" would be a good start):
Technical aspects are easy to solve, and learn (and also to outsource). The difficult part is to find smart problems, and to understand how you can solve some things faster than your competitors by combining bioinformatics with other approaches.
BTW: I really like your idea to approach bioinformatics from the hard-ware side (also see evolvable hardware).

Yes I read about evolvable hardware, it sounds so awesome. Unfortunately I have the feeling it isn't much researched any more, for whatever reason. (Maybe all the more reason to get into it.) And thanks for your advice, I'm going to look for that book.

My advice is to make contact with biologists in your own university.
You say you want real problems, and I applaud this as addressing real problems is the best way to avoid wasting your time (which is an all-too-common fate of forays of this kind). How to make contact? Presumably social media is the way to go. At your age you should know how to use it. You need to aim at PhD students and staff, though, not undergraduates.
Reading books is all very well, but until you know what the problem you're takling is you won't know what to focus on. And biology is too wide and unstructured to master by reading.

I would rather recommend contacting a PI directly then using social media. Many PIs are happy to hire a student who shows interest.

@Remi.b — Sure, whatever works. Would an undergraduate know what PI to contact? Anyway, my point is that a young internet savvy student should use that savvy in his own environment to advertise his willingness to get involved in a project. He should know better than me.

Thanks for your answer. Do you think it is better to contact someone from the bioinformatics department of my university, or to directly contact biologists?

@Kevin I'd definitely go to the bioinformatics dept. They presumably have projects with the biologists already, but if you tell them what your skills are they may well have something you can do. At the very least they can aside you.

I am a Computer Engineer myself and never taken Biology in even my high-school. (Maybe people here would start hitting me but I confess I used to hate Biology to bits - maybe bytes or Megabytes)
In autumn, 2013/14, it was the same Pavel Pavenzer and Philip Compeau of Rosalind, who introduced me to Bioinformatics (I enrolled into that course totally by chance) and Bioinformatics sounded pretty cool. Firstly, since programming was pretty cool as all I had to do was apply string algorithms and later on I was fascinated by beautiful design of Genome by Almighty Allah.
Well here is summary of my experience to share with you:

Buy a good book on Genomics (PS. Verma and V.K. Agarwal is pretty good one - I have found it good enough)
Master yourself in the basic Bioinformatics algorithms (ones you will find on Rosalind)
Check sites like TCGA, ICGC for Gene Expression data. Its in numeric form and you will enjoy applying statistical algos like PCA, Regression etc on them
If you are interested in sequence data classification, then I would suggest you to read String Kernels by C.S. Leslie et al. (I can provide you its implementation using SVM on C++ if you would like)
Most of Bioinformatics courses teach you Sequence-Alignment algorithms or HMMs. They will waste your time. Don't take them too seriously. You will find the reason to reject HMMs in the String Kernel paper (HMMs use Heuristic approach and are very slow and inefficient as compared to SVMs)
There is lot of work yet to be done on Epigenetic data. With little effort, you can contribute to community by publishing your research. I would recommend you to check that aspect as well. But again, take one thing at a time and you are going to start from Nature Scitable (use only this website for first couple of weeks - keep your mind clear and take one task at a time. I have wasted my time by being greedy for learning too much until I came to Nature Scitable and man! It was exactly what I was looking for.)

While bioinformatics presently is a bit heavy on fairly standardized problems involving sequences, you might also consider topics such as computer vision (and to some degree control theory), which are presently seen in many leading computational biology publications.

Aside from what was suggested in other answers, you should also try to get to know the state-of-the-art in bioinformatics, i.e. read up on what was done in the last few years, have an open eye for new publications in the field and let you inspire by what other people are/have been working on.
This post by Stephen Turner nicely summarises a number of bioinformatics-related journals/RSS feeds, blogs, mailing lists, email alerts/subsriptions and twitter accounts you should assign to or check regularly for staying up-to-date.


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Mammal Statistics about Natural Death Versus Being Killed?
Is there data determining what percentage of mammals die a natural death (disease, old age) and what percentage die due to being killed and/or eaten by other mammals?
In watching wildlife documentaries over the years I'm accustomed to footage of mammals killing each other. So it makes me curious if wildlife mammals are more or less likely to be "murdered" by other mammals than humans are to be murdered by humans.

Incidentally I posted the question here, as there's no SE site for wildlife, and this thread directed me here.

This question is wrong on meta, I move it accordingly.

I think this question is very broad because "mammals" are a very diverse group, and because predators often target the weak and sick: do you count their predation as a natural death or not? "Murder" is also not a concept that should be applied to animals in the natural world because murder is a human social construct.


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Metabolic activity postmortem
I read some papers about studies on metabolism in post-mortem tissues in human, but I do not exactly the reason about why our brain continues to have activity after death.

Welcome to Bio. Could you link those papers? I also think the definition of post mortem is important. Do you have one at hand?

Many definitions of death include brain death which is often defined as cessation of electrical activity in the brain (i.e. no metabolic activity).

Your question is a little vague and as Christiaan mentioned, linking to the papers would be useful. If I understand, though, you want to know why cellular metabolic activity that takes places after someone dies?
If that's the case, the answer is essentially that whatever kills a complex organism in the sense of causing the heart to cease beating, doesn't immediately cause every cell in the body to stop functioning at the same moment.
Now for a slightly longer answer...Consider someone who suffers a heart attack and dies. Blood stops flowing through their veins and cessation of breathing means gas exchange stops. For cells with extremely sensitive oxygen and nutrient demands like cardiac cells, cell death begins to occur rapidly. Other cells farther down the blood and oxygen supply chain have a greater tolerance to disruptions in nutrient supply and would have at least some store of nutrients to work with after blood flow stops. Those cells will keep doing whatever they were doing for a little while; metabolizing nutrients, transporting metabolites, transcribing genes, etc.
After a while, though, even they will feel the lack of oxygen. At that point, most cells will switch over to anaerobic respiration. The eukaryotic fraction of cells in our body isn't particularly good at this, but can struggle on for a little bit until they simply run out of fuel and begin to die, largely through apoptosis.
Apoptosis of some cells will actually help prolong the lives of some of the cells neighboring the apoptotic ones, an effect that probably encouraged the evolution of apoptosis. After a while, though, too much apoptosis will have occurred and an uncontrolled sort death called necrosis will begin, leading to cascades of cell death and cessation of cellular metabolic activity. This process can take days to occur, depending on many variables surrounding the death of the organism.
So far, this has all been about eukaryotic cells; cardiocytes, adipocytes, myocytes, etc. These are the smallest fraction of cells in our body, by cell count. The rest of our bodies are composed of prokaryotic, or bacterial cells. This is our microbiome and this is where (for me) things get really interesting.
Although our microbiome exists in a symbiotic relationship with our eukaryotic cell fraction, many members of the microbiome are less dependent on the nutrients found in our blood system than those eukaryotic cells. The cells of our microbiome are also frequently much more capable of surviving in low-oxygen or even anaerobic environments. These parts of us will continue to thrive for some time after we "die".
Some of our microbial cells, if left to their own devices, could even find new environmental niches outside our bodies and continue to live long after "we" have died. The quotes around 'die' and 'we' become necessary at this point because from here, questions of identity and life branch into the philosophical.
This became a lengthy answer, but I find it a really interesting topic. Here's a nice article from the Guardian, that discusses post-mortem cellular metabolism and our microbiomes in particular: https://www.theguardian.com/science/neurophilosophy/2015/may/05/life-after-death

It all comes down to what death is I guess.

True that. Definitely not a cut-and-dry definition... =P

I edited the tag wiki in an attempt to clear things up a bit. +1 for your efforts

Nice description @Forest (+1), especially how you took the topic from biology to philosophy ;-)

To elaborate on the comments - I think the question hinges on the definition of 'death'.
A brain-dead person is considered clinically dead. However, vital functions such as respiration and blood flow can be maintained artificially and pretty much indefinitely. So under active ventilation, a person in a brain-dead state feels warm to the touch and seems to be breathing normally. Yet, the person is dead (source: WebMD).
So as to your question I dare say that after death, there is no neural activity.
Conversely, when there is still brain activity I do not think the person is declared clinically dead. For example, cardiac and respiratory arrest can be acted upon by resuscitating the person. If the brain of such a person ceases to show activity, then little chance such a person will survive.
Reference
- Goilar & Pawar, Indian J Crit Care Med; 13(1)
PS: I edited the tag wiki to define human death more strictly

I would like to know what happen in the brain exactly

@user22053 - you really have to be more specific than that -


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What is the shortest mRNA the ribosome can read to produce a peptide?
This question came as a comment on a previous question regarding non-ribosomal peptide synthesis, and why Glutathione cannot be synthesized by the ribosome.
In general, Glutathione has a "gamma" peptide bond, thus cannot be synthesized by the ribosome. However, is there an actual minimal length that ribosome can process?
I understand that the mRNA is more then just the codons, however, does it still require a minimum set of condos, e.g., say 18 nucleotides, to produce a peptide?

Haven't read this yet, but it looks promising: http://www.nature.com/nrg/journal/v15/n3/full/nrg3520.html

prokaryotes or eukaryotes?

Reading the paper linked by @canadianer and its references was pretty illuminating. It's a straightforward paper except for its conclusions, and the most convincing part is the evidence of actual translation. There's some evidence that transcription start sites are used as a regulatory mechanism by displacing other things that might otherwise bind. An unknown fraction, but most(90%+), very short bioinformatically detected ORFs are not translated.
Some, however, are. See this table for the experimentally verified translated micropeptides. The shortest is a nearly unbelievable 6 peptides long.


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Stability of RNA including Thymine nucleobase
Does an RNA double strand containing the nucleobase T instead of U has a lower free energy?
Or more precisely: There are tabulated values for the change in free energy of the canonical neighboring base pairs here.
Do you know of any source where values for neighboring base pairs of e.g. GT/CA got compared to GU/CA?

I think you mean bond energies.

If you want you can call "free energy of neighboring base pairs" the bond energy. But I think it is less precise.

I was under the impression that you could only measure free energy changes, not free energy. And presumably bond energies would be equivalent to the free energy changes in breaking a hydrogen bond. But my chemistry is a little rusty, so do point me to sources that measure actual free energies of base pairs of any sort.

Ah no, you are right! It is change in free energy. I adapt my question.

I think my problem with bond energy is that the change in free energy is not simply the breakage of hydrogen bonds. It is an interplay between stacking (pi-pi) and hydrogen bonding.

But the stacking would depend on the neighbouring bases. There have been lots of studies in this area, but It’s not my field. Naively I would think a rT-rA bond would have a similar energy to a rU-rA bond. But do many actually occur? I would think most rT bases are in tRNA where the T is generally in a loop and has to be generated by enzymatic modification.

I would also guess rT-rA is similar to rU-rA. I don't know if rT-rA is frequently occurring. But I am not a biologist. I would like to know that more concerning prebiotic evolution.

I don’t know because I wasn’t there, but the current thinking is that thymine arose late. There is no rTTP, only dTTP. I have an answer somewhere about thymine and the RNA World hypothesis, and discuss the biochemistry. As I said, the only place I know rT occurs naturally is as a modified base in tRNA and I don’t think it’s in base-paired stem but I would need to check that.

When you say there is no rTTP you mean there is no rTTP found in current biological systems, right? I mean you can probably make it somehow in a chemistry lab.

You certainly could. But my arguments relate to the evolution of biochemical pathways. I think if you want to take this further you need to tell us what your hypothesis is, or spend some time combing through the literature of synthetic nucleic acid duplexes.

I think my question is clear though.


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Are there ribozymes that cut double strands
the header already says:
Are there any ribozymes known that cut double strands?
A kind of ribozyme equivalent to the Ribonuclease III.
With cut, I mean that the backbone of both strands, forming the double strand, is opened/broken.
Reaction:
one double strand -> two double strands

Please tell us what research you have done to try to answer this question yourself, and what you have found. Also use standard English if you can: “really cut like” doesn’t cut it, and I find it difficult to see how one can cut something that is already broken. It would be more useful if you specified whether you are referring to RNA or DNA. Context would do no harm either.

I tried to clarify the answer according to your suggestion. I do not mind if it is RNA or DNA that becomes cut, that is why I did not mention it.

I think you need to read about ribozymes a little before formulating questions. As they are thought to be relics of an RNA world they are not going to cleave DNA. As dsRNA is not central to modern organisms, even if it had been in early life, it would be unlikely to have survived.

Could you be more specific? And if the answer is obviously "no", then would you be so kind and answer the question and explain why it is not possible? I still do not understand your question regarding specifying if it is DNA or RNA that becomes cut, as e.g. hammerhead ribozymes cleave or ligate both DNA and RNA.

My question is not "did it survive" ;) I would also be happy to know about an artificially created ribozyme that cleaves double strands. But dsDNA is central in Biology. As a ribozyme constitutes the core or the Ribosome, I was conjecturing that there might be a ribozyme at the core of an enzyme able to cut double strands.

Sorry specifying hammerhead ribozymes in this context was wrong. I found this: "A highly conserved ribozyme in the human and in other species is the hammerhead ribozyme. Ribozymes are active in the cleavage or in ligation of RNA and DNA as well as participating in various RNA-processing reactions, such as RNA splicing, the biosynthesis of tRNA and in viral replication.", here

As far as I am aware from scanning recent reviews, most natural ribozymes act in cis, and none act on DNA. Do you have a reference to the contrary?

See the one above and here. Admitting that they report that the activity was less for DNA compared to RNA.

But like mentioned above, I do not mind if you can not find it in Biology. The question is, if it exists at all and if no, if there are reasons why it is not possible to create one.

The first reference you cited was a book chapter on protein synthesis in which there are 28 references to the ribozyme nature of peptidyl transferase. Please make sure you give correct references before wasting people’s time.

For completeness, here is one that states that a hammerhead ribozyme was used to ligate RNA with DNA. Kind of a mixed case.

"unphysiological" Are you kidding me? I did not ask if it exists in cells. It is a general question. There are people that develop self-replicating ligase ribozymes.

I just came across a paper where they found a DNAzyme that cleaves RNA https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1283523/

Ribozyms are generally known to have a potential to introduce strand breaks. However, it's indeed a good question whether those may include double strands!
Unfortunately I don't know the answer as it's generally difficult to prove non-existance, but in this paper, they go as far as to imply that translation needed to evolve due to the lack of helicase activity of ribozymes.
In additional literature for helicase activities (which is generally associated with introduction of double-strand breaks), all ribozymes with helicase activity seem to be attached to proteins to be functional. So maybe it's indeed possible, that there are no ribozymes that cut double-strands.

It is well documented that they make single strand breaks, usually on themselves.

Yes, on themselves on homologius sequences. By the way, I felt the premise of the question was that it's impossible for rybozymes to introduce double-strand breaks.


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How much does an experiment on monkeys cost?
Including legal fees, the paperwork, the housing, the food etc. (provided there is already a lab with biomedical lab equipment and space for the housing) for let's say the final testing phase of a novel drug over a duration of 3-5 months. what are the monthly and per monkey costs (for the questions sake let us say we have 10)? And how would the costs compare to a similiar study on mice?
I'm just curious because I could not find any figures on the internet.
EDIT: Provided I would get the get legal approvement,
EDIT2: and it is based in the US.
EDIT3: in California.

Welcome to biology SE! This particular question has many answers based on the location of your study, Institutional costs, legal costs which differ between countries, Insitutional costs also take into account the fees paid to the technical staff. If you provide your country/location it would help the people here provide a better answer.

As far as my two cents go. I met a PI at a conference who had to get some brain surgeries done on mice and he said that he was looking at approximately 30K $ per monkey. He worked in the US.

I'm voting to close this question as off-topic because its about managing experiments, not science

@KoustavPal per month?

@rg255 could you tell me where such a question would be better situated?

sorry he mentioned it for monkeys. That was the cost he would incur per monkey from housing, feeding until the completion of a single experiment on a single monkey. Nope, now that I remember correctly I think it was more like 5K for the facility and 25K for the surgery

@rg255 don't you think this question would fall within this site as per the on topic guide http://biology.stackexchange.com/help/on-topic. I would consider it to be in the third category, "questions about techniques in a biological or biochemical laboratory"

Questions on interdisciplinary subjects like bioinformatics are also welcome, as long as they focus on the biological part of the subject. - I would say financial management of experiments does not focus on biology

@rg255 playing devil's advocate somewhat, but this isn't interdisciplinary, it's 100% biology. I'd say it falls under "questions about techniques in a biological or biochemical laboratory", which doesn't actually require "focus on the biological part of the study" (the way the on-topic page is worded). Personally, I also think it's an interesting and useful question, and I can't think of another SE that would be able to cover it better.

@rg255 but you should also consider the fact that only an Investigator or a scientist who has written a grant for experimenting on monkeys can provide a reasonable answer to this.

I would not consider this off-topic but  the cost of the experiment will very much depend on the kind of experiment, the country of residence (local laws and taxes) and the kind of monkey as well. Therefore the question is broad. @daveid you should talk to someone near you for better understanding. BTW, check this out.

Also there's no attempt to work out the costs for themselves (lack of effort so "homework") and is very broad - the cost will vary greatly with the type of experiment

@rg255 I would say this is specific enough - I know some scientists who do animal experiments (not on primates and not in the US, otherwise I could attempt an answer) and generally all you need for a grant application costing is the number (and type) of animals, the experiment duration and the containment level (if the work requires it). And to be honest this is an area where there is so little public information it would be difficult for the OP to get any information themselves.

I contacted http://www.understandinganimalresearch.org.uk/ and they've offered to send me some information about this next week.

@arboviral +1 above and beyond!

I attended a seminar yesterday by Prof. Martin Hofmann-Apitius which described literature/data mining to generate the knowledge of a subsystem (+ bel) correlated against the funding invested into that subsystem. You can use this to find which parts of a system are over-funded (and exhaustive) or underfunded and incomplete, and this can potentially guide you to a more efficient answer. Although I see the point of this question, a much more apt question is "How much does a result cost when studying disease/system X?" I now see those questions will be much more answerable in a few years time!


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How to dialyze large amounts of precipitated enzyme solution (ammonium sulfate)?
I am no biochemist, but I want to purify some liters of solution through dialysis. What I know are those dialysis tubes in glas vessels on stir plates for labs. But how is this done in industry for bigger quantities in an affordable way?
Background: The solution contains a precipitated enzyme (183 kDa) with ammonium sulfate (132 Da). I want to take away the ammonium sulfate to get back the active state of the enzyme.

Ammonium Sulfate (AS) precipitation is used to concentrate protein. After AS precipitation, you would centrifuge the sample to pellet the protein and then resuspend it in a small volume of water or buffer. You can then dialyze this small volume.
There are other methods of concentrating large volumes of protein, including chromatography and ultrafiltration.