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Effect of sex-ratio on the effective population size
As stated on this wikipedia article, the effective population size $N_e$ when the sex ratio differs from $\frac{1}{2}$ is
$$N_e = \frac{4N_mN_f}{N_m+N_f}$$
I understand the biased sex-ratio decreases the effective population size and the formula is quite simple. However, I would fail to prove that this formula is right.
Can you demonstrate to me that $N_e = \frac{4N_mN_f}{N_m+N_f}$ is true?

The reason that an unequal sex ratio affects the effective population size is because offspring are produced by one male and one female parent, and an unequal sex ratio increases the rate at which genetic drift will occur.

"...the smaller number of males still contributes half of the genes in the next generation..."

In other words, assuming the male population is smaller, the genes passed on by the males/fathers are sampled from a smaller population than that of females/mothers. As you know, smaller populations are more prone drift.
Imagine the classic drift example with a bag of blue and red marbles, but have the parental generation with an unequal number of marbles in either bag.
Hartl & Clark illustrate (see figure 4 here) the relationship between sex-ratio and effective population size, where a sex ratio of 1:9 gives an effective population size of around 36% the actual size (given by $100 \times (N_e/N)$). This means that the rate of inbreeding and drift in the focal population is equivalent to that of an idealised population which is 0.36 times the census size of the focal population.
$$N_e = \frac{4N_mN_f}{N_m+N_f} = \frac{4 \times 1 \times 9}{1 + 9} = 3.6$$
The population is diploid and dioecious; each parent carries two genes, and each parent must be replaced within the population so each pair must produce two offspring. Consider the case where $N_m = N_f = 1$ (and thus $N = N_e = 2$). The number of genes in this population is four. Therefore, to maintain the same population size, four genes must be drawn from the ancestral population.

Further reading:

Hartl & Clark (Page 123-124, Random Genetic Drift: Unequal Sex Ratio)
Conner & Hartl (Page 62, Chapter 3)

While (personally) I can't prove this mathematically, I can demonstrate it using simulation. I've written up a simulator of genetic drift in R, which can cope with unequal sex ratios.
The first four graphs are populations with $N_E = 360$ at various sex ratios ($N_M / N_F$ = 0.11, 0.33, 0.67, 1.00), for 100 replicate populations simulated over 80 generations, with an initial allele frequency of 0.2. The four simulations have different census population size, but equal effective population size, because of the sex ratio. The four groups of populations behave similarly (rates of drift are similar for the simulated populations under the various conditions).

These four use larger populations ($N \times 15$), at the same sex ratios, where $N_E = 5400$ in all cases simulated over 400 generations. Again the groups of simulations behave similarly.

Update:
I've added histograms to ease viewing of the pattern, using $P = 0.5$, for 1000 populations simulated over 25 generations, where $N_E = 360$ and census population size/sex ratio varies between simulations. This distributions are similar despite the different census population sizes.

Thank you for your answer. As stated in the post I understand the biased sex-ratio decreases the effective population size. I fail to prove that $N_e = \frac{4N_mN_f}{N_m+N_f}$ is true (while $N_e = \frac{\left(N_mN_f\right)^2}{4(N_m+N_f)}$ is wrong for example)

Hum... no it does not quite help. I am looking for a mathematical proof that $N_e=\frac{4N_fN_m}{N_f+N_m}$. In other words, I am looking for a mathematical proof that the rate of loss of heterozygosity of a population with $N_m$ males and $N_f$ females is the same as a Wright-Fisher population with $N=\frac{4N_fN_m}{N_f+N_m}$ (by the definition of the effected population size $N_e$).

@Remi.b made some edits, still I don't prove mathematically though

Wow. You definitely deserves a +1 for a al of that. Thanks

thanks - I've updated the scripts (available in the linked page) to give sex ratio rather than $N_M$ and $N_F$ and it shows it with fewer replicate populations which is a bit nicer to look at - I did 100 reps here to show the general trend (i.e. how the trajectories spread out over time) but that's quite ugly to look at


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what are examples of experimental designs on exposing materal for degradation
if one wanted to compare how sources of DNA would degradate in various conditions(environmental) how would they do this in an experimental fashion but also be best comparable to real world examples of Enviromental conditions? Sorry if this question is worded poorly, any suggestions would be appricated.
For example, if I were to expose my own blood to various conditions such as a wet enviroment versus a dry ennviroment, how would I best replicate these enviroments in real life(ie: bloodly water in a cup versus dried blood on a floor) without introducing confounding varables?
I would need some type of "standard" yes? And if so, then would using sterile controled conditions be appropriate, or should I literally be using these real world situations for "better" results?
I tired finding papers, but I guess my research methods are too poor to get anything useful.
EDIT:
My facilities I have access to are a small academic institution, I know basic autoclave use and have access to gel rigs and pcr machines. My samples do not have to be blood, it could be any human tissue or sample, like hair or spit. I suppose I would use the same sample, but kept in a sterile condition for a controo, maybe a petri dish?
I guess my mental protocol would be to try different degradation conditions and extractions, but starting with a boiling DNA extraction to see how effective a certain condition was compared to a control.
I could set up a time table of like 2 weeks to perform the experiment, and every 3 days or so, extract DNA from the control and the sample to then pcr with some human primers(I think we are using the fbi's CODIS primers that they use in foriensics, but only a subset due to cost) and then run an agarose gel to determine degradation( poorer resolution meaning more degradation I suppose?).
Another wuestion that popped to mind, for my time table and my DNA extractions, would I have to perform the pcr and subsequent gel elecrrophorsis as soon as I am done with my extraction, or could I store the extraction samples until I am ready to run a large batch of pcr tubes and a large gel? Would they degrade in a -80°C freezer?

You are going to need to add more details to your question. What kind of facilities to you have access to? If you are doing this in an academic or commercial lab, there are likely protocols for handling human tissue that needs to be followed. Human blood is a biohazard and there are likely strict rules in place as to what you can and cannot do. Also, what is your plan for processing and examining the DNA after your experimental time. PCR amplification, sequencing? What are your controls? Until you give these details, then it is hard to say.

@AMR.            I added more details, thanks for the suggestions. This is an academic lab, I have access to autoclave, pcr, gel rigs etc..(we are not rich, state school). I was using blood as an example, there are other tissues I can use, although I can get authorization for blood if needed. Controls would be a sample of tissue or product that is kept in sterile conditions, like a perri dish maybe? Or would that be a bad idea. A lot more detail is in my post above.

Since you mention examples, a colleague did a project on DNA degradation using cotton swabs with saliva (definitely not as hazardous as blood!). What I don't know for sure is if she used normal PCR, but I do know she didn't have access to qPCR (and she was really good at agarose gels!). My bands were never perfectly regular, though, and I was just testing for presence or absence.

Have you heard of qPCR? This method quantifies the amount of DNA in the sample. Another quantitative PCR method you might look into is taqman PCR. Traditional PCR + agarose gel electrophoresis is not going to give you a quantitative measurement of the DNA in your sample.
Here are the wikis on taqman and qPCR.
taqman https://en.wikipedia.org/wiki/TaqMan
qPCR https://en.wikipedia.org/wiki/Real-time_polymerase_chain_reaction
Also, if you have the choice between intercalating agents and fluorescent probes, go with fluorescence. Intercalating agents are hazardous.
Hope that helps.
Edit Adapted from comments -
We don't have access to a real time pcr intrusment sadly. All we have is a traditional pcr machine. Can I get your opinion on this quote I found on the quantitative messures of traditional pcr: '"No, though comparing the intensity of the amplified band on a gel to standards of a known concentration can give you 'semi-quantitative' results." From thermofisher.com/us/en/home/life-science/pcr/real-time-pcr/…. Are there ways to work with the intensity of the bands I get to be " more reliable"? – Ro Siv
Yes, quantification from traditional PCR can be done, though the accuracy is questionable. One method I have heard of uses a computer to analyze the intensity of the bands. You could probably pull this off with some Python code (check out the scikit-image python library). The other option is to do what you said, compare to known concentrations.
If you are familiar with HA titers in virology, you might be able to contrive a similar method, in which you carry out 10-fold dilutions of the sample until there is no more detectable DNA left. The point at which there is no DNA left is called the experimental end-point, and the titer of the original sample is simply the inverse of the dilution factor at the end-point. Check out hemagglutination(HA) in the context of virology. I think a method similar to this would be better than simply eyeballing the intensity of bands, because you will have some quantitative evidence.
If you want to eye-ball, you should use control bands at several different concentrations, so that you can say, 'the intensity of the band falls between control bands A and B, and so the concentratin of the sample is between concentrations A and B'
I bet you could pull off the serial dilutions. It will be good practice, too. To make a 10 fold dilution, just add 1ml of sample to 9ml of saline. Then, from that new solution you just made, do it all again. Take 1ml and add to 9ml saline. Repeat. Each time you decrease the concentration by 10^-1. You can scale it down too - 1ul sample to 9ul of saline. Repeat. Here is a SOP on HA. Honestly, I would go with the serial dilution thing. I bet ur professor would help you out with this. It is cheap, easy, and widely used. cfsph.iastate.edu/HPAI/resources/SOPs/HA_HI.pdf
Question: If I were to do both methods, then would ImageJ be a possible substitute for scikit-image? rsb.info.nih.gov/ij I think its GUI interface is alot more workable for me.
Response: From just skimming that link it looks like it might. You would probably be interested in the density analysis part of the software, but I dont think a computer is necessary, and ya you will have to produce that gradient of concentrations any way. If it were me, I'd first try to do the experiment without computer analysis. Produce the gradient of control DNA concentrations, compare your sample to the control gradient and see where your sample falls.
Then repeat the experiment while varying the independent variable, lets say its time. So take a sample at 5 min 10 min 15 min etc. and produce a plot of surviving DNA concentration vs time. It will probably end up looking something like a sigmoid curve. If you decide you need more precision in your measurement of the DNA concentration, then consider using the image software, but I doubt you will need it, though I admit it would be twice as badass.

We don't have access to a real time pcr intrusment sadly.  All we have is a traditional pcr machine. Can I get your opinion on this quote I found on the quantitative messures of traditional pcr: '"No, though comparing the intensity of the amplified band on a gel to standards of a known concentration can give you 'semi-quantitative' results." From https://www.thermofisher.com/us/en/home/life-science/pcr/real-time-pcr/qpcr-education/qpcr-vs-digital-pcr-vs-traditional-pcr.html.  Are there ways to work with the intensity of the bands I get to be " more reliable"?

Yes, quantification from traditional PCR can be done, though the accuracy is questionable. One method I have heard of uses a computer to analyze the intensity of the bands. You could probably pull this off with some Python code (check out the scikit-image python library). The other option is to do what you said, compare to known concentrations.

If you are familiar with HA titers in virology, you might be able to contrive a similar method, in which you carry out 10-fold dilutions of the sample until there is no more detectable DNA left. The point at which there is no DNA left is called the experimental end-point, and the titer of the original sample is simply the inverse of the dilution factor at the end-point. Check out hemagglutination(HA) in the context of virology. I think a method similar to this would be better than simply eyeballing the intensity of bands, because you will have some quantitative evidence.

If you want to eye-ball, you should use control bands at several different concentrations, so that you can say, 'the intensity of the band falls between control bands A and B, and so the concentratin of the sample is between concentrations A and B'.

My lab skills are lacking and I feel like I would mess up easily, do you have any "dummy" sources for doing the serial dilutions or using the imaging software?

I bet you could pull off the serial dilutions. It will be good practice, too. To make a 10 fold dilution, just add 1ml of sample to 9ml of saline. Then, from that new solution you just made, do it all again. Take 1ml and add to 9ml saline. Repeat. Each time you decrease the concentration by 10^-1. You can scale it down too - 1ul sample to 9ul of saline. Repeat.  Here is a SOP on HA. Honestly, I would go with the serial dilution thing. I bet ur professor would help you out with this. It is cheap, easy, and widely used. http://www.cfsph.iastate.edu/HPAI/resources/SOPs/HA_HI.pdf

This is the scikit-image website, though if you havn't used python before this might cause you some headache http://scikit-image.org

Either way, I think your best bet is to do some type of serial dilutions (either to your control or to your samples like in HA) and calculate a titer. Check out the link to the .pdf I sent you, but dont look at the HI section of it, just learn the HA part. If you like biology, you will have to learn serial dilutions at some point. There are used everywhere. Good luck! You can do it!

If I were to do both methods, then would ImageJ be a possible substitute for scikit-image? http://rsb.info.nih.gov/ij/      I think its GUI interface is alot more workable for me.

From just skimming that link it looks like it might. You would probably be interested in the density analysis part of the software, but I dont think a computer is necessary, and ya you will have to produce that gradient of concentrations any way. If it were me, I'd first try to do the experiment without computer analysis. Produce the gradient of control DNA concentrations, compare your sample to the control gradient and see where your sample falls.

Then repeat the experiment while varying the independent variable, lets say its time. So take a sample at 5 min 10 min 15 min etc. and produce a plot of surviving DNA concentration vs time. It will probably end up looking something like a sigmoid curve. If you decide you need more precision in your measurement of the DNA concentration, then consider using the image software, but I doubt you will need it, though I admit it would be twice as badass.

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BLAST(Basic Local Alignment Search Tool) is heuristic?
How can we say that BLAST is based on a heuristic algorithm, as after finding one common word in the query sequence and a database sequence it performs pairwise alignment by dynamic programming - which is an exhaustive algorithm? Also, BLAST provides quantitative analysis by giving bit scores and E-values. As it gives quantitative results, why do we say it is based on a "heuristic algorithm", such as 'word algorithm'?

I didn't quite get what you meant by "word algorithm" - if it's important to your question, you may want to expand on that point.

You might be confused about what "heuristic" means. "Heuristic" doesn't mean random or arbitrary, instead, an algorithm is termed "heuristic" if it employs a shortcut which means that it does not necessarily yield the theoretically best result.
For BLAST, this shortcut is the assumption of first matching the fixed-length words prior to extending the match. Hypothetically, there could be a query sequence and a database where the best scoring match for the query sequence doesn't contain any k-length sequences in common with the database sequence. In this case, BLAST would be unable to find that match. - So the heuristic portion of the algorithm isn't in the dynamic programming portion, it's in that first step of finding pairs which are to be aligned.
The failure of BLAST to find a match is likely to be rare, though, especially with short word lengths. If you find a decent match, it's highly likely that there is a 3-mer (5-mer, etc.) of identical sequence in the pair. But because it's not a guarantee, the use of k-mer word in the process means that BLAST is a heuristic algorithm.
The ability for BLAST to provide quality and statistical metrics is not limited by its heuristic nature. To build an e-value, you don't need to know that BLAST is able to find the absolute best match. Instead, you just need to be able to build a model of the sort of matches BLAST would find by spurious random chance, when applied to a similar database with no "true" matches. Similarly for bit-score. You don't need to know what the absolute best match would be, you just need to know how BLAST would behave on a hypothetical true-match-free database of similar properties.

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How does waking up from an alarm clock work?
During sleep, one's brain is shut down. All it can do is to see some dreams from the semi-conscious mind.
Then how does it hear when the alarm clock rings?

The brain does not "shut down" during sleep. While not everything about sleeping is understood, we do know that certain areas in the brain remain active during sleep. There is a good overview on sleep on the website of the National Institute of Neurological Disorders and Stroke.

Until the 1950s, most people thought of sleep as a passive, dormant part of our daily lives. We now know that our brains are very active during sleep. Moreover, sleep affects our daily functioning and our physical and mental health in many ways that we are just beginning to understand

As for hearing, that part of the brain doesn't shut down during sleep - and for good reasons. Sudden, loud noises for example may be a sign of immediate danger. Any animal that just stops hearing a third of the day would be at a huge disadvantage.
The brain even processes the sounds we receive during sleep and doesn't wake on every loud noise. You might find the following article interesting: How do we hear while we sleep?

Using electrodes implanted directly on the human cortex, a Johns Hopkins University undergraduate has located the part of the brain that appears to process sounds while people sleep. This site, in the frontal lobe, may be part of a vigilance system that, for instance, rouses a mother when her baby cries but lets the woman sleep when a truck rumbles by.

Alarm clocks are usually designed to just get louder and louder until we do wake up. Even despite that, some people actually do manage to sleep "through" the sounds, for example of they were very tired and haven't yet had enough sleep. This is speculation, but maybe in that instance the brain prioritizes sleep.
Other articles on the subject are for example Odd Sound Processing in the Sleeping Brain and Auditory information processing during human sleep as revealed by event-related brain potentials, but the main point is that we don't stop processing what happens around us just because we are asleep.


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What will happen if a foetus is Rh- and the mother is Rh+?
If a mother has Rh-negative blood and her foetus has Rh-positive blood it will result in rhesus incompatibility and lead to erythroblastosis fetalis. What will happen if the reverse occurs, when a mother is Rh+ and the foetus is Rh-?

Nothing. Rhesus incompatibility results when people who are Rh- develop antibodies against Rh+ blood after exposure. People with Rh+ blood do not show any such reaction to Rh- blood.
In a way, it's comparable to blood types in that regard. People with the blood group O can develop antibodies against type (for example) B blood. People with type B don't develop antibodies against type O blood, and can thus receive blood donations of type O.
Also, rhesus incompatibility during pregnancy is only a concern in second or subsequent pregnancies (or after miscarriages). The antibodies develop through the blood being "mixed" during the birth (or miscarriage) and are then an issue if the next fetus also has Rh+ blood, which is just assumed if the father is Rh+ or has an unknown blood type to be on the safe side, and can be addressed medically.

Injections of a medicine called Rh immune globulin can keep your body from making Rh antibodies. This medicine helps prevent the problems of Rh incompatibility. If you're Rh-negative, you'll need this medicine every time you have a baby with Rh-positive blood.

-What is Rh Incompatibility
Also, as you can read in my answer to a similar question about blood groups and pregnancy
How does a fetus retain a blood group different from its mother? the maternal and fetal blood usually only mix during birth due to the placental blood barrier. If you are wondering whether the fetus should have a reaction, the immediate functions necessary for that don't develop until more than six months after birth.

Does it warrant stating explicitly that the foetus does not (for practical purposes relating to the rejection of Rh+ blood) get exposed to the mother's blood in utero? The questioner might be imagining that the Rh- foetus "should" reject the Rh+ mother. And even if the blood were mixed, I'm not sure whether a foetus has the antibody mechanism for Rh+ rejection active yet.

@SteveJessop good idea, added a paragraph

Steve: that would be specific immunity, so your hunch is correct: it isn't developed yet at that stage.


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How exactly are petri dishes used (e.g. in medicine)?
I know that petri dishes with a growth medium are used to grow micro organisms. I guess this works as follows:

The petri dish has to be kept sterile. To make it easier, I guess one could cool it.
The microorganisms are somehow put on the petri dish.
The petri dish is put in an incubator (e.g. 37 °C if one wants to simulate the human body).
After some time (how long?) one can look at the colonies.

Does one only look at them with the naked eye or is there a way to make more detailed studies?
For example, when I have an illness, can the doctor (for some illnesses) simply use this petri dish / naked eye technique to confirm a hypothesis what kind of illness I have?

What exactly is your question? Please read http://biology.stackexchange.com/help/dont-ask Petri dish with appropriate medium can be used to count number of cells in liquid culture. You spread 100uL of liquid and after incubation count colonies. Each colony comes from exactly 1 cell if you dilute liquid culture enough.

My answer to this question, http://biology.stackexchange.com/questions/40750/how-sterile-is-working-next-to-a-bunsen-burner/40755#40755 , may give you an idea of the steps that might be taken to prevent contamination when working with plates, though in a diagnostics setting, it is unlikely that the plates will have an antibiotic on them. Also in a modern clinical laboratory, there would be other methods used, but the basic principles of asepsis are still the same, keep your work area clean and do your best to prevent any airflow onto the surface of an uncovered plate.

Also a trained technician or clinical scientist will recognize the morphology of the bacterial colonies that grow on the plate and whether or not they grew where the plates were streaked or on an unstreaked area. Contamination will pretty much cover the plate where as sample will only grow where the plate was streaked.

I think this is too broad, there are various uses depending on the objective which is probably an extremely long answer, if you have a question about how to test for specific diseases using petri dish methods that would be better. Petri dishes are just a piece of very broad use lab equipment.

I think the petri dishes you are referring to are also called agar plates. Agar is a 'growth medium' for microorganisms. It provides the nutrients that the microorganisms need to survive. It can also contain main other 'things', such as antibiotics or pH color change indicators. There are many types of agar, for example, tryptic soy agar is used to grow E. coli. I think the oven you are referring to is called an incubator. Incubators provide the atmosphere, particularly temperature, needed for the organisms to grow. There are many types of incubators. Some microorganisms actually cannot grow in oxygen rich environments, and some only grow at specific temperatures. These organisms must be incubated under their preferred conditions in order for them to grow.
And yes, a lot can be learned from simply looking at the agar with the organisms on it. What exactly can be learned depends on the growth medium (agar or other medium).
To summarize, petri-dishes are just the plastic dishes that contain growth medium. And incubators are usually refrigerator looking things that provide the proper temperature for the organisms to grow. The goal is generally to mimic the natural environment of the organism, but as I stated, scientists often add many other things to the environment for experimental and diagnostic purposes.
Here is a list of common agars used in bacteriology http://learn.chm.msu.edu/vibl/content/differential/

Oh, as for the time, this depends on the organism. Some grow very fast, E. coli replicates about every 20min under 'log growth' conditions, and some grow very slow, like Mycobacerium tuberculosis. The rate at which the organism replicates is highly dependent on the environment in which the organism is living. Some bacteria only grow at very high temperatures, like Thermus aquaticus, which was isolated from a hot spring in Yellowstone National park.

Also, cooling a petri dish will not sterilize it. In  fact, low temperatures are often used to preserve bacteria. To sterilize a petri dish, one must autoclave the petri dish. An autoclave is like a big steaming pressure cooker.

I did not think that cooling a petri dish will sterilize it. I was talking about keeping the petri dish sterile. My thought was that when you produce a petri dish, it will probably get "contaminated" by just being surrounded by bacteria. Or that "sterile" probably only means that there are very few bacteria on the plate.

Why is it called 'log growth' condition when the number of bacteria grows exponentially (with respect to time)?

Well, log base 10 is 10 to the power of some number. Example 64 = 2^6 so log base 2 of 64 is equal to 6. It just implies exponentiation.

Sorry, didnt mean to say you thought cool = sterile.In case you were thinking of experimenting yourself, and you do want to keep your petri dishes sterile, you should keep the lid on them and probably keep them in the plastic sleeve they are shipped in until you are ready to use them, and avoid exposing them to the air, because there are microbes floating around in the air that can contaminate your dish. But I guess you were just asking out of curiosity. At any rate, perhaps it supplements the answer.

Hopefully Im not talking too much, but to answer the question of sterility, sterile by definition means no organisms. Sanitary is often used to describe what you were saying - very few organisms.


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Why don't housekeeping genes have TATA Box regions in their promoter sequences?
Housekeeping genes are genes that are continuously transcribed. Like all other genes they have promoter sequences, but they don't have TATA box sequences that are used to specify from where transcription is going to begin.
Why don't housekeeping genes have a TATA Box in their promoter sequences?

It seems that there are 10 types of eukaryotic promoters, and only 32% are TATA-containing promoters, the rest of the eukaryotic promoters don't have a TATA box: http://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-13-512

The TATA-box element (and notion of house-keeping genes) are classical textbook examples of trying to explain complex biology in a simplified manner.
In fact, most mammalian genes do not have a TATA-box element and most transcription start sites (TSSs) are spread over a larger area in the 5' end of the gene. Each TSSs contributing to differences in gene expression strength and gene product. This phenomenon has been extensively investigated using cap analysis of gene expression (CAGE). For a short summary of the major findings you can refer to Rikens website here.
Sandelin and Carninci et al wrote an excellent review on the findings of the first CAGE experiments here, and how this contradicts classic textbook promoter structures Nature.
In addition, the CAGE technology, has been used to map out cell-type specific enhancers which contribute hugely to the correct gene regulation, Anderson et al. Nature.
I know this answer does not directly address your question, but rather raises a lot of new questions.

Two possible answers:
First, TATA boxes has been found to cause increased "noise" in gene expression, such that the expression of genes that have a TATA box is highly variable. See this review for example.
A different set of results suggests (here) that TATA acts only as an amplifier of expression.
Regardless of whether TATA amplifies expression or also increases expression variance, this is not suited for housekeeping genes, which generally have low and constant expression.

Quick googling located online version of Lodish et al Molecular Cell Biology. 4th edition.
From TATA Box, Initiators, and CpG Islands Function as Promoters in Eukaryotic DNA section:

These genes, which generally are transcribed at low rates (e.g., genes encoding the enzymes of intermediary metabolism, often called “housekeeping genes”), do not contain a TATA box or an initiator

Also, from Transcriptional Regulatory Sequences of the Housekeeping Gene for Human Triosephosphate Isomerase (Boyer et al, J Bio Chem 1989):

In contrast to facultative gene promoters, these promoters are
  characterized by [...] and, notably,
  the lack of an appropriately positioned TATA box
  [...]
  Based upon these structural differences,
  the possibility exists that initiation of housekeeping and
  facultative gene transcription proceeds through distinct mechanisms.

I can imagine you can google more information, but it seems to me that reason for lack of TATA is necessity for constant low-level expression (hence no strong promoter) and separate mechanism of regulation (hence some common structure). Last point might arise from redundancy argument: when regulation of TATA-containing genes become faulty, housekeeping genes regulation stays same because it is somewhat independent.
However, you should be aware that your original assumption is at least controversial (from same J Bio Chem paper):

Unlike most housekeeping gene promoters that have been
  described to date, the human TPI promoter harbors a canonical
  TATA element (5’ TATATAA 3’) that spans positions
  -27 to -21. LS mutagenesis demonstrated that this TATA
  box clearly represents a control element, the integrity of which
  is essential for the maintenance of both the fidelity and the
  frequency of TPI gene transcription initiation.


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Do any dogs have blue iris - not just sclera?
I was looking in to the question of whether any dogs in fact have "blue eyes"...
A quick search gives plenty of information on and images of dogs with blue sclera and black iris.
Every "blue-eyed" canine I know of personally or could google up has black iris and blueish sclera.
It is unclear if any dogs have blue iris.
(BTW there are many popular articles on the "four typical reasons" that canines can have blue sclera).
Humans with "blue eyes" of course have blue iris / white sclera.  But the only dogs I have found with "blue eyes" in fact merely have blue sclera and black iris.
I did find a couple of poorly-written lite info sites that mention blue iris, but appears to be basically a typo, the articles appeared to mean to refer to blue sclera -- I cannot find any actual scholarly articles on the issue --
(I"m sure, everyone on this site knows that regarding humans with "blue" iris, it's not "really" blue, but a Tyndall effect. Popular article on that.)
And don't mention cats - it's commonplace that cats have "blue eyes" but every image I've seen is of a feline with blue sclera, and black iris. One could ask, do any felines have blue iris?
In short my question is ... do any canines have blue iris??

What evidence have you that blue-eyed dogs actually only have blue sclera? Do you suppose their irises to be colorless then? That would make their irises red, as albino eyes.

Hi Anon!  "blue-eyed" dogs have black iris, as I think I mention in the question.  My only evidence for this is that every "blue-eyed" dog I have ever seen has blue sclera / black iris, and every photo I have been able to "google up" is blue sclera / black iris.  Further, I have exhaustively googled "dog with blue iris" and there are none I could find -- hence, I am asking the experts!!!

I think you are confused. The iris is colored, the pupil is black. The sclera can be white, tan, or bluish-white. I myself have never seen a black iris in dogs or humans.

I think you are confused. When dogs look straight at you, their sclera is not visible. What you are seeing is their iris and pupil.  It is only when they glance off to the side that you can see the sclera of a dog's eye. Humans are pretty much the only mammals where the sclera is normally visible. In a dog, the iris entirely takes up the area which in humans would be sclera.  So malamutes, huskies, etc. will have blue irises black pupils. And pupils aren't actually black, they are an aperture, so the light passing through the lens is not reflected back so it appears black.

@AMR I'd never thought about humans being unusual like that, great thought, I wonder why it evolved - the cooperative eye hypothesis seems plausible at least

Ahhhhhhh!   I was mixing-up the iris and sclera since the iris is so big in dogs!!!!  Nice work, Anon and Amr

Why would anyone down-vote this question?  (I couldn't care less - but why?)

@rg255 Christiaan gave a very informative answer to that question. http://biology.stackexchange.com/a/40680/16651

I have no idea why you cannot find reputable sites that discuss eye color in dogs. Dog breeds with blue eyes should satisfy you; I can't see that they would have any reason to dissemble. In case it doesn't, the references below should. Of course dogs, like humans, cats, and many other animals, can have blue eyes (and by that, I mean irises. Dog irises are not substantially different than human irises. Neither are dog sclerae. They do have a more interesting retina, however.)
This is one of my dogs, a Border Collie, one of several breeds in which complete heterochromia is common. Her right eye is a pale blue, her left is dark brown. Her sclerae are off-white and the conjunctiva are usually somewhat injected; her pupils are black, because they are simply an aperture through which light passes to the retina.

The pupil is large (dilated) because this is a night-time photograph.
Many breeds of dogs have blue-eyed varieties. As with some cat breeds, blue eyes are sometimes genetically linked with deafness.

Blue eyes were positively associated and patches were negatively associated with deafness in the Dalmatian.

(The pink stuff on her forehead and nose is beet juice.)
Deafness prevalence and pigmentation and gender associations in dog breeds at risk
Brainstem Auditory-Evoked Potential Assessment of Congenital Deafness in Dalmatians: Associations With Phenotypic Markers


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Why aren't plants' roots as diverse as leaves?
I have been doing some gardening recently and I suddenly realised that all plants have superficially identical non-woody roots of the same size from gigantic trees to small fruiting plants and vegetables. They are all white, no more than 1 mm across, long and flexible with no distinguishing marks. Only when the root start to become woody do they become different in appearance.
Leaves are very diverse even when they have just started to grow, i.e. before they have reached their full size. I can recognise many different plants from their smallest leaves alone but I wouldn't be able to differentiate plants by looking at their roots. So why aren't roots anywhere near as diverse as leaves?

If you consider rhizomes, corms, bulbs, tubers, nitrogen-fixing nodules, etc. as part of the root system, there's more variety than you give credit for. But an interesting question none-the-less. +1.

@anongoodnurse A potato, which is a tuber, will still put out roots that look like any other plants'. But if you consider that almost every plant can be visually identified by its leaves alone, why not roots?

I was agreeing with you; the roots are very similar. But I wouldn't go so far as to say that every plant can be identified by its leaves alone, if you want me to disagree with you. :)

@anongoodnurse I know you are agreeing with me. I was just saying that, as far as I know, plants with more complex root systems still put out simpler roots that fit my original question. I have personally seen these on rhizomes, bulbs and tubers. I'm not sure what a corm is or what a nitrogen-fixing nodules looks like. I'll have to increase Wikipedia's traffic...

I think the perceived diversity is biased by the relative obscurity of roots and familiarity of leaves as well as the scale at which a human observes these organs with the naked eye. I suspect functional diversity of roots is greater than leaves. One reason for this is that roots compete for and acquire a more diverse set of resources and interact with a larger diversity of organisms than do leaves. In short, if you could observe the metabolome and microbiome I would expect the opposite to be true.

Maybe we can't see the huge diversity of roots because we cant see most of roots which are underground.

The submerged part of an iceberg easily remain unnoticed

Besides various bizarre-shaped storage-roots, roots of other-functions such as roots for mechanical support, climbing, floating, respiration, capturing rainwater/atmospheric moisture, parasitism, and even photosynthesis, seen

From developmental-origin and structures also, roots are diverse. The root system could be primary (obtained from seed) or adventitious (originated from some-other parts like stems or leaves). Diversity is possibly more in adventitious roots. There are seen diversities in root caps and root hairs. From internal anatomy secondary growth could be seen, and a lots of special anatomical structures could be there. Root-stem transitions also vary a lot.

The pattern of root growth and branching is different in different-species, and are ecological adaptations.

@anongoodnurse Underground parts does not necessarily means root. Corms and rhizomes are stem-modification. Tuber is quite informal term and tuber commonly indicate stem-tuber. (However some storage roots are also called root-tubers or tuberous roots). Bulbs of lilies and amaryllids are usually a structure made up of stem, leaves as well as roots. Basic types of plant-organs, like root, stems and leaves are well-demarcated from their developmental-nature and anatomy.

To answer this type of question, we should start by defining 2 concepts: the functions of the root and the external condition that brought to a specific evolution.
Evolution is a necessary process to all organisms, which evolve to optimize a specific function and to better adapt to the external conditions.
There are 3 main and common functions between all land plant's roots: fix plants to the soil; absorb water and minerals; establish specific relationships with other organisms, principally fungi and bacteria. The external conditions of roots (soil) are quite stable, even though, the different "physical" composition of soil, that is the quantity of sand, clay and rocks, change the physical appearance of size and proportion between the main and the lateral roots.Therefore it is plausible to say that it is not necessary to have a great variety in root's structure; since all roots must carry out same functions, all plant's root underwent a similar evolution.
For the leaves it is a bit different. Leaves must also carry out specific and common functions, as: exchange gas (CO2 and O2); contain photoreceptors to "absorb" light for photosynthesis. However, the external conditions of leaves are shortly and continuously changing and highly different (consider the vary regions of the world, as desert and rainforest) with reference to roots. Therefore each plants underwent evolution depending on these types of external conditions, so as to, of course, optimize their functions but at the same time protect themselves as much as possible. Consider, for example, the intensity of sun's radiation, which, if too strong, can destroy cellular structures, the quantity of CO2 in the air, or the high biodiversity of insects, which can carry diseases, ecc...
Interesting book about evolution is: J.C. Harmon, S. Freeman, "Evolutionary analysis", where it is given an idea of the type of evolution, different species, could undergo.
(hope my english is not too bad)


text:
Who and when was the first human diagnosed with hemophilia, or considered a carrier?
The earliest case I can find is Queen Victoria of England, who ruled from 1837-1901. Is this the first hemophilia case on record?

The disease hemophilia has been known for much longer than that. At the time the Talmud was written, for example, it was known that if some boys in a family died from circumcision, the next were also at risk. This might have been because physicians recognized an inherited blood disorder.
Abulcasis, an Arab physicians of the 10th century, wrote about families in which male members died from bleeding out after injury.
In 1803, John Conrad Otto wrote about

a hemorrhagic disposition existing in certain familie

Tracing the condition back three generations in that family named Smith, who lived in  Plymouth, New Hampshire. So there were definitely earlier cases where we even know the names of the patients, eben before the disease was named.
The word haemorrhaphilia, later shortened to hemophilia was first used in 1828 by Friedrich Hopff, before the birth of Queen Victoria.
Queen Victoria herself did not have the disease, though, she was a carrier. At least one of her sons had the disease and at least one of her daughters was also a carrier.
The history of hemophilia
History of Bleeding Disorders


text:
Stabilizing forces between the protein sequences?
we know that Protein structures from secondary to Quaternary are maintained by noncovalent or weak interactions including electrostatic interactions,van der Waals forces & hydrogen bonding. What is the significance of these weak interactions why they are preferred by nature rather then strong covalent interactions?

Proteins often undergo conformational changes. The activation energy required to undergo a conformational change in a protein with only covalent interactions would be much higher compared to that of a protein with weaker bonding forces. An example of a conformational change seen in enzymes is the change in conformation during allosteric regulation, in which an effector molecule binds a site on the enzyme distant from the enzymes active site. The binding of the effector molecule induces a conformational change that exposes the active site of the enzyme. Another example of conformational change is the change in conformation seen in Toll-Like-Receptors (TLRs). Additionally, many proteins change their conformation in response to pH. These changes would likely not occur if the protein only contained covalent bonds, and the ability of proteins to undergo such changes makes them responsive to the environment, as well as allowing them to carry out their enzymatic actions, if such actions exist for that particular protein.
Here is the wiki on allosteric regulation https://en.wikipedia.org/wiki/Allosteric_regulation
Here is a figure on conformational changes in TLRs http://www.nature.com/ni/journal/v8/n7/fig_tab/ni0707-675_F1.html
And here is the wiki on activation energy, a concept used in chemistry (see section on catalysis and Gibbs free energy) https://en.wikipedia.org/wiki/Activation_energy

There are examples of covalent interactions that influence tertiary structure. One such example is a disulfide bridge. Check out this figure, where the two yellow balls constitute a disulfide bridge and influence tert structure https://i.ytimg.com/vi/ysPt1lIllcs/hqdefault.jpg

I know that one of the covalent interaction exist such as disulfide bridge my question was that majority of stabilizing forces are non covalent and what is significance behind this.

Please see my answer above. I believe it is what you are looking for. The non-covalent interactions allow the protein to easily change conformation. This makes the protein dynamic and responsive.

Conversely, if the protein only contained covalent bonds, its structure would be rigid, and it would require much higher activation energies to change conformation (compare the changes in enthlapy between breaking a covalent bond and breaking a hydrogen bond).

yes, I find it useful..

The word DonJulian uses for proteins — "dynamic" — is very well chosen. Life is dynamic, proteins underpin living things, and their dynamic properties help convey dynamism to life.


text:
Which is better adapted for global warming: deciduous or evergreen trees?
Evergreen photosynthesise for longer and don't lose their leaves all at once, whereas deciduous plants do and enter periods of hibernation during winter, among other differences (correct me if I am wrong).
Is there any significance in these differences considering the future impact of global warming on trees?

Please edit your question so it takes into account rules of thiw site http://biology.stackexchange.com/help/dont-ask there is no actual problem to be solved: “I’m curious if other people feel like I do.”

Which kind of tree do you see as you move towards the equator? That should give you a pretty good idea of what matters in warmer climates.


text:
Can you knockout specific receptors in an adult?
Sorry I don't have a good understanding of this topic, but I'm guessing that "receptor knockout" is related to/a part of "gene knockout"?
And If I understand correctly, gene knockout is currently not yet possible to do in an adult (maybe possible in a small area/specific organ, but not systemically) ?
So does that mean a systemic receptor knockout is not possible and maybe possible in small specific areas?

Short answer: yes, it is possible.
But there are some requirements for your delivery system. "Gene knockout" ("gene KO") means such DNA modification that is permanent (get inherited by cell's progeny) and deleterious to gene function (e.g. protein no longer get produced).
So your system must deliver DNA "mutation agent" to all cells (of organism or small specific area). This can be done by using viruses and, for example, CRISPR/Cas9 system for genome editing. Idea  is that virus will get in the cell, start expressing component for genome editing, multiply and infect neighboring cells. Modification in virus can make it non-lethal and less harmful, so you don't kill tissue in process. Virus delivery can be site-specific (e.g. direct injection into the area), it also might be cell-type specific if virus is tailor accordingly.
Also, remember that CRISPR/Cas9 and other similar techniques have efficiency well below 100% and also that you often have two copies of the same gene. This means that total KO probability goes as square of single copy KO probability. If for one event probability is 50%, for both it will be 25%; 10% becomes 1%.
So, all principle component for such experiment already exist.


text:
Focusing on flowering plants, are there reasonable explanations why pentaploids would be more fertile than triploids?
For the genus Rhododendron, triploids are sometimes fertile but pentaploids appear to be often fertile. Once Rhododendron seedlings gets above the triploid level, aneuploids not near euploid appear to become more viable at least in greenhouse situations. What mechanisms best explain this increase in fertility of odd ploidy and viability of aneuploids as ploidy levels increase?


text:
In glycolysis, what is the source of the electron that makes NAD+ into NADH instead of NADH+?
I looked at the formula for the glycolysis reaction. The overall reaction seems balanced, however, I don't see anything on the left hand side of the equation that would provides the electron to convert NAD+ to NADH. Where does that electron come from?

This question would be much better if you included the reaction (then it would be considered your research) in the body of your question, the whole 'equation', including the enzyme(s). One reaction in detail would be sufficient. Otherwise, this reads like a homework question, even though it may not be.

If it were a proton transfer, it would be NADH2+ (You already had a plus charge on the NAD+ cation). What is another of a molecule picking up a hydrogen and an electron in exactly the same step?

@Hal I agree with anongoodnurse above - question as stated is vague... are you trying to balance the NAD+ and NADH?

@VanceLAlbaugh The question isn't vague, it is just that Hal is forgetting that there are ways other than proton transfer for a molecule to pick up a hydrogen.


text:
Why even if all requirements for natural selection are met, it may not happen?
In the book written by John Endler Natural Selection in the Wild p. 4
it says that even if condition a, b and c are met, evolution by natural selection might occur,

[...] , but not necessarily, [...]

See last paragraph of the image.
Endler, J. A. 1986. Natural Selection in the Wild. Princeton University Press.
I’m wondering in which case it’s possible that everything is in place for natural selection to occur, but is not having any effect.
It seems to me that if every condition of natural selection are met, there will absolutely a change in the phenotypic distribution? Why does the text say evolution is not guaranteed to occur?

if all the living things are killed for instance there is no natural selection.  if the environment does not affect the outcome of reproduction, i suppose that natural selection is not occurring, but its hard to imagine such a situation

Hi @mbeausoleil - could you respond to the comments under remi.b's answer - we could do with clarity

What does the sentence below mean?

As a result of this process, but not necessarily, the trait distribution may change in a predictable way.

To my understanding, but not necessarily means that other processes than natural selection can affect the trait distribution in a predictable way.
Other than natural selection, what affects the trait distribution in a predictable way?
I am not trying to make an exhaustive list but I am just providing here two obvious examples.

An intense gene flow (migration) from a nearby population will also cause the trait distribution in a local population to change in a predictable way.
Genetic drift, will reduce genetic variance and therefore reduce the variance of the trait distribution. While the change of the mean of the trait distribution is not predictable under genetic drift, its change in variance is predictable.

Note that the book has been published in 1986 and the vocabulary and science is probably slightly outdated. If you are learning about evolutionary biology, you can probably find better source of knowledge. For example Understanding Evolution is a free online introduction to evolutionary biology. There are many textbooks that offer very good introductions to evolutionary biology.

I'd add genetic correlations - selection on one trait (a) may oppose the selection on another genetically correlated trait (b), so when studying a all conditions would be met but no change (or lesser than expected, or opposite to expectation, change) occurs

Sure I could add that. However, as you said, this is NOT an example of when something else than natural selection can affect the trait distribution in a predictable way. It is an example of when selection is counteracted by something else.

Upon reading the question again, I think the user is asking why evolution doesn't always occur (in the predicted way) if the conditions for natural selection are satisfied. A question of why doesn't selection always give a response, rather than how else can predictable evolutionary change occur.

Hum... indeed. However, there is contradiction in the sense of the question between the actual question and the citation that the question is supposed to tackle. As a consequence the post would deserve being closed as unclear.

Agreed, need the OP to come back!

Actually, the answer of @Remi.b is clear and is in relation to what I asked. If you want to go deeper, you can ask the question: is it possible if all the conditions (a, b and c) are met that natural selection, regardless of other processes considering that they have no effect, is not changing the trait distribution?
In other words, if the conditions a, b and c are present, is the trait distribution changing all the time?

Evolution, a change in the trait distribution of a population, occurs by four mechanisms; drift, mutation, migration, and selection. E.g. These mechanisms cause a change in the mean of trait, or variance in a trait etc.. Just to summarise the conditions you gave:
a) Trait $i$ has variation
b) Trait $i$ covaries with fitness ($\omega$)
c) Trait $i$ is heritable from parent to offspring
Genetic drift is the random loss of genetic variance from the population by stochastic processes. Mutation (generally) generates new genetic variation within populations. Migration can lead to loss (emigration) or gain (immigration) of genetic variation from a population, as variants come or go from a population.
Selection is mechanism underlying adaptation. This is what is in condition b of the conditions you gave. We can predict the response to selection using some simple quantitative genetics in the form of the (multivariate) breeders equation.
$\Delta z = G\beta$
Where $\Delta z$ is the response in the trait, $G$ is the genetic (co)variance matrix, and $\beta$ is the selection.
In a simple toy example we could look at a single trait, $i$. We allow $i$ to satisfy all of the above conditions. This means that both $G$ and $\beta$ are non-zero, and therefore, $\Delta z_i$ will also be non-zero. Just putting some random numbers in to the equation to make it clear, if $G = 0.5$ and $\beta = 0.8$ then;
$\Delta z_i = 0.5 \times 0.8 = 0.4$
Mutation, drift, and migration could all oppose or distort the effect of selection. In other words, they can cause the actual and predicted response to be different from one another (i.e. $\Delta z_i \neq 0.4$), and there will not necessarily be a change in the phenotypic distribution.
However, selection is also factor that could cause a difference between the predicted and actual response to selection in trait $i$. This is because genetic correlations can arise among traits, either by linkage (close proximity in the DNA) or pleiotropy (when one gene affects more than one trait). For example, we may see no response at all in $i$ ($\Delta z_i = 0$) when both $G_i$ and $\beta_i$ are non-zero, if selection on a second unmeasured trait, $j$, opposes selection on $i$ ($\beta_i = -\beta_j$), and trait $j$ has equal variance ($G_i = G_j$) and is perfectly covarying with $i$, $cov_{i,j} 1$. Approximately this would be;
$\Delta z_i = (G_i \times \beta_i) +  (G_{i,j} \times \beta_j$)
$\Delta z_i = (0.5 \times 0.8) + (0.5 \times -0.8) = 0$
This is a major issue in the study of evolutionary biology. Genetic correlations can cause severe disparity between the actual and predicted response to selection and univariate methods are insufficient as a result. More studies adopt multivariate methods these days, though these are generally limited to just a handful of traits so its still not perfect. In reality methodological and logistical constraints present a huge obstacle to being able to predict $\Delta z_i$.


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Why is alcohol purged from the body more slowly when we sleep?
It is a popular belief that when you get asleep after drinking alcohol, in the morning you have higher level in your blood than if you stayed awake the whole night.

Is this true?
If so, why? Is it because the liver works more slowly while sleeping, or because the intestines work more slowly and there is still more alcohol in the morning to be processed by the liver?

I never heard of that. That'd be great if you could provide a link to prove that it is a noticeable claim? Note that your question would also be on-topic on Skeptics.SE.

@HonzaZidek agree with comment above - this is a flawed question - alcohol is not purged more slowly when you sleep and you don't wake up with more alcohol in the morning - check out zero order kinetics if you want to learn more about alcohol metabolism

You are right, Culprit is Ethanol in Alcohol. It contains 2 carbon atoms, 6 Hydrogen atoms and 1 Oxygen atom.

Ethanol is readily soluble in water, so it easily dissolves in the
bloodstream and gets carried to various parts of the body. The most
affected areas of the body include the liver and the brain. In the
brain, ethanol adversely affects Glutamate receptors, which causes
slurred speech, memory loss, slow reaction to stimuli, and other
common side effects of being a bit too tipsy.
Not only this, ethanol molecules bind with GABA (gamma-aminobutyric acid) receptors, which is able to slow down the
activity of brain. Unlike glutamate receptors, ethanol actually makes
GABA receptors more receptive, causing the brain to slow down even
further. However, alcohol doesn’t just act to slow everything down in
the body. It also stimulates the production of dopamine and
endorphins, chemicals that produce feelings of pleasure. This is the
reason why people choose to get that alcohol “high”, despite knowing
the negative consequences that it may lead to.

So basically when you are physically working body needs more oxygen while Ethanol only has one oxygen atom, and Since Liver starts to work on regular pace, Which plays a central role in all metabolic processes in the body.
Everyone's oxygen levels in the blood are lower during sleep , in fact while sleeping or in meditation body needs very less oxygen to survive.

Why would I need to wear oxygen while sleeping?
Everyone's oxygen levels in the blood are lower during sleep, due to a
mildly reduced level of breathing. Also, some alveoli drop out of use
during sleep.
If your waking oxygen saturation is greater than about 94 percent on
room air, it is unlikely that your saturation during sleep will fall
below 88 percent. However, your doctor can order an overnight oximetry
test if there is a question about your oxygen saturation levels while
you are sleeping.

In general, metabolic rate is higher when you are awake, because then you tend to be moving about doing stuff.

Welcome to Biology. This answer just touches the question. Further, sources are lacking and this is mandatory when quoting stretches of text

@AliceD Thanks, I will get better if you give me a few more chances.


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Resolution of X-ray crystallography
A structure determined by X-ray crystallography has a resolution of 1.5 Å. When I look at the coordinates, I find every backbone C-N distance is 1.32 Å.i.e. Accurately predicted. If resolution is not good why every C-N bond distance is accurately predicted?

The structural model of a protein is obtained using both experimental data and prior knowledge about geometry of macromolecules. As a structural model is refined, interatomic distances are also restrained. So, the C-N distance isn't really predicted. Alternatively, knowledge about this distance is used to construct reasonable model.
In response to the comment below I'll cite Rupp's Biomolecular Crystallography, the most comprehensive book on this subject. Refinement and restraints are covered in Chapter 12, Model building and refinement.

An observation does not have to be an experimental observation
  (measured data) specific to the particular structure, but can be any
  type of general prior knowledge regarding molecular stereochemistry.
  Known stereochemistry can be exploited and implemented in
  macromolecular refinement in the form of geometric constraints and
  restraints. [...]
We know from accurate and precise small molecule and peptide fragment
  structures [...] that bond lengths and bond angles show distinct and
  relatively narrow distributions around their mean positions. [...]
Refinement programs read restraint target values specific for each
  residue and each ligand molecule from restraint library files, which
  are subject to continuous empirical update.

The value given in this book (Table 12-1) for peptide bond C-N is 1.336 Å with variance 0.023 Å.

it's always helpful to include resources for external validation - it may seem silly when the answer is common knowledge in your field, but it is very helpful to those outside of a specific field.

@VanceLAlbaugh: I've added a citation


text:
Electrode locations for neuron study in stereo EEG?
I am thinking where to put optimally depth electrodes in stereo EEG outside sulci in studying the functioning of neural transmission of N neurons over one perivascular space in rodents, mice or rat, where I would like to know how small N can be. The theoretical minimum is one neuron but I would like to understand the Physics how small current you can measure by EEG reliably with not too high Signal Noise Ratio (SNR).
I did not find any meta-analysis about EEG electrode locations in DynaMed Plus.
I am not sure about the anatomic therminology of Neurology so I use the terms cerebral cortex, sagittal and coronal planes in describing directions.
Definition of electrode's location somehow in cerebral cortex
The further the electrode is away from the source, the lower SNR.
This proposes me that there has has to be at least 20 neurons to minimize the variance.
What is the average distance between two neurons?
Here my conjunctures about location of electrodes where the picture is from Virginia's university Nature publication here:

where the electrode is surrounding N neurons and one blood vessel such that one electrode is below the neuron and one above.
It is contraindicated to put the electrode too close to the blood vessel.
Definition of electrode's Coronal-Sagital locations
I am interested in

how close perivascular space can the electrode be? Stereoelectroencephalography (SEEG) implantation method has a safety distance minimally 2 mm but practically more than 5 mm of depth electrodes. [TODO cite]
how superficial can the electrode #2 be? 1.0 - 1.5 mm in microelectrode EEG here i.e. mostly in superficial layers.
how deep can the electrode #1 be? I think mostly in superficial layer i.e. 1.0 - 1.5 mm with microelectrodes. SEEG with depth electrodes - minimally 2 mm but practically more than 5 mm.

Stability of electrodes
The stability is affected by many processes discussed here.
The array of electrodes is allowed to float with the motions of the cortex due

heartbeat
respiration
...

Sources

Talairach J, Bancaud J, Szikla G, et al. Approche nouvelle de la neurochirugie de l’epilepsie. Méthodologie stérérotaxique et résultats thérapeutiques. Neurochirurgie (1974) 20 (Suppl. 1): 1-240.
Cossu M, Cardinale F, Castana L, et al. Stereo-EEG in the presurgical evaluation of focal epilepsy: a retrospective analysis of 215 procedures. Neurosurgery (2005) 57: 706-718.

How can you define evidence-based locations of stereo EEG electrodes?

I am not sure why this question received a down vote. It is usually good to give an indication if it isn't plainly obvious what the problem is. That said, I am assuming that you are asking about rodents, mice or rat. Please clarify with an edit to your question.

@AMR - The downvote was probably the result from trying to measure single cells with EEG, that's impossible. This question is on depth electrodes for single-unit recordings. Further,  the answer to this question is opinion based, because there is no strict definition of where an electrode needs to be. The further away from the source, the lower the SNR.  What is acceptable and what not is pob.

@Christiaan Thank you for your comment! I made the body clearer. The one neuron study is just a theoretical model. I want to understand how you can estimate the amount of neurons required to be optimally within the distance in the cerebral cortex in EEG measurement, minimizing the variance.

The question is still unclear. An EEG is performed with noninvasive scalp electrodes in humans, or, perhaps, with transcranial epidural electrodes in special cases. The figure implies depth electrodes which is per definition not an EEG as far as I know.

@Christiaan Depth electordes are done with stereo EEG so EEG.

That's interesting. I didn't know that. +1


text:
How many virus infections does the average human have?
According to the WHO:

67% of the population  are infected with herpes simplex virus type 1 (HSV-1)

Presumably there are other viruses as well that infect a lot of people. How many infections does the average person have?

What do you mean by "have"? Should we count short-term infections that can be caused by countless cold viruses from many different families? Or should we count persistent viruses only, such as HSV and HPV?

@EliKorvigo : I would call all of them.

There isn't really an average person; I doubt this can be answered as asked. If you live on a remote island, you won't have all that many; if you live in an overcrowded city, you'll likely have a ton; if you live in cold regions, your risk of many viruses is lower than in temperate or tropical regions. If you travel a great deal, you're exposed to many more than someone who stays put. Etc., etc., etc. Then there's everything in between. Maybe the only real way to get an answer to this is to look at rates for every known virus and add? I don't know. I think it's too broad.

You also need to make the distinction between being infected and becoming sick. The immune system can keep infections subclinical, but they will still remain present in the body.

This is likely very different depending on location. Most people live in Asia (China, India) or Africa. Most of the studies are done in North America or Europe.

Ignoring short-term (acute) viral infections, so only considering persistent viruses, probably on the order of 5-10-ish.  There are 8 human herpesviruses known, of which 6 (herpes simplex I, EBV, CMV, VZV, HHV6, and HHV7) are very common in humans, generally infecting 50-90% of a population.  There are over 50 strains of human adenoviruses, but only a few are very common and persistent; hAb2 and hAd5 are probably the most likely.  Then there may be a human papilloma virus or two persistently infecting many people, though the prevalence is lower than herpes or adenoviruses.  So, it's reasonable to assume that most people have somewhere around 5-10 persistent viral infections.
If you add in acute infections, and ask about all exposures during one's life, you're probably looking at thousands or tens of thousands of viruses, but the questions about what's a different virus and what's an "infection" become trickier.

I really like the this answer, but can you give a reason for "thousands or tens of thousands of viruses"?

About a hundred strains each of rhinovirus and enterovirus, plus multiple strains of influenza viruses, noroviruses, adenoviruses, RSV, parainfluenza, rotaviruses, reoviruses, coronaviruses, parvoviruses ... probably around a thousand already, and these are only the agents that have been identified and that are known to cause disease. New pathogens are still being discovered, meaning we're undoubtedly infected with many unknown viruses, and there's very little known about viral infections that don't cause disease, even though those are probably common too.

Thank you for this answer. I'm not an epidemiologist, so forgive me if I am very mistaken, but are you saying that we've all (on average) been infected by a hundred strains of enterovirus? Maybe we have, but that seems a bit high to me. With rhinovirus I won't disagree. I doubt that the "average person" has actually been infected by a great many influenza strains, and the numbers sound too high to me. But I repeat, I'm not an epidemiologist.

That's why I didn't want to answer that part.  Questions  of "what's a different virus" and "what's an infection" come down to shrugs and handwaving.  As soon as I say something, you focus in on the details, and they don't matter. It makes no difference whether we're infected with 10 or 20 or 50 enteroviruses, because the vast dark matter of viral infections outweighs all of them  If you don't like my answer (I'm not an epidemiologist either, just a virologist) then make your own; you can define strains the way you like, and come up with any answer you want.

I didn't intend to offend; I asked because that was the OP's question, and on SE, the answers are supposed to answer the question. If there isn't an answer, I'm certainly not going to try to give one. That was the point of my comments to the OP.


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CNS lymphatic vessels around ventricles lat et 4th?
I am searching for precise locations of the lymphatic vessels of the CNS based on the applications of the article here.
However, I did not find any when having a focus on the immediate region around ventricles (lateral and fourth).
I know this 2D visualization of the lymphatic vessels:

and this visualization at perivascular lobes

I am interested in how much the lymphatic vessels cover the lateral sides and ventricles.
I know this Blender application here where I consider Full hemispheres, each as a single mesh most useful.
However, I have a problem in adding those small membranes on top of each hemispheres and there lymphatic vessels because I do not know how evenly I should put those in the model.
I am particularly interested in the ventricles and how lymphatic vessels are around them.
How can you visualize the CNS lymphatic vessels around the immediate neighbourhood of ventricles (lateral and fourth) in 3D?


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Is high metabolism linked to high evolutionary turnover?
I recently read The Dinosaur Heresies by Robert T. Bakker, a 1986 popular science book presenting arguments for an active lifestyle and high metabolic rate in dinosaurs.
One of the arguments that Bakker presents relates to the pattern of species and genera in the fossil record over time.  He states that "warm-blooded" animals (i.e. animals with high metabolic rates) are expected to have higher turnover of taxa and faster rates of diversification.  Dinosaurs have high species and genus turnover and rapid diversification, which Bakker interprets as evidence for a high metabolism.
This argument rests on the claim that high metabolism is correlated with high evolutionary turnover.  Setting dinosaur physiology aside, I wonder how reliable the underlying assumption really is.
Is there good evidence that metabolism and evolutionary rates are causally linked, perhaps due to the ecological strategies that warm-blooded animals tend to adopt?

The question is very interesting. I don't think you express any argument though but only a hypothesis. From your post, the hypothesis that "animals with high metabolism have higher rate of speciation" seem to come from nowhere. Can you try to express Bakker's  logic behind this hypothesis?

@Remi.b Bakker argues that dinosaurs had a high metabolism, based on the rates of divergence and extinction in the fossil record.  However, this argument relies on the claim that high metabolism is in fact correlated with high evolutionary turnover.  My question is whether this underlying claim is indeed well-supported by evidence.

Oh ok. It is not an argument then. It is a claim that such evidence exist. An argument should follow a logical thinking, an argument is not a non-referenced claim. So, you are asking if the claim is supported by evidence or not.

Metabolism and evolutionary rates are linked, but not in the way you describe.
First consider that metabolism is intrinsically linked to body size. The larger an animal is, the smaller amount of energy per unit mass it takes to maintain that body. This can then be extended to many things about an organism, such as life span, gestation time, population growth, etc. (see Brown et al. 2004 for more detail).
Next consider that metabolism changes with temperature. Take an ectotherm (an organism who's internal temperature is the same as the ambient environment, traditionally called cold-blooded creatures) like a lizard, which will go thru temperature fluctuations throughout the day. It will have higher metabolism when the temperature is higher. A lizard living in a warm environment like the tropics will have an overall higher metabolism than a lizard of the same size living in a temperate climate. With that higher metabolism comes a different life span, gestation time, population growth, etc. even though their body sizes are the same.
When temperature is considered and corrected for, all organisms have attributes that scale directly with body size. A plant literally has the same metabolic rate as a lizard if they are a similar mass and live at the same temperatures. (Seriously, see the Brown paper).
Now onto evolution. Rates of evolution depend on many things, but primarily two. Generation time (the time for 1 generation of a population to reproduce) and mutation rates of DNA.
A longer generation time decreases the rate of evolution. For example a single celled organism reproducing every month will evolve faster than an elephant reproducing every decade.
Larger rates of mutation in DNA increase the rate of evolution. If DNA does not change then evolution cannot happen. So the faster DNA changes (thru mutation rates) the faster the potential evolution can be.
Generation time increases with increased body size/metabolism (Brown et al. 2004). Mutation rates decrease with increased size/metabolism (Gillooly et al. 2005).
With those two general patterns, one can say that the rate of evolution decreases with increased metabolism.
Now onto dinosaur evolution. You said that R. Bakker observed that dinosaurs had a higher rate of evolution than expected. With the hypothesis that a higher metabolism caused this. I'll assume they had the same physiological constraints as animals of today, which is reasonable considering they are ancestors of birds. Which everything I just laid out I would propose R. Bakker hypothesis is false, since a higher metabolism means a higher generation time and lower mutation rates, which would lead to decreased rate of evolution.
The latest science says that dinosaurs were endothermic (regulate their own temperature) up to a point (Witze 2014), so their internal temperatures were not as warm as mammals, but probably warmer than most fish and reptiles.
So when accounting for size they likely had lower evolutionary rates than mammals, and higher rates than fish, reptiles, insects, or other ectotherms.
Why then does R. Bakker observe higher evolutionary rates in the fossil record then? I can think of just a general reason why. The timescale of dinosaurs is on the order of 10's of millions of years. Much longer than the tiny amounts of evolution that we have observed in the past 100 years of science. There could easily be processes happening at those long time scales that we aren't considering.
References
Brown, J. H., Gillooly, J. F., Allen, A. P., Savage, V. M., & West, G. B. (2004). Toward a metabolic theory of ecology. Ecology, 85(7), 1771-1789.Link
Gillooly, J. F., Allen, A. P., West, G. B., & Brown, J. H. (2005). The rate of DNA evolution: effects of body size and temperature on the molecular clock. Proceedings of the National Academy of Sciences of the United States of America, 102(1), 140-145. Link
Witze, Alexandra  (2014). Dinosaurs neither warm-blooded nor cold-blooded. Nature. 2014 Link

Interesting, and thanks for the "metabolic theory" links.  However, what you say in the third-to-last paragraph is actually the opposite of what you said in the preceding paragraphs.  Higher metabolism means lower generation time and higher mutation rates, and hence a faster rate of evolution.  This is in agreement with Bakker's arguments.

Regarding dinosaur mesothermy, the debate is far from settled.  While some researchers favor a "mesothermic" model, one can find other papers arguing for complete endothermy like that of modern birds and mammals (e.g. Seymour 2013).

Regarding the last paragraph — much of what we know about evolution comes from the fossil record, so I'm not sure what you mean by "processes happening at those long time scales that we aren't considering".  When Bakker says that evolutionary rates for dinosaurs in the fossil record are high, he's comparing them to other groups in the fossil record, not just to recent observations over the last hundred years.

Pretty sure my comments are consistent throughout. As metabolism increases generation time increases and mutation rates decrease. That's what observations from today tell us. Assuming dinosaurs followed the same patterns then you can't say that their higher than expected evolution rates are due to high metabolism.

Process at long time scales could be many things. For example, how should we interpret the evolution of a small bodied creature to a large bodied one over several million years? I have no idea, but something like that could affect how we compare evolution in the fossil record with evolution we see in laboratories.


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What would the resulting karyotype be if someone with Klinefelter syndrome fertilized an "empty" egg?

Endoreduplication: is a form of nuclear polyploidization that results in multiple, uniform copies of chromosomes. This process is common in plants and animals, especially in tissues with high metabolic activity, and it generally occurs in cells that are terminally differentiated.
Investigating the hows and whys of DNA endoreduplication. - Larkins, et. al.

What would be the karyotype of the sex chromosomes of a complete hydatidiform mole that was the result of a sperm (monospermy) of someone with Klinefelter syndrome (47,XXY) fertilizing an "empty" female egg?
I know that in a situation without Klinefelter syndrome the sperm inside the egg would double all it's chromosomes by endoreduplication (since the mother's chromosomes are all missing), but in this situation there would not be a need to double the sex chromosomes if the sperm already contains "XX" or "XY" (Since Klinefelter syndrome has 4 possibilities for a sperm : Y, X, XY, XX).
Or would it be that the cell doubles every chromosome if there are too many missing?

I added some links to your question for those that might be unfamiliar with molar pregnancy, etc - it's always a good idea to add links for clarity to help others understand your question


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identifying which SNPs sit in TFBS (Yeast)
i have a set of ~11k SNPs for Saccharomyces cerevisiae, baker's yeast and i would like to identify which ones of these sit in transcription factor binding sites and if they do information on the relevant TFBS.
i've scoured this site and the internet and i couldn't find a downloadable database that would give me locations of all known/verified TFBS for yeast. i've studied the YEASTRACT website thoroughly but didn't find such database to download information about TFBS for all the ORFs/genes in one go.
moreover, when i tried getting the information manually through YEASTRACT search on-line i found results confusing. for example: searching for TF for ORF "YOL166W-A" returns a list of 4 TFs. clicking on one of them, say Sok2p, takes you to another page which says, amongst other things, that the corresponding TFBS is "acMTGCAKg"... what does it mean? (i know the ACTG alphabet but what are the 'a', 'c', 'K' and 'g' symbols?) and what does this tell me about the actual location of the binding site? do i have to BLAST the whole genome to identify it? (shouldn't there be a database with this info for yeast already?) if so, how do i BLAST for symbols like 'K' and 'g'?
i have background in stats but currently work in genetics applications, hence extracting relevant bioinformatics data is very confusing for me on occasions. any help will be appreciated.

I agree it can be extremely confusing sometimes to find the right data.
Do you know RSAT (Regulatory Sequences Analysis Toolkit) ?
If you go in "help & contact", and "motif databases", you'll find the Yeastract database: http://rsat-tagc.univ-mrs.fr/rsat/motif_databases/Yeastract/
I thought it would also be on JASPAR, but couldn't find it.
Then for your analysis where you look for SNPs in the motifs, there is a tool on RSAT, that unfortunately works only with the Metazoa database right now, but you might be interested to check it out, and the corresponding paper: http://rsat-tagc.univ-mrs.fr/rsat/variation-scan_form.cgi

In addition to the 4 nucleotide letters, there are letters that mean "the letter is one of these two or three:
M = aMine = A or C
R = puRine = A or G
W = Weak (two hydrogen bonds) = A or T
S = Strong (three hydrogen bonds) C or G
Y = pYrimadine = C or T
K = Ketone = G or T
B = not A
D = not C
H = not G
U = not T
I would guess the the lowercase means that those letters are not as important as the uppercase ones in terms of determining binding.


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Why can't men produce milk, just like women?
This might seem a bit weird, but why can only women produce milk? Wouldn't it be more beneficial to our species if all humans could produce it? I can't think of any reason only one gender would need it, unless it would somehow be harmful to men.
I know that men can secrete milk in some cases, but why not in general?

The words beneficial to our species very much suggests that you misunderstand evolutionary processes.

Why do you say that, Remi? Traits that are detrimental tend to not be selected for in many ways, while traits that are beneficial increase the likelihood that an organism will pass on those traits to future generations. That is the theory of natural selection in a nutshell.

Evolution does not primarily work for the benefit of the species @DonJulian

related/possible duplicate: Why only female mammals have well developed mammary glands?


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Is honey in hot green tea unsafe?
I used Google to try to figure out what kind of mixture honey has with hot water, and I found several Ayurvedic sources claiming that honey in hot water is toxic.
For example:

Honey – NEVER Put It in Hot Water/Teas
5 Reasons You Should NEVER Cook With Honey
Honey: A Must Read For Those Who Eat It Regularly

What I would like to know is how does heating honey make it toxic?
Is there something that happens at the molecular level that changes the chemical properties of honey when it is heated? If so, are these chemicals harmful, as claimed?
Are there any other reasons other than heating that may make honey toxic?

Could you provide references to your claim?

I assume you are talking about sites like http://markbunn.com.au/honey_never_in_hot_water/ or http://www.mockingbirdmeadows.com/2013/11/19/reasons-you-should-never-cook-with-honey/ ? Basically claiming that heating honey will kill us all (well, maybe not kill, just make us very sick)?

@YviDe, I added some information from an Ayurvedic Research journal that addresses those issues. There concern is an increase in HMF, but HMF is a breakdown product of hexoses, and will be found in anything that contained fructose and glucose that was heated, not just honey. However HMF has not been found to be correlated to any illnesses in humans, so the significance of the find is questionable.

I am voting to reopen this question. In answering the question, I realized that there was a biochemical process at work when honey is heated that transforms hexoses into hydroxymethyl furfuraldehyde. As such, there the question and its answer would be relevant from a biochemistry. I have edited the question to bring it more in line with a question on topic for Biology S.E while trying to maintain the question the OP was trying to find out which is what makes heated honey toxic and is honey in tea safe to drink.

Nice edits @AMR

Heated Honey and HMF
In this paper, Studies on the physicochemical characteristics of heated honey, honey mixed with ghee and their food consumption pattern by rats, by Annapoorani, et.al.;International Quarterly Journal of Research in Ayurveda, 2010 Apr-Jun; 31(2): 141–146.doi:  10.4103/0974-8520.72363, the report finds a statistically significant increase in the compound hydroxymethyl furfuraldehyde (HMF).
The compound was studied by the National Toxicology Program of the U.S. Department of Health and Human Services in Mice and Rats and the results were published in a report dated June of 2010.

5-(Hydroxymethyl)-2-furfural is formed when reducing sugars such as fructose and sucrose are heated in the presence of amino acids. 5-(Hydroxymethyl)-2-furfural is ubiquitous in the human diet and occurs at concentrations greater than 1 g/kg in dried fruits, caramel products, certain types of fruit juices, and up to 6.2 g/kg in instant coffee. 5-(Hydroxymethyl)-2-furfural also occurs naturally and has been identified in honey, apple juice, citrus juices, beer, brandy, milk, breakfast cereal, baked foods, tomato products, and home cooking of sugar and carbohydrates.

- NTP toxicology and carcinogenesis studies of 5-(Hydroxymethyl)-2-furfural (CAS No. 67-47-0) in F344/N rats and B6C3F1 mice (gavage studies).; Natl Toxicol Program Tech Rep Ser. 2010 Jun;(554):7-13, 15-9, 21-31 passim.
HMF is a breakdown product of Fructose, Glucose, and Cellulose (hexoses) and is found in many products, especially high fructose corn syrup, after heating, and is excreted in the urine. However, it has not been correlated to any diseases in humans (4). In the NTF toxicology and carcinogenesis studies, the conclusions were that

under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in male or female F344/N rats administered 188, 375, or 750 mg/kg. There was no evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in male B6C3F1 mice administered 188 or 375 mg/kg. There was some evidence of carcinogenic activity of 5-(hydroxymethyl)-2-furfural in female B6C3F1 mice based on increased incidences of hepatocellular adenoma in the 188 and 375 mg/kg groups. Administration of 5-(hydroxymethyl)-2-furfural was associated with increased incidences of lesions of the olfactory and respiratory epithelium of the nose in male and female rats and mice.

- NTP toxicology and carcinogenesis studies of 5-(Hydroxymethyl)-2-furfural (CAS No. 67-47-0) in F344/N rats and B6C3F1 mice (gavage studies).; Natl Toxicol Program Tech Rep Ser. 2010 Jun;(554):7-13, 15-9, 21-31 passim.
As is shown in the NTP report and the other sources above, HMF is not only found in honey. It will be found in any product that contained sugar or high fructose corn syrup that has been heated, such as baked goods. The reason you are likely to encounter it in honey is foremost that honey is 70-80% reducing sugars (5) and also that bee keepers often supplement HFCS for actual flower nectar when there is not enough flower nectar available for the bees to use to produce honey.
Toxic Honey
One thing to note is that there are toxic forms of honey, just as there are poisonous mushrooms and edible mushrooms. Honey derived from rhododendrons can contain Grayanotoxin, however it is rarely fatal in humans. If you are buying your honey from a supermarket or a reputable keeper, then there is almost no chance that your honey will contain grayanotoxin.
Why is Honey Harmful to Infants?
The issue with honey is that it can contain Clostridium botulinum spores. If the spores germinate, the resulting bacteria release botulinum toxin.
Botulinum toxin, which is the cause of botulism, is a neurotoxin that causes dystonia, and can be lethal in minute doses (ng/kg doses).
For most adults, the risk of botulism from the spores found in honey is minute. The gut microbiome and immune system proteins such as defensins will prevent C. botulinum colonization, so even if the spores germinate, they will not grow to a critical mass to produce enough toxin to do harm and will be excreted.
This however is not the case for infants less than six months of age. Their microbiome is still developing and their immune system is not fully formed. Also, as they have less mass, it takes a lesser absolute amount of the toxin to cause illness and death.
C. botulinum spores are heat resistant, though they can be killed by boiling (7), which means that the internal temperature of the spore needs to reach >85°C for over 5 minutes. Pasteurized honey should already have had this treatment, however you will still see the warnings to not feed to infants less than six months to one year of age, as commercial heat pasteurization may not kill all of the spores (7).
So unless you are immunocompromised, have no gut microbiome, are an infant less than six months of age, or your boiled water does not stay at a temperature greater than >85°C for longer than 5 minutes, and are using raw honey, then you shouldn't be at too much risk.
Edit
Information has been reorganized to better reflect edit to question.


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Where can you find the quantities of each amino acid of a particular protein or food?
Taking a potato as an example. If I wanted to know how much µg or % of each of it's amino acids there are in 1 gram of pure potato protein, where can I find this information?
Is there a freely accessible database online with these statistics? Or, one that contains something for each protein from which this could be derived? (and if so how?)

you mention as an example a "potato" - I put a link to the USDA database that lists a number of foods and protein sources and the known nutritional info

Both excellent answers so far, I'm a bit short on time so I haven't figured out yet which answer is effectively best to accept, though I've been looking into both, but rest assured there will accept properly and upvote in a day or 2 max.
P.S.: Should I expect much fluctuation in bio-availability of the amino acids for each protein? Or is bio-availability more of a thing to worry about for other compounds and not at all for proteins and amino acids?

The bioavailability shouldn't fluctuate much for the protein, which should be fairly constant for each of the individual amino acids - I can't comment what the bioavailability is for the nutrients other than the macro nutrients (i.e. Carbohydrates, fats, amino acids)

There's a fantastic database available from the United States Department of Agriculture that includes almost 9,000 common foods, including their nutritional information. This database is searchable and available from the USDA Agricultural Research Service. Here is a link for the online searchable database.
Within the database you are able to search for a number of parameters; including, food composition, water content, individual amino acid content, fatty acid and total fat content, vitamins, minerals, phytonutrients, and more! One of the nice things is that you can ask it to rank the foods in order of nutrient composition. For example, ranking all the foods in the database in order of protein content or a specific amino acid (or whatever else you're interested in).
It's a great database, especially for researchers that need a database of trusted nutrient data.

Within the database you can search by nutrient or by food, whichever you are curious about. For example, as you mention in the question, I entered potato and in the second screen shot below you can see the listing of all the nutrients in the potato. These are listed as % weight per 100g of potatoes - with or without the skin.

To get to the amino acid content breakdown, click on Full Report (All Nutrients) at the top.

Which question to upvote between you and Samuel is a brain breaker. The original question was per gram protein, I assume you changed my question to account for foods that contain additional lose amino acids. However I effectively needed per gram pure protein from the food rather than per g of food. Anyhow I've upvoted your question.

@Happy the USDA database gives you both the total amount of protein and the total amounts of amino acids (as well as all the other nutrients) - you can divide one by the other to get amino acid per gram of protein. Now I think I'm confused by what you're saying... ?

Yeah in Samuel's case an additional calculation seems to be also needed so I think I'll just settle on your answer as accepted one.

Original link no longer works. New site seems to be https://fdc.nal.usda.gov/

Go to WolframAlpha and enter 1g potato in the input field:

Then scroll down in the results to Protein and amino acids and click the more button in the top right hand corner to get the following list of amino acids with their compositional values for one gram potato:

you need to know the protein sequence to be able to do this.
Paste the protein sequence into this tool and press 'Compute Parameters'. This will give the percentage amino acid composition of the protein.
http://web.expasy.org/protparam/
Otherwise if you mean 'generic protein from potato' then as a quick google reveals this
http://journals.cambridge.org/download.php?file=%2FBJN%2FBJN12_02%2FS0007114558000271a.pdf&code=829c6412f21656bf0e528452fc6608c7
I am not sure there is a database of amino acid composition of foods
EDIT
Actually I found this resource, might warrant further inspection
http://www.fao.org/docrep/005/AC854T/AC854T00.htm

Good answer, I've upvoted, sadly for example for almonds the amino-acids are expressed only with A: mg/g total nitrogen, which I don't understand how to interpret as it differs wildly from B: mg/100 g food. So I don't have usable data for almonds. Oh and thank you for the cambridge article, interesting to consult it in comparison to the database.


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Does the second law of thermodynamics cause aging?
What is the current understanding as to why organisms age and die? In the following explanation on Ask an Engineer, entropy is not even considered (despite it being answered by an engineer). Unless you consider

accumulation of damage to an organism over time

as a result of entropy ?
In the end, is the eventual death of any organism a result of how the laws of universe? In the paper Aging of the brain, entropy, and Alzheimer disease, the author states that

Increasing entropy, manifest through a complex network of interacting ARCs, is seen as the fundamental driving cause of neural and cognitive decline in the elderly

where the abbreviation ARC stands for age-related changes.

Living organisms are not closed systems, and as far as I am aware, the laws of thermodynamics only apply to closed systems.

Second law of thermodynamic and ageing
The second law of thermodynamic applies to closed system. Organisms are not closed system. The second law of thermodynamic is a fundamental principle of our universe and any biological processes do follow the principles of physics. However, stating that biological ageing is (partially) caused by the second law of thermodynamic suggests a big misunderstanding of what the second law of thermodynamic is.
To have a better understanding of the second law of thermodynamic, check up the wikipedia article or one of the many other sources of information on the subject and ask questions on Physics.SE if needed.
Ageing and its evolution
The evolution of ageing (or senescence) is a big subject and has already been subject of a large number of questions on Biology.SE. Have a look at the questions tagged . Below are two examples of post that will interest you:

Why do we age? or Do we have a theory of senescence?
Why does evolution not make our life longer?

There is also a wikipedia page on the evolution of ageing.
Note btw that biological immortality and negligible senescence do exist.