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Does the cell have a mechanism to determine DNA sequence from protein?
Something like a reverse genetic code.

No. Why would it need to?

@MattDMo - That's the answer. Post it as such.

For the same reason some bacteria introduce foreign, viral, DNA into their own genome.

@TMOTTM I'm not sure I understand your reasoning. Some bacteria integrate foreign DNA into their genomes as a means of testing defensive mechanisms and evolving in a rapidly changing environment. I still don't see any possible reason to "reverse translate" a protein, for the reasons Remi.b and I discuss below - the number of possible mRNA or DNA sequences per protein sequence is absolutely astronomical, and would do the organism no good at all, as it wouldn't be codon-optimized. I simply don't see a reason for doing it.

Sure, the number of possibilities are astronomical. The cell has various mechanisms to proof-read DNA, still, certain proteins get translated wrongly and are over-active --> for this protein, the proof-reading at DNA level fails.

"Reverse translation"
Translation is the process by which an mRNA is "translated" into a protein.
It is impossible to get the exact DNA sequence from the protein sequence because a large number different DNA strands could code for the exact same proteins. In other words, there is a loss of information in the translation process. See codon redundancy and I am not even talking about introns and UTR.
Now, it is theoretically possible to get one of the large number of possible DNA sequence from the protein sequence. I am not aware of any natural process that does this job.
"Reverse transcription"
Transcription is the process by which DNA is "transcribed" into a mRNA.
It is possible to get the DNA sequence from an mRNA. And it just so happen that such process does exist! A "reverse transcription" if you want. The enzyme that does this job is called reverse transcriptase. Reverse transcriptase is mainly found in retro-viruses but there are a number of non-retro viruses that have a reverse transcriptase.

"several different DNA strands could code for the exact same proteins." I think you're dramatically underestimating here. A polypeptide 400 AA long could conceivably correspond to exponential numbers of possible DNA sequences when you calculate the number of alternatives at each and every position. "Several" just doesn't cut it.

Ha ha, yes indeed. I replaced "several" by "a large number".

A Reverse Translatase, if it was discovered, would be the biggest discovery in biology (maybe in science generally?) in the last 30 years. We would LOVE to be able to treat proteins as strings of information in the same way as we do nucleotides.
But there are good theoretical reasons why it's unlikely. As already mentioned above - the RNA->protein map isn't unique, so the enzyme would only give you one possible mRNA for the protein. But there are bigger issues. DNA, and to a lesser extent RNAs, all have pretty similar physical properties regardless of sequence. proteins really, really don't. Any enzyme going from protein to RNA would have to be ridiculously complex and versatile (much more so than the already bewildering ribosome), to disassemble the almost infinite varieties of protein. Moreover proteins almost always get further modifications that aren't clearly encoded by their RNA sequence - they get chopped up, bonded to themselves, and have extra chemical groups, sometimes big ones, stuck on.The map from RNA->protein is really, really complicated. And this is kind of the point of proteins.
Going from DNA to RNA or backwards is like converting between the master copy of a blueprint, and the working copy used on a building site. It can be done almost perfectly. Going from protein to RNA is more like going from the building itself to the blueprint. The difficulty of the problem is of a completely different level.

I understand. But assume, the protein was first partially degraded.

What is involved  in making a specific antibody to a specific antigen? The immune system recognizes an unfamiliar epitope on a molecule and a dance of enzymatic activity begins where V and J gene segments are cleaved and spliced, d-nucleotidyl transferases may insert nucleotides in V and D segments, with as many possible choreography as there are possible antibody specificity. The master choreographer for all these possible scenarios must by necessity reside ultimately in our germ cell line. Ultimately, even if some predisposed somatic mutations take place, we must assume that this ability to respond to any antigen, even the myriad of synthetic antigens created in modern laboratories, is inherited. And therein lies the problem.
Back in 1976, I wrote the following to Dr. Marvin Fishman, one of the pioneers in Immune RNA research at St Jude Children Research Hospital:

It is hard to conceive how genes for antigens that had yet to come
  into existence would have been preserved through eons of evolution
  since there would be absolutely no natural selective pressure to
  insure their continuation in the germ line. One possible mechanism for
  the generation of antibody diversity is the formation of informational
  RNA in certain specialized cells in response to a given antigen and
  the distribution of this RNA to other cells involved in the immune
  response. Your work has shown the existence of I-RNA and its
  informational role. Its mechanism of formation is not yet known. It
  seems unlikely to me, for reasons stated above, that the macrophages
  responsible for making I-RNA carry this information in their genome.
  It would have been evolutionarily simpler to develop an enzyme system
  capable of making the appropriate I-RNA when it comes in contact with
  the Ag in question. This system would only have to provide information
  for the combining site of an immunoglobulin. Once this piece of RNA is
  made, it can be incorporated into the macrophage’s genome by the
  reverse transcriptase at the appropriate site and then the information
  for a whole specific immunoglobulin could be released through
  transcription. This hypothesis can be checked by adding an inhibitor
  of the reverse transcriptase along with the antigen. This should
  prevent release of I-RNA capable of coding for a whole Ab in a cell
  free system. Actinomycin-D would also inhibit the release by the
  macrophages of I-RNA...

What I was proposing to Dr. Fishman and all of my professors at the time was the existence of “Reverse Translatase”, an enzyme that could read the epitope site of a foreign protein and encode the proper nucleic acid sequence that would then become the template on which the amino acid chain that would constitute an anti-epitope could be assembled. At this point, let me provide a little background on Immune RNA.
It was found that a percentage of macrophages from peritoneal exudates, induced by injection of mineral oil into the peritoneal cavity of mice, incubated in vitro with antigens the donor animals never came in contact with, could process these antigens and elaborate specialized RNA that could transfer immunity. The first hints that macrophages played a crucial role in antibody production came in the late 50s when Fishman et al. showed that antibody production to a specific antigen could be initiated in vitro in lymph node fragments after their stimulation with cell free extract from macrophages that had been incubated with the antigen in question. It was shown that adding the antigen itself to these fragments initiated no response. Only the extract from the macrophage-antigen soup elicited a response. Furthermore, treating this extract with RNase before adding it to the lymph node fragments totally destroyed its capacity to stimulate antibody production in those fragments. Immune RNA was born. Later the standard experiments were conducted with spleen cell cultures mainly instead of lymph node fragments.
It seems to me that the most economical system that could have evolved is the capability to process antigens with a Reverse Translatase system of enzymes that would then transmit information that would be incorporated in the hypervariable or combining site of a specific antibody. This new RNA could then be inserted in the appropriate gene segment of B cells via Reverse Transcriptase that would henceforth become memory cells capable of a secondary immune response. It would be a much more efficient and more easily attainable way for nature to achieve specificity rather than the cleavage, splicing and recombination of gene segments in a predetermined choreography with a billion variations. A few experimental facts that were known in the 70s on the elaboration of I-RNA seem, if not confirm, to at least suggest such a hypothesis.

The addition of Actinomycin D, rifampicin or dimethylrifampicin inhibit the formation of I-RNA by these specialized macrophages indicating the need for RNA polymerase and Reverse Transcriptase activity for its formation. This is what one would expect if a new nucleic acid chain was formed by reverse translation and then had to be incorporated into the macrophage’s genome before a completed I-RNA could be transcribed.
And this is a most important point: the formation of RNA-antigen complexes that is found in those peritoneal exudates macrophages as a precursor to the completed I-RNA strands was not inhibited by either Actinomycin D or rifampin suggesting that the RNA formed in those complexes during the antigen processing phase was not transcribed but formed in another manner, perhaps by Reverse Translatase.
The ability of I-RNA to stimulate antibody production in spleen cell cultures is not inhibited by Actinomycin D nor rifampicin indicating clearly that there is no need for transcription of any gene for the antibody produced. The information for the whole antibody must be completely contained in the I-RNA.

So the evidence suggests that some antigens are first sequestered by a specialized sub-population of macrophages that process them by first forming RNA-antigen complexes. That RNA does not need to be transcribed from any gene region since its formation is not blocked by inhibitors of RNA polymerase, but is perhaps elaborated by a Reverse Translatase that probably makes up the major protein component of those complexes. The next step seems to be incorporation of that RNA into a gene region by reverse transcriptase and then transcription of the complete strand of I-RNA. This I-RNA is released and picked up by B lymphocytes that can then initiate an antibody response. Once this I-RNA is incorporated in the appropriate gene region of the B cells by reverse transcription, they become committed memory cells capable of a more rapid secondary immune response if stimulated again by the antigen.
Proof of the existence of such an enzyme would be in RNA-DNA hybridization studies. If one could extract the RNA from the RNA-protein complexes that seem crucial as a precursor to the formation of I-RNA in those specialized cells and show that it would only hybridize with DNA from V or D gene segments of committed memory B cells but not unsensitized B cells from the same donor, it would be a powerful argument for the existence of reverse translation. An assay for such an enzyme or enzyme system by demonstrating uptake of an appropriate tritiated nucleic acid could also be attempted. Its most likely source, if it exists, would be those RNA-protein complexes found in peritoneal exudates cells exposed to antigen.

Can you please format your answer by including paragraphs? At the moment this is very hard to read. Additionally please also add some references.


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autosomal recessive population numbers
This question is background research for a science fiction / fantasy novel, my knowledge of genetic is very basic.
It seems obvious to me that for genetic disorders that are autosomal recessive, if those disorders prevent affected individuals from reproducing, the carrier and affected rates in a population will naturally be smaller. I'm not sure if this is the entire reason why say, blue eyes are more common that cystic fibrosis, but it definitely seems to be a contributing factor.
My question is this: say you have a (fictional) autosomal recessive trait that does not prevent reproduction. Let's call the initial carrier rate in the population for this trait C and the initial affected rate A.
In case it matters, the fictional trait I'm considering might reduce the chance of reproduction (as the people may be shunned, or considered less desirable as a mate) but there is nothing preventing reproduction. Something like "bright purple hair" where there is a stigma against affected individuals -- "your hair marks you as tainted" or something. I'm thinking A is around 0.1% (1 in 1000 births). (And if I understand the math right, C would then be around 6%, or 1 in 16 -- so that C * C / 4 gives A.)
Now let's say an oppressive government decides to prevent all affected individuals from reproducing (but carriers are left alone). Let's assume a 100% success rate for the government at rendering affected people infertile thus preventing their reproduction. What will happen to C and A over time? Is there some simple way to estimate how they will trend over several generations?
I don't need exact numbers but I'm having trouble with even coming up with a guess.

Welcome to Biology.SE. I am not sure I understand your C and A correctly. Is it true that C+A=1?

Sorry @Remi.b, my terms come from common stuff like literature given to family members of babies born with a genetic disorder (I have some personal experience there). C is what they call the "carrier rate", the proportion of the population that is a carrier. I'm not sure if "affected rate" is a real term, but I mean the proportion of the population born with the disorder.

Oh ok... so any individual that carry the recessive allele counts in the frequency C regardless of whether it has the disease, is that right? Btw, red hair is not a disease, as you said they can procreate!

Oh so maybe the terms I used like 'carrier' are more appropriate to disorders/diseases? I thought they were generic enough to apply to any trait!!

Um, hmm yes I think individuals with the trait do count as part of frequency C. But if it made explanation/calculation easier it would be fine if you want to redefine the terms so that C does not include the "affected" individuals.

In population genetics, with a simple one-locus two-allele model, we consider the frequency of the two alleles to be $p$ and $q$ where $p + q = 1$ (and thus $1-p=q$ and $1-q=p$). When an allele is recessive it is only expressed at the phenotypic level when the individual carries two copies of the allele.
Following from your example, gene $A$ might be responsible for hair colour, with alleles $A_1$ and $A_2$ where $A_2$ is a recessive allele responsible for purple hair. I will denote the frequency of $A_1$ with $p$ and frequency $A_2$ with $q$. This means that the frequency of individuals with purple  hair ($f_{A_2A_2}$) is $q^2$ and the frequency of people with not-purple hair is $p^2 + 2pq$ (assuming an idealised population). As such, a population of 500 diploid individuals* where there is 100 copies of the $A_2$ allele would have the following genotypic (& phenotypic) frequencies:
$$f_{A_1 A_1} = p^2 = 0.9^2 = 0.81$$
$$f_{A_1 A_2} = 2pq = 2 \times 0.9 \times 0.1 = 0.18$$
$$f_{A_2 A_2} = q^2 = 0.1^2 = 0.01$$
So the allele for purple hair would be present in 19% of the population, but the trait would only manifest in 1% (only ~5.3%, $\frac{1}{19}$, of the people that carry the purple hair allele exhibit the trait). Therefore selection would be quite inefficient at removing this allele from the population, even if you could prevent all purple-haired individuals from reproducing. To find the frequency of $q$ required to give a genotypic/phenotypic frequency where 1 in $x$ individuals have purple hair just take the square root of $1/x$. E.g. to get 1 in 1000 individuals expressing purple hair
$$q = \sqrt{q^2} = \sqrt{(1/1000)}$$
What does this mean for evolution? Alleles that are recessive deleterious are very hard to remove from the population because, at low frequencies, they rarely produce the detrimental effect. Assuming complete dominance ($A_1 A_2$ = exactly like $A_1 A_1$), denoted by $h = 0$, selection only acts on $A_2 A_2$ homozygotes. The frequency of the $A_1$ allele increases at the rate $1/(1-sq)$ where $s$ is the relative fitness advantage. Mutation can also introduce more copies of the $A_2$ allele to the population such that there will be an equilibrium, balanced by the rate of loss due to selection, and rate of gain by mutation. Furthermore, to further build on your analogy, a neighbouring population, where purple-hair is not selected against, may bring copies of the allele in by migration.

Suggested further reading on evolution here and reading on eugenics would likely be of interest to you.
* 500 diploid individuals = 1000 gene copies. Thus $q = 100/(500 \times 2) = 0.1$

That helps immensely. And even better, one of your links led me to find the free PopG program which seems to provide a way of exploring these values over time, while doing the calculations and graphing for me!

Just noted a couple minor correction -- in the third equation I think you mean q-squared not p-squared is 0.01. (sorry I don't know how to write equations)
Also after you define the rate 1/(1-sq), I think you meant "where 1-sq is the relative fitness advantage" but I'm not sure.

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mVenus fluorecent protein, life time? luminosity?
If fluorescence proteins get excited by radiation, how long does it usually take for the excitation to decay (at room temperature)?
I guess, if the life time is too long, the luminosity will be very low. Do you know something about how luminous the fluorescence can be?

what exactly you wanna know? Life-time of fluorescence is on the order of nano seconds

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When do 3 germ layers form in embryo? And why is there only one mature egg formed?
During the process of pregnancy, when do the 3 germ layers form in embryo? Is it after formation of gastrula? Also, during oogenesis, why does only one mature egg form? Why don't use polar body egg instead? During oogenesis, is there a crossing over occurring? If yes, at which stage?

This seems more like a homework question, but still I answered it because the second part of the question (polar body egg) is rather interesting.

I'll bifurcate the question and answer each part one at a time.
Germ layer formation: Gastrulation is a phase early in the embryonic development of most animals, during which the single-layered blastula is reorganized into a trilaminar ("three-layered") structure known as the gastrula. These three germ layers are known as the ectoderm, mesoderm, and endoderm i.e. the layers are formed with gastrula, or simply gastrula is the structure which contains these 3 layers.1

Polar body egg: Polar bodies generally don't have the ability to get fertilized as they are just residual parts of oogenesis. They are formed just to maintain haploid number in oocyte, so they don't even get sufficient amount of cytoplasm to survive (most of the cytoplasm is given to oocyte to provide nourishment to embryo). So they apoptose and disappear, but in some cases (like this), they are considered important and can even lead to unusual phenomena like polar body twinning, in which twinning occurs when the egg cell and polar body are both fertilized by separate sperms.2.
Cross over: In oogenesis (or specifically, ootidogenesis), cross over occurs during the conversion of primary oocyte to secondary oocyte and first polar body. Meiosis I of ootidogenesis begins during embryonic development, but halts in the diplotene stage of prophase I until puberty. For those primary oocytes that continue to develop in each menstrual cycle, during puberty, synapsis occurs and tetrads form, enabling chromosomal crossover to occur. As a result of meiosis I, the primary oocyte develops into the secondary oocyte and the first polar body.3
(In mammals, the first polar body normally disintegrates before dividing, so only two polar bodies are produced.)
References:

https://en.wikipedia.org/wiki/Gastrulation
https://en.wikipedia.org/wiki/Polar_body
https://en.wikipedia.org/wiki/Oogenesis
Polar bodies—more a lack of understanding than a lack of respect
Rare Forms of Twinning


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Is saturation of olfactory cells able to create a feeling of another odour when it stops?
I'm looking for at least one scientific study about how odours could impact human olfactory system and create some phenomenon that could be loosely compared to retina remanence.
As an example, with standard eyes, when you look at a cyan area for a long time and then look at a white paper, the paper looks yellow for a while (see some fun experiments here). This seems to be called an afterimage.
In the type of study I'm looking for, if it exists, the olfactory cells would be involved instead of the retina.
Being exposed to a strong odour for some time would make the subject smell an other odour (a complementary odour?) when the strong odour disappear even if nothing casts this new "complementary" odour to the nose. We could call this an "afterodour" or a "complementary ordour".

The problem with odors is that no known odorant hits only one olfactory receptor. A saturating concentration of compound X for receptor A might be saturating another receptor B, but not receptor C. If you now decrease the concentration, receptor A is still saturated, receptor B is only partially activated and receptor C is not activated at all. Since smell is perceived as the sum of inputs from all olfactory receptors, the smell at the different concentrations will be perceived totally different because of the different receptor activation. Exposing a nose to a strong stimulus will always stimulate more than one receptor, so saturation will occur at more than one receptor.
Perception of light on the other hand depends on finely tuned receptors which are specific for a certain wavelength range. Once the receptors were tuned to have few very specific receptors and once they were tuned to have a lot of unspecific receptors. I like the idea but I doubt it can be confirmed in the lab, also I couldn't find any reports supporting, not that this is any proof.

Yes, there is something like an "odor afterimage", at least in rodents. This is the paper:
http://www.pnas.org/content/110/35/E3340.abstract
But have in mind that this phenomenon is quite different from visual afterimages. First, it doesn't depend strictly on "adaptation", because adaptation is a property of the sensory organ, not of the brain. Second, besides all the qualia questions, it doesn't seems to create different olfactory sensations, or a "complementary odour" as you said. One of the reasons for this lack of "complementary odour" is that the complexity of olfactory receptors (simply put, the number of different receptors and their activity) is way higher than that of visual receptors, so, it's not a simply matter of receiving more impulses from the non-adapting receptors than from the adapting ones, as in vision.

Very interesting! Not exactly what I'm looking for, but pretty close subject. I'll try to contact the study authors. Thanks.

No worries. But I believe that, in the end, the answer to your question would be "no". An analogy with the true visual after image doesn't hold water in several aspects, the most important being the white color. The white color is a mix of wavelengths that stimulates equally all the 3 cones. That's why you see red if you look at a white paper after seeing a green color for a long time: the CNS doesn't receive the "white" information because the R cone is adapting. To have the same regarding odour, we'd have to come with a "white odour", a mix of all possible odorants. (continues below)

(continuation) Then, after giving the person just one odorant for a long time, give him/her the "white odour" and check if the odour he/she feels is the same white odour without adaptation (because the saturated receptor, adapting, will be firing less). And I reckon that such an experiment is simply not doable.

Thanks for this comment. Note that I'm not looking for something that says it is real. I'm looking for studies that could either say yes or no. Your answer gives me a lot of tips to head my searches. I'll tell here if I find something.


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Is it possible to make a contagious cure to a virus?
In a TV series I've been watching The Last Ship, - spoiler alert - a scientist develops a cure for himself for a virus, but actually continues to remain a carrier, and sort of weaponizes the virus accidentally, killing 3 billion people. In response, another scientist develops a cure for that virus, a vaccine, and eventually makes that contagious by close contact as well, based on data gathered from the lungs of the scientist that infected/vaccinated himself with the weaponized version.
The science behind this might be totally ridiculous, or potentially realistic / possible I don't know. Is this possible? Can a vaccine / cure to a virus be engineered into a contagious version, to cure everyone in a chain reaction?

Cure or prevention? There are several vaccines that can and do spread, such as the smallpox vaccine (vaccinia)

Arrived at this question looking for the same thing, though from a different TV show - Doctor Who, S02E01, New Earth, in which the doctor cures thousands of infected humans by disinfecting a few, and getting those few    to pass the "cure" on. The way it was actually done was ridiculously unrealistic, but raised an interesting question for me.

There's also this, very directly related to your question: https://www.geneticliteracyproject.org/2015/10/19/tnts-the-last-ship-shadows-ebolavirus-crisis-how-realistic-is-a-contagious-vaccine/

Fun question!
I think that to make a transmissable ("contagious") antiviral vector, you would need to design a virus that can infect people and that codes for something like an antiviral drug compound, which targets specific viral proteins.
As easy as that was to write down in one sentence, I think that execution would be extremely challenging.
Making the anti-virus out of another virus seems necessary to me, as there is little alternative. You would need something capable of efficiently spreading from host to host, that can generate many copies of its therapeutic payload and that is relatively simple to engineer. A virus is the only thing that I can think of that fits the bill.
You could theoretically engineer an antiviral virus that is mostly non-pathogenic to other people, although this wouldn't be perfect. Even if it didn't code for specifically pathogenic proteins, it is a foreign molecule that is likely to raise an immune response, risks integrating into an important location in the host genome and would divert cellular energy to production of its proteins and away from other cellular processes.
Say that you get this to work, that it's minimally harmful to its host and can effectively target the more pathogenic virus, against which you've designed it. What happens when the job is done? Is it still in the host body, pumping out more copies of itself and/or its antiviral proteins? If so, then it could end up causing more damage to the host in the long run, as it uses host resources to fill cells with no-longer-helpful foreign molecules.
Given more thought or time (than I have), you could probably image more ways to tweak the design of this theoretical anti-virus, but as a brief answer, I think that the above considerations can give you a quick idea of what it would take to bring this system from the realm of science fiction to that of hard science. :-)

Can a vaccine be contagious?

Yes.
Most currently used human vaccines are not transmissible. That is to say on vaccinating one individual, the vaccine cannot infect another individual. Oral poliovirus vaccine (OPV) is an exception. OPV is a live attenuated vaccine that replicates after administration (as all live attenuated vaccines do). Unlike other live attenuated virus, the virus in OPV sheds in substantial amounts and can be transmitted from person to person. Transmission is, as with other enteroviruses, fecal-oral, via contaminated food and water, hands or fomites (see Murray Medical Microbiology, Ch 56).
Vaccine derived virus can circulate in communities for some time. This is, in some ways beneficial, because it allows for more broad vaccine coverage and improves herd immunity, but can cause problems. Vaccine derived poliovirus can revert to what we call neurovirulent poliovirus, causing what we call Vaccine Associated Paralytic Poliomyelitis. In the US, we use a formaldehyde killed inactivated poliovirus vaccine (IPV) that does not replicate and is not transmissible. It is less effective at producing an immune response, but cannot cause disease. Strategies for a global move to IPV are an active area of investigation.

Definitely possible, assuming you have access to sci-fi technology.
Consider a virus specifically rigged to produce epitopes (the immunizer) matching pathogenic infections. It has to survive in its host while causing negligible damage and having reasonable access to the bloodstream for immune recognition.
Next, it would have to be extremely specific to a narrow type of cell preferably exposed to the air. Immediate obvious candidate cell hosts are palatal tissue cells - exposed to the air plus reasonable bloodstream access. In this case, full upper respiratory tract is largely a non-starter since it would likely cause constant allergies similar to a rhinovirus.
Minimum damage principle: the most practical approach would be a partial lysogenic cycle where the contagious "antivirus" contents stay in host cells for a limited period of time (after which the foreign DNA/RNA is programmed to destroy itself), creating copies which grow off the surface of the host cell and shed. Preferably the contagious antiviral particles would immediately deactivate themselves on entering a host cell that happens to be strapped for resources (if the concentrations of certain needed materials are insufficient, then deactivate).

The original vaccine was the infectious disease cowpox, which elicts a good enough response from the immune system to smallpox that it effectively prevents the infected from getting smallpox.  It's just not particular contagious among humans.
But it might be possible to engineer a virus which has a very mild disease course, but is antigenically similar enough to something nasty that it provides protection, and is contagious.
But delivering a medical treatment without consent is ethically dodgy.

It turns out vaccinia virus is different from cowpox virus, but it is transmissible, even recently.  Good answer! I'll upvote if you add a reference.

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What's the name of this bug?

A friend of mine found this bug in Germany. He sent the picture and asked if anyone knew what kind of bug it is. Since no one knew and I didn't find anything similar via google search, I decided to ask it here. Since he only sent me the image I can't really give good information regarding size.
So can anyone identify what type of bug this is?

It's the Jedi bug. Do you see the green laser sword?

I would put it in the family of Curculionidae (true weevils or snout beetles). The problem with that is it comprises about 86,000 species worldwide and about 900 in germany. Maybe someone else can narrow it down

@timbernasley that's at least a start and definitely better than nothing.

Do you know if it had fully developed wings? It looks like the head is on the right, and the abdomen is on the left, like Sudachi mentions in his answer below. It looks to me like this might an immature nymph form of a species that undergoes incomplete metamorphosis. That would help narrow down the order of insect.

I'm quite sure that it didn't have fully developed wings. But it's definitely possible that it had some sort of wings.

It looks like it's the other way around to me. More likely a member of Auchenorrhyncha, which includes cicadas and leafhoppers. I say this judging from the leg structure, abdomen shape, and the eyes. It is however missing wings... perhaps they were removed by another organism?
It somewhat looks like Philaenus spumarius, the "meadow froghopper" which is found in Germany. As for the green tail bit, I am not all that sure.


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What were the camels' humps good for back in the polar areas?
I've heard that camels lived in the North America formerly and just in the last few thousands years they've migrated to the hot deserts. Thus they allegedly utilized the adaptations against the cold weather in the tropics.
One of this adaptations have been their humps. Clearly, it is useful not to have a thick fat layer all over your body in the hot weather. (I see it like a neural spine sail (which helps with thermoregulation to the desert fauna).) But how about the polar areas? All the other polar animals don't see to be restricted by the fact they save all the fat under their skin in any way.
So what were the original reason for the evolution of the camels' humps?

Do you have a reference for "Clearly, it is useful not to have a thick fat layer all over your body in the hot weather."?

@kmm I suppose so, since nomads don't wear fury coats, but I think I don't really catch the whole concept, so there is probably a different reason.

In my opinion there might be two reasons why the camel hump (rather than bump) might be one of the adequate adaptations of camels to living in the cold (additional to their flat feet giving hold on both snow and sand and tooth structure, Rybczynski et al., 2012). Both match the humps being fat storages in modern camels.
The first is also provided by Rybczynski et al. (2012):

Their iconic hump(s), containing fat, also may have been adaptive. As seen in high-latitude ungulates today (Parker et al., 2009), fat deposits could have been
  critically important for allowing populations to survive and reproduce in harsh climates characterized by 6-month long, cold, winters.

Note that this refers to the nutritional value of the fat deposits and does not necessarily relate to maintaining body temperature.
The difference to modern camels would be that the fat storage in modern-day camels serves indirect water deposition (water can be easily gained from the fat stored in the humps and storing the water condensed in fat molecules is way more efficient than storing water directly). This relates to the second reason which, however, is more speculative from my part.
Cold - especially in plants - also implies drought as frozen water is not available. This does not need to apply to mammals as they can thaw ice, e.g. by licking. However, this might be critical as the body might lose some temperature during that process. Accordingly, fat storage might already then have been a means to storing water while keeping body temperature.
Alternatively, and maybe even more likely, the camel hump might have undergone a switch in function from storing a food source in archaic camels to storing water in modern camels as both can be achieved with fat deposits due to the chemical properties of fat.

Beat me to it by seconds! Was even going to use the same reference. Well played, sir... :-)

Is there actually a good support for the hypothesis that many of the particular camel features have evolved in a cold environment or is it still just a good hypothesis?

@AlexDeLarge Ok, I have heard about the water acquisition by decomposing the fats. But about the first reason: Surely, fat is used as a nutritional storage in all mamalls but what is the advantage of storing it into a single place? Other polar animals play the opposite strategy.

@Remi.b: I am not a camel expert but as far as I know the paper cited in my answer (and some fossil record papers) is pretty much what is out there. The evidence that ancestors of modern camels evolved in arctic areas seems to be strong. What traits actually evolved in response to cold does not seem to be clear.

@Probably: I don't know. Might be that there is absolutely none. In cases like this, I often think that the contingency of evolution is the most plausible explanation. There is, however, one thing I could think of (again, speculative). According to the cited paper, camels evolved during a warm period - eventually indicating that there were harsh, cold winters but mild summers. Unlike in todays 'always cold'-arctic where a layer of fat is nice, this could have been disadvantageous in the warmer summers compared to a condensed storing in the humps.

@AlexDeLarge Ok, thank you, I'll read the paper and wait if someone comes with a better explanation.


text:
Is there selection against long proteins and long genes?
Background thought
Titin and TTN
Titin is the largest protein in the human genome with 33423 amino acids. Titin is coded by the gene TTN that must be at least $3 \cdot 33423 \approx 100kb$ long. Looking at NCBI entry for the gene TTN indicate that TTN is actually about 240kb long.
Transcription rate
The average transcription rate (Ref.) is around 1.5kb per minute. It therefore takes about $\frac{240k}{1.5k * 60}$ 2.5 hours to transcribe TTN in mRNA. This mRNA then need to be spliced before being available for being translated. Per consequence, I don't think it is possible for translation to happen in the same time as transcription but might well be wrong.
Translation rate
The translation rate is about 8.4 amino acids per second (Ref.). It therefore takes about $\frac{ 33423} { 8.4 \cdot 3600}  \approx 1$ hour to translate the protein. Sure, several ribosome can translate the mRNA in the same time but it still remain that it takes 1 hour to synthesize at least one protein.
Transcription + Translation rate
Assuming translation does not occur in the same time as transcription, the total time to create the first protein of titin is about 3.5 hours.
Half-life
The half-life of a typical human protein is 6.9 hours (Ref.). Intuitively I would expect a negative correlation between mRNA size and mRNA half-life.
Half-life and Transcription + Translation rate
Because the time to produce the first protein is about half the half life, it means that a quarter of every single mRNA that is being produced would never give rise to even a single protein because it would degrade before either before or after translation has started.
It sounds like an important cost and would be surprised if a gene or a protein could be any longer.
Question
Is there evidence of selection against long proteins and long genes?
Are there proteins that are much longer than Titin in other species?
Do I exaggerate the cost it represents, either by not considering that an average rate (such as transcription rate) is not representative of the actual rate for typically long gene/protein or by assuming that it is costly to create tons of mRNAs that won't never be translated?

You are forgetting that there would be a lot of ribosomes on a single mRNA.  Also, there could be multiple RNA polymerases transcribing the gene.

Sure. It still remain that it take 3.5 hours to synthetize the very first protein and I'd expect it to fail 25% of the time.

Let's say it does take 3.5 h to make a single protein from the point when transcription is initiated. However, titin is a structural protein and is not some kind of protein that has to quickly respond to stimuli. Once the protein reaches steady state then it is just continuously made. Imagine a transcription event that started at time t which culminates in the protein production at t+3.5h. Let's say there is another transcription event that started at t+0.1h which will end up making protein at t+3.6h. You are getting a protein molecule at every 0.1h. Do you get my point?

Similarly, there are multiple ribosomes on the mRNA. If it takes 1h for a single ribosome to traverse through the ORF and let's say there are multiple ribosomes on the mRNA placed 0.1h away (convert that to #codons), you'll end up getting a protein molecule from a mRNA molecule every 0.1h.

I think I get this point. I understand that it is feasible to produce proteins at a constant desired rate. It still remain that plenty of mRNA will degrade without being of any use and that plenty of mRNA will degrade during the translation, leaving half synthesize protein that are of no use either. All of this represent a cost that is much more important for a long gene and long protein than for a short gene and short protein. Thanks for your help!

The mRNAs can be quite stable.

Is there evidence of selection against long proteins and long genes?

I am not aware of any such evidence and cursory googling did not reveal studies that researched a correlation between gene selection and gene size. However,  the larger a gene, the larger the probability of a deleterious mutation within said gene so I expect that there is some limit to the size genes can reach and be stable through evolution.

Are there proteins that are much longer than Titin in other species?

To date, titin is the largest known protein

Do I exaggerate the cost it represents, either by not considering that
  an average rate (such as transcription rate) is not representative of
  the actual rate for typically long gene/protein or by assuming that it
  is costly to create tons of mRNAs that won't never be translated?

I really like how you estimated the time cost of producing titin. However, as you already suspect, I believe that you have several flaws in your assumptions.
First of all, the stability of mRNA and proteins varies a lot and depends strongly on their sequences. The half life of proteins can vary from minutes to Years. The Titin protein has a half life of ~70 h.
Similarly, mRNA stability varies from minutes to > 12h. Especially household and structural genes were identified to have mRNAs with long half lifes.
Both protein and mRNA stability is not simply governed by random decay but rather by tightly regulated degradation. For proteins, an example is ubiquitinylation which is a process where certain amino acid sequences are recognized and cause the protein to be ubiquitinylated which in turn triggers the degradation via the proteasome. For mRNA, the secondary structure is crucial since certain loop structures can be recognized by RNAses. Thus average protein/mRNA lifetimes do not help to estimate the actual turnover of a specific protein.

+1 Thanks for your answer, that was very helpful. In addition to confirming what I suspected might go wrong with my quick estiamtions, I especially realized that a random negative exponential decay is not a good model for mRNA decay. I appreciate that you make reference to the mutation (which is of $e^{-uL}$, where $u$ is the mutation rate per base-pair and $L$ the size of a gene in infinite population) as it is likely a much more important factor that the one I brought about in my quick estimations. Thanks

I'd expect that genes with the larger probability of a deleterious mutation would be under the stronger evolutionary pressure. Paper http://genome.cshlp.org/content/24/9/1497.full states that "Longer genes are less likely to produce duplicates and more likely to exhibit alternative splicing".

Related to your questions: one thing that is known is that older genes, meaning genes that appear earlier in evolution are longer than new genes. Also new genes evolve faster than old ones.
So new genes are usually short and tend to get larger with time.
Inverse Relationship Between Evolutionary Rate and Age of Mammalian Genes


text:
Why are treatment periods with antibiotics longer than 1-2 days?
Antibiotics are given prophylactically for several indications (e.g. prior to dental surgery).

Why are the treatment periods for prophylactic antibiotics much shorter than when treating an infection?

Example: Prophylactic antibiotics may be the day before surgery, but in the case of infection, they are often given for 10-14 days.

Is there something different about pre-infection bacteria (or the body) compared with after the infection has set in?
Looking for general concepts here, as I recognize there are many different types of bacteria and antibiotics.

Generally when you have an infection, pathogenic bacteria have colonized a tissue, and you need to keep antibiotics circulating in that tissue long enough to kill all/the great majority of them. To prevent infection, you only need to kill the few that might be able to settle in and multiply (which would lead to infection down the line.) If the antibiotic level is already acceptably high in the target tissue before a procedure, the bacteria will die, not colonize and infect. Is this an adequate explanation?

@anongoodnurse I think your comment answers the question nicely. Why not post it as an answer?

@anongoodnurse In the case of a septic surgery, most infections are localised sepsis, hence I do not think that the main concern is to just prevent bacterial seeding, as they might not need to undergo a hematogenous spread before infection ensues. Not sure though.

@SatwikPasani - It doesn't matter where the bacteria might end up (though some places are more likely than others.) Oral antibiotics generally cover the entire body with obvious limitations. Dental procedures are covered in susceptible patients to prevent hematogenous seeding of a heart valve. Does that answer your question or have I misunderstood your comment?

@anongoodnurse That is a good explanation thanks!


text:
Simple computational biology project for AP Biology class. Ideas?
Our teacher assigned us a project to do with an extremely open-ended prompt and it should be completed within a month.
I was planning on doing something related to computation and evolution in terms of biology although I'm not really sure where to start. I say simple because I'm not a professional programmer, rather, extremely interested in the field and I hope to use this as an opportunity to stretch by skills.
Any ideas on a project or where to start would be greatly appreciated.

Welcome to the site. Unfortunately, Biology.SE is not a forum, and your question is quite opinion-based. From the [help/dont-ask], If your motivation for asking the question is “I would like to participate in a discussion about ______”, then you should not be asking here. However, simple Google searches will turn up plenty of hits for project ideas as well as sites where this type of discussion would be on-topic, such as Reddit or Quora. Good luck!

This could be an appreciated discussion at Reddit bioinformatics. Ask where to start, what are easy to use and quick tools, and how to get something meaningful out of the results.

You can use BLAST or NCBI resources to do an analysis of something like the duplication of a gene in the HIV virus, for example. If you're looking for a place to start, I would recommend just learning the NCBI database resources.

In addition to what Ham Radio suggested, checking out Galaxy might not be a bad idea for doing any sort of computation/analysis that would otherwise have to be done on the command line. In particular, check out tools for sequence alignment (BWA and Bowtie), genome assembly (Velvet, Spades, IDBA-UD), and variant analysis (Freebayes, Mpileup, GATK). Good luck!


text:
Cell cycle-regulated genes and mRNA
I am a mathematician and my knowledge about biology is close to zero. I am reading a bioinformatics paper and I would like to understand a bit more about the biology task they are talking about. I cite here the first paragraph of the paper:

The identification of cell cycle-regulated genes through
  the cyclicity of messenger RNAs in genome-wide studies is a difficult
  task due to the presence of internal and external noise in microarray
  data. Moreover, the analysis is also complicated by the loss of synchrony
  occurring in cell cycle experiments, which often results in additional
  background noise.
  [De Santis, Marianna, et al. "Combining optimization and machine learning techniques for genome-wide prediction of human cell cycle-regulated genes." Bioinformatics (2013): btt671.]

I've searched online for some explanation of this topic and I understand that cell-cycle is a set of events that cells go through for duplicating themselves. I also understand that there are some molecules that are responsible for the regulation of the cell cycle. I know that mRNA is a class of nucleic acid that is responsible for transferring the informations from the DNA inside the nucleus to the ribosomes in order begin the amino acids synthesis. Microarrays are matrices obtained by DNA sequences inside some chip.
What is the cyclicity of mRNA? How is it related to the cell cycle?
I just need a very simple explanation, without any detail, as it is not my field but I am concerned to understand the background.

It is assumed that in order for a cell to divide it must progress through a series of gradual stages. At each of these phases certain proteins have to be manufactured through mRNA and/or modified post-transcriptionally in order to serve an specific proliferative or anti-proliferative role, which overall eventually orchestrates the transit to the subsequent stage.
Conventionally the cell cycle is comprised of 3 "interphase" stages prior to execution of Mitosis itself: G1 (growth, metabolically active), S (synthesis of DNA to duplicate genetic material in preparation for its splitting into two daughter cells), and G2 (gap phase where a numerous of quality control checks are undertaken in the form of surveillance of the newly produced DNA for example to ensure viability of the progenies).
Under these premises, the protein content of a cell at an specific phase is expected to cycle or oscillate in accordance with its requirements, and this is linked to mRNA cyclicity as the most direct responsible process for modulation of protein abundance. It is then related to the cell cycle in the sense that in order to transit from the G1 phase for instance, proteins involved in DNA synthesis will need to be produced, and thus protein factors released for the transcription of those certain mRNAs to take place.
Experimentally such dissection of cell cycle-regulated genes is tricky. Extracting mRNA from pure sub-populations of cells at specific stages of cell division is challenging as the isolation of such cell sub-populations is normally through chemical enrichments and sub-optimal synchronisation procedures. The signal to noise ratio is not ideal under these circumstances.
In brief, the cell cycles through stages in order to divide and such cycling is in itself due to the cycling of certain proteins, the most renown ones are called precisely "cyclins", which are protein markers of cells division. Cyclin D, E, A, B prevail differently at different stages of the cell cycle as a result of the balanced equation of mRNA transcription and post-transcriptional protein modifications (phosphorylation events mark them for degradation for example).
Overall an intertwined and well-coordinated process.
*** EDIT
For a suitable selection of some basic bibliography on the subject, robust sources covering the subject with rigour (less specific and dense than the journal articles I comment bellow) please refer to the following links:

Molecular Biology of the Cell
Molecular Cell Biology
Cell Cycle Regulation
The Cell Cycle Principles of Control

& even a review of the latter here.
HTH

Welcome to Biology.SE - can you add some references to your answer? it would definitely make it stronger!

@VanceLAlbaugh I think most of this is given in textbooks. Ana, you can add a textbook reference or provide wikipedia links wherever you think they are necessary (cyclins for an instance). The OP can refer to these links. You can also give a reference for one of the genes that undergo such changes (p53-Mdm loop perhaps). I think overall the answer is fine.

@WYSIWYG agreed

Thank you so much Ana. Can you indeed give me some reference? Even just the book you studied from is fine

A quick search in <www.pubmed.com> with the desired key words would bring you myriads of examples. For a recent computational article see here: http://bioinformatics.oxfordjournals.org/content/early/2016/05/20/bioinformatics.btw309.abstract

The work on Cyclins and CDKs (cyclin dependent kinases) received a Nobel prize in 2001. http://www.nobelprize.org/nobel_prizes/medicine/laureates/2001/press.html

Another fairly recent article on the subject, this time from a more experimental angle: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4595013/

Now, although textbooks give a glimpse into the subject, the area is still subject of active investigation as some tuning is still required to gain better insight of cell cycle regulation. The basic solid knowledge was mostly achieved in simpler organisms such as yeast. Mammalian cells, and pluricellular organisms altogether, being more complex have proven a challenging target in the field of systems biology.


text:
My BRIG run is suspiciously quick. What is a typical length of time for a run?
I use the BRIG (BLAST Ring Image Generator) program to compare prokaryote genomes. It executes a local BLAST+ and visualizes the results as rings around the reference genome. I downloaded three genomes (~5 million to ~5.5 million base pairs long) from the NCBI to test the application with. It only took 5 to 10 minutes for BRIG to finish. In my personal experience, BLAST is never that fast. Certainly not while comparing entire genomes. I'm also quite sure my computer is not thát fast and changing BLAST parameters doesn't do much difference. The output appears to be good however.
Is my input just small, is my PC better than I know or is it something I'm not aware of?
What would be  a typical time for a run of that magnitude?

Sources:
Website BRIG
Genomes used:

Accession: BA000007.2 GI: 47118301
Accession: AE006468.2 GI: 973795115
Accession: AL513382.1 GI: 30407157

If the output looks correct and there are no errors then it could be perfectly fine. The web versions can take a lot longer because the servers are receiving so many queries.

@James That makes sense. I just got this weird feeling that something, somewhere is not right. This speed doesn't correspond with my own experience at all. I'm used to BLAST runs that take hours and even days while using grid computing. With this input I expected a run-time of at least a couple of hours because I don't have my grid anymore


text:
Is the "freeze response" really a remain of our reptilian past?
I'm looking for any reliable sources relating the common-known human reaction on a stressful situation, humans sometimes freeze and can not move. From some materials found on the internet I got that it is supposed to be a remain from the bugs' playing dead. But it doesn't seem to be an advantageous reaction from the point of view of big mammals.
My explanation is that the brain just can't process the new complex signals. Are there any studies about this topic?

It would be helpful if you posted some of the sources that led you to this question. The "materials found on the internet" might be useful for better understanding your question.

While it's not a solid answer, this article might lead you in the right direction.  If you want a more substantive and scientific read, this article will be a good jumping-off point.

Freeze response is also a part of the fight or flight response. See this paragraph below from Wikipedia:

The fight-or-flight response (also called the fight, flight, freeze, or fawn response in post-traumatic stress disorder, hyperarousal, or the acute stress response) is a physiological reaction that occurs in response to a perceived harmful event, attack, or threat to survival.

This, being enough of a definitiin, does not explain the point in your question i.e. how could the freeze response help our ancestors in some dangerous situation (and thus become evolutionarily helpful)? Its actually quite simple. Let me first explain how the fight and flight responses would've helped us.

For the fight response, imagine a simple situation: a small animal (say, cat) runs towards you to attack you. Now, fight response immediately turns on. Hormones in your body tend to make you feel more powerful and aggressive, so that you easily fight off the cat and make it run away. This would be helpful for someone who would've otherwise done nothing and simply get a couple of injuries from a notorious cat.

In flight response, imagine a simlar situation: you are being attacked by a larger animal (say, bear). You know that you just can't fight with it, but if you run fast enough, you can outrun that bear. Now, flight response rapidly takes over. Hormones, like adrenaline and nor-adrenaline, tend to get more blood to your legs (so that you can run faster), dilate your pupils (so that you can see everything more clearly), etc., everything required for a faster sprint. This would be beneficial for someone who would otherwise not run away and reach a near-death situation.

So, how does the freeze response help? Consider another (last one) situation: you're being attacked by a lion. In this case, you know that you can neither fight with an angry lion nor outrun it. What should you do? One immediate idea would be to play a dead man's role in front of the lion so that (maybe) it will leave you. Of course, it doesn't pay off everytime, but surely it does, sometimes. And in such a case, this would be better for someone who would otherwise either try to fight with the lion or to outrun it. And, obviously, it is a better option for many other organisms too. So it indeed seems that this response developed much earlier in time, maybe even long before first chordates appeared.
With the above part explaining why it is beneficial, one part still remains i.e. how does it work? For this, see the paragraph below:

Studies show that particular connections from the periaqueductal grey (brain region located along the spine) to the pyramis at the base of your skull are integral to the freeze response. When these connections are activated, it causes the body to freeze. They can be activated by things that are actually dangerous and by things that aren’t, so even irrational fears can cause us to freeze. While giving a presentation, you might not actually be in danger, but your body responds like it is and causes you to clam up.

Below are images of the periaqueductal grey in spinal cord and pyramids in brainstem to help you understand their locations.

To conclude, freeze response is not a mere "remain" of our reptilian past, it is still beneficial for us.
References:

https://en.wikipedia.org/wiki/Fight-or-flight_response
https://www.psychologytoday.com/blog/evolution-the-self/201507/trauma-and-the-freeze-response-good-bad-or-both
https://joyable.com/blog/fight-flight-freeze/
https://www.slideshare.net/mobile/dr_ansari2000/the-brain-stem-ii
http://slideplayer.com/slide/4637165/


text:
Standard notation for dominant and recessive allele
I'm reading through some science that could come up in my GRE equivalency.
I've never been much of a biologist, more of a chemist/geologist....though it does interest me massively!
I'm just seeing this question in a textbook....
Q) Assume eye colour in humans is controlled by a pair of alleles of a gene where the allele giving brown eyes is dominant to the allele giving blue eyes. Both parents of a blue eyed man, John, were brown eyed. He married a brown eyed woman, Sara, whose father had brown eyes and mother blue eyes. Sara had a blue eyed sister. John and Sara had a brown eyed child.
Fill in the boxes and circles on the family tree below to show the genotype of each individual.

I just wanted to ask how exactly we mark out genotype in science? Do we use D's and r's?
Thanks!

Conventionally, a pair of contrasting alleles are shown with the first letter of the dominant trait as capital for dominant, and the first letter of the first letter of the dominant trait in lower case for recessive. For this case, it'll be B for brown and b for blue. Someone homozygous for blue would be bb, someone homozygous for brown would be BB and someone heterozygous (brown) would be Bb.

@MalharKhushu -- You should put that in the answer box. :) It's correct AFAIK -- Capital letters for Dominant, lower-case for Recessive, and works fine as long as it's within a Mendelian framework.

Out of curiosity, what is a GRE equivalency?

Thanks, @MCM, but that would require citations, and so on, and for such a short answer, I don't really want to hunt out articles or studies

How can I distinguish between who is homozygous and who is hetrozygous?

So am I right in suggesting that John and Sara's sister are bb?

And both of John's parents are Bb, because they are brown eyed...which is dominant, but clearly they are heterozygous because John has blue eyes.

Thanks for all of the help I've received with this one....I'll have a go!! John's parents are both Bb
John is bb
Sara is Bb
Sara's sister is bb
John and Sara's child is Bb
Sara's mum is bb
Sara's dad is Bb

[H]ow exactly we mark out genotype in science? Do we use D's and r's?

General rule
The general rule is to indicate the dominant allele with a upper-case letter and the recessive allele with a lower-case letter.
The most commonly used letter is the first letter of the alphabet. The two possible alleles are a and A and the four possible genotypes here are therefore aa, aA, Aa and AA. Only aa has blue eyes in your example. Note that it is very common to merge together Aa and aA (that is to not consider whether the A allele was inherited from the father or from the mother) and just call it Aa.
More than 2 alleles OR no clear dominance relationship
It is quite common to use A1 and A2 as well but when doing so, we don't implicitly indicate a relationship of dominance. This notation also has the advantage to be able to deal with cases where there are more than two alleles segregating in the population (A1,A2,A3). Note that in reality perfect dominance is quite rare.
More than 1 locus
When dealing with more than one locus, we generally use A/a for the first locus, B/b for the second locus, C/c for the third etc... However, in general when dealing with several loci, authors don't have identical loci ad therefore they directly name them and use appropriate letters. For example, in models of recombination under control of a modifier locus, the modifier locus can often take the values M and m, while a random linked locus under purifying selection would take the letters A and a.

Thank you, this is so incredibly helpful!!
So brown eyes are dominant over blue eyes

Just to make sure you got it: I am not stating that brown eye allele is dominant over blue eye allele (actually genetics of eye color is a little more complicated). I only described the standard notation used to designate different alleles. That was your question right?

Thanks for this, sorry silly comment by me.
Am I right in suggesting that

John's parents are both Bb
John is bb.
Sara is Bb
Sara's mum is bb
Her sister is Bb
Her dad, is harder to figure out for.....is he BB or Bb and why?
Finally, the brown eyed child is Bb.

I'm assuming that the father is Bb, because amongst his children there is one dominant allele and three recessive

It looks like there were an implicit question in your post about the genotypes of the different individuals. I thought the post was about notation. Next time make sure to make your question clear and to limit your posts to only one question. If it was a homework question you should have used the homework tag too.


text:
Do trees have genes for stopping growth?
Do trees have genetically encoded to stop growing at some height, to keep dividing the cells only to a certain amount, or to pump nutritions only till it's advantageous because they've already overgrown their companions? Or do they just keep growing till they can?
I was inspired by this article, according to which the height limit is about 130 m. Since if the second one was true, it would be possible to grow a 130 m tall tree with enough nutritions.
Also, the evolution of trees wouldn't mean to getting more genes of height, but to use nutrients more efficiently.

mildly related: Why is it beneficial for trees to grow tall?

'Trees' are widely different - are you asking about Redwoods in particular? Also note that the paper is specifically referring to the physiology of Sequoia sempervirens, and tradeoffs in this species, not trees in general. Most tree species cannot grow to be more than 100m, no matter how much nutrients you dump on them.

Yeah, I'm asking about trees in general.

Plants can go through temporary dormant ("perennating") phases i.e.  meristem activity suppressed. As well; a major line of plant cells after certain stage of development, become "permanent tissue" (parenchyma, collenchyma etc.)... i.e. doesn't divide anymore (until they are dedifferentiated by any factor, human or natural). Sclerenchyma, the dead tissue, is a result of programmed-cell-death. So, certainly plants have some genetic machinery to pause or stop growth.

The answer I got from Jan Kolář of Charles University:

Traits of trees like height and mass are a result of the genes and
  environment. The determinative factor for the studied plants and
  animals is a big amount of various genes. When we get to know all the
  functions of all the genes, we should be able to determine the most
  important ones but for now we know just that gibberelin and auxin are
  very important for the growth of the tree, so we'll be looking for those
  genes which control the level of those hormones.
In case of trees, a big part of the height they can grow are utterly
  mechanical factors. The stem and the main branches have to be enough
  strong not to break with their own weight and the roots have to be
  enough firmly rooted in the soil. This limit is determined mainly by
  genes that control the grow of the cell walls, their mechanical
  resistance etc.

also at a certain height it isn't prossible anymore for the tree to transport the water to the top of it

@RickBeeloo If you talk about the atmospheric pressure limit I disagree

Take a look at this article: http://www.nature.com/nature/journal/v428/n6985/full/nature02417.html @Probably

@RickBeeloo Thanks, what's the principle behind this "constrains" (if you have it avaiable)?

What do you mean with "this constrains" which constrains?

In the abstract they say "Current hypotheses of height limitation focus on increasing water transport constraints" which isn't really specific.


text:
After hysterectomy does FSH secretion stop?
This question came in an exam, and my reference book says yes, it does. But it hasn't explained why.
If the ovaries are also removed, then the menstrual cycle should stop. In absence of hormones oestrogen and progesterone, there would be no inhibitory effect on FSH, so its secretion should continue.
Or if it stops, then why?

Strictly defined, a hysterectomy is removal of only the uterus.  But sometimes the ovaries are also removed, depending on the reason for the surgery and age of the woman.
If the ovaries are also removed, there would no ovarian or uterine cycling, true.  But without the negative feedback effect of ovarian steroids (progesterone and estrogen), levels of both FSH and LH would be persistently, abnormally high.  The same happens in postmenopausal women (ovaries still present but no longer producing steroids) and spayed pets.
If the uterus is removed but the ovaries left in, the ovaries would continue to mature follicles that release estrogen, ovulate, luteinize and produce progesterone, etc, etc. Even though there is no uterus for the steroids to act on (and no menstruation), the steroids would feed back to the anterior pituitary gland and FSH/LH levels would fluctuate in the normal patterns.
Without the obvious sign of menstruation, it would be tricky for the woman still with ovaries to know whether or not she had reached menopause.  The first woman (ovaries removed) would be thrown into a 'surgical menopause', an abrupt (and nasty) withdrawal of all ovarian steroids.

Could you add sources (references to papers, books, websites etc.) to allow users to background read on your answer?

It would be better if you could add some sources. I had searched Google, but did not find satisfactory results.

It's been already shown that women subjected to hysterectomy but retaining ovaries reach menopause earlier than intact women, so hysterectomy may have an effect on the secretion and feedback pattern of FSH and LH. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3223258/
If what Heidi says is true, ie "If the uterus is removed but the ovaries left in, the ovaries would continue to mature follicles that release estrogen, ovulate, luteinize and produce progesterone, etc, etc. Even though there is no uterus for the steroids to act on (and no menstruation), the steroids would feed back to the anterior pituitary gland and FSH/LH levels would fluctuate in the normal patterns.", it would mean that steroids acting on the uterus would do their job and get back to the blood stream and exert the feedback effect on the hypothalamus.
What happens after they have entered the uterine endometrial cells to exert their effect? Are they metabolized within the cells? Are they excreted with the deciduous cells during menstruation? If that's the case, the amount of circulating FSH and LH in the blood stream of hysterectomized women would be higher than the average levels of intact women and maybe that's the reason why they experience ovarian failure earlier than expected. Another possibility is that the uterus is not a passive organ, but that remains to be proved. Damage to the ovaries during surgery has been speculated, but giving the same results (early ovarian failure) after key hole procedures (laparoscopy), it seems that's not the case.


text:
What are the binding sites (or receptors) of cortisol?
I am in the process of a OCR GCSE Case Study, and my question is "Do the benefits of anabolic steroids outweigh the risks, which has an obvious conclusion.
I need to know the scientific name, or a scientific analysis of why it causes an increase in protein synthesis,  for the binding of cortisol to understand this quote:"Anabolic steroids may block the binding of cortisol to its receptor sites, which would prevent muscle breakdown and enhances recovery.". For without enough understanding i can't explain it.

might be nice to know what OCR GCSE - would be a good change/update to question

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. What research have you done so far to answer this on your own? What have you found out, and where exactly are you stuck? This is not a forum or tutorial site, we expect you to have done previous research on your own. Google searches and Wikipedia are excellent places to start, as is PubMed.

The intracellular receptor for cortisol is called NR3C1.
http://www.uniprot.org/uniprot/P04150
To my knowledge, a direct (competitive) effect of anabolic steroids on the binding of cortisol to NR3C1 has never been proven. The anabolic effects can easily be explained by other targets. A good starting point for further reading might be this review:
https://www.ncbi.nlm.nih.gov/pubmed/22101547


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Why would a mother reject her offspring if it has been "interfered" with by humans?
There was a recent incident at Yellowstone National Park in which tourists placed a bison calf in their vehicle, and that eventually led to the calf being euthanized.
The National Park Service issued a statement in which they said:

In addition, interference by people can cause mothers to reject their offspring. In this case, park rangers tried repeatedly to reunite the newborn bison calf with the herd. These efforts failed.

Why would a mother reject her offspring if it has been "interfered" with by humans?

Several ungulates and other species such as seals and primates are known to initially use odour to discriminate their offspring. Most relevant work to study this has been done in sheep; sheep are ideal for studying attachment because there are ethical and logistic difficulties that limit laboratory and research use of most other species known to develop selective mother-young social relationships. In addition domestic sheep are common worldwide, easily bred and handled, and well-understood in terms of behavior and natural history, providing a solid base for more intricate study (more information here).
According to this paper ewes are attracted to amniotic fluid for a few hours after birth, which stimulates nuzzling, sniffling and licking behaviour; after a relatively short time she becomes familiar with the lamb's unique odour. Thereafter, lambs without this odour are almost always rejected. After some time the ewes learn to use visual and auditory cues to identify their lambs and smell becomes less important. The Wikipedia article on the subject gives some information about the neurobiology of the process.
From a selective advantage point of view, I would speculate that this would evolve to reduce the risk of being exploited by 'free-loader' genotypes that engage in behaviour similar to brood parasitism in birds (i.e. leaving their offspring to be cared for by other ewes).
This can work both ways; in addition to the risk of disrupting the smell of a lamb by excessive handling, shepherds have recognised for centuries that lambs which are rejected by their own ewe, or whose ewe has an inadequate milk supply, can be fostered by other ewes who have lost lambs using a technique historically called skin-grafting, where a dead lamb is skinned and the skin tied around the foster lamb. The odour is thus transferred to the foster lamb for long enough for the ewe to accept it and become familiar with its visual and auditory identifiers, after which the odour is no longer important. The paper I cited above above describes a study that found that cloth 'stockinettes' could be used in place of a skin to achieve the same outcome.
edit: Interestingly, the responses to this question at skeptics.SE suggest that the popular notion that odour-based attachment results in abandonment following human interference with birds is probably untrue.

I know that in at least some species  of birds it is untrue.

Actually, once humans or any other animal touches the infant, especially before the mother has recognized it as its own, the scent of the "foreigner" stays on the infant/offspring. Thus, the mother does not recognize the infant or believes it to be "tainted". This is true for a lot of birds as well as wild animals. If anyone "disturbs" the bond- forming during parental care of the newborn, the newborn is often abandoned by the parents.


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Extraction of arthropod embedded in animal tissue
I'd like to extract an ectoparasite from a biopsy of animal skin for subsequent identification. The mite is small, about 100 um, and embedded in a column of tissue. It's too small to manually excise under magnification. Currently preserved in 70% ethanol.
Ideally I would isolate it by loosening or dissolving the surrounding tissue without destroying its features. I'd like to conduct a visual inspection prior to sequencing for species identification. Specific suggestions and techniques welcome.
See photo:


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Why is flash light harmful to what aquatic life forms?
When visiting an aquarium, it's often not allowed to take photographs with a flashlight on. It is said that the flash light with very high intensity is harmful to the displayed life forms.
I respect that and try to capture images without flash.
I'd still like to know how flash light interacts with the animals (or even the plants) in an undesirable way? Is it harmful because they are not used to it?
The light emitted from the arc of a welder for example is so intense, that it destroys the human eye. Laser is another example. Technology is so advanced that we can produce harmful light sources that not even the winking reflex can protect us against. Maybe a flashlight used for photography is the welding arc for aquatic life?
Additional light can increase growth of algae, which would in turn influence the (very little) ecosystem in an aquarium. On the other hand, I don't think the short bursts of light from photographic flashes introduce enough light to have an impact. Or do they?
The motivation for this question is not to be knowledgeable about what creatures are not harmed by flash in order to fry them in light. Advancements in camera technology make it unnecessary to add more light to the scene in the form of flash light. What made me curious about it is that except for the industrial light sources mentioned above, we rarely consider single bursts of light to be dangerous for us humans. We are much more concerned about the continuous sunlight.

I am sure the main reason is that flash lights, certainly in a dark aquarium, are very frightening and might cause temporary blindness for the animals. If someone flashes in your eyes, you can't see for a few seconds as well. That will cause distress for the animals and distressed animals live considerably shorter.
The total amount of light is indeed much to small to cause algal growth and real blindness is not likely from camera flashes.
EDIT:
I've found this article that will certainly be of interest to your question.


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Given the number of individuals who have a recessive disorder, how can one calculate the probability that the disorder was inherited?
Just to be clear, this is not homework.
Suppose a biological family has five children, two of whom have a certain recessive genetic disorder that is not sex-linked. The parents themselves do not have this disorder.
I want to estimate the probability that the parents are carriers. How can I do that, short of getting this probability directly from a lab study?
This problem appears to be where Bayesian statistics can help. All I need to know is:
1) the probability of the parents being carriers, given they don't have the disorder, but 2/5 of the children do.
2) The probability of the parents being carriers
and 3) The probability of the children having the disorder.
3 I can probably find without too much effort. #2, I'm guessing, is a Hardy-Weinberg problem - I just need to find the relevant statistics for people of the parents' backgrounds. But I have no clue how to start with #1.

You should read the homework policy. You will understand why I have voted to close as homework.

Assuming...

The parents are the real biological parents (no cheating allowed!)
There is a purely dominance/recessivity relationship between the alleles and no individual can express the disorder without being homozygous for the disease causes allele
De novo mutations for the disorder are rare enough to be ignored in the calculation of this probability
Trisomy and monosomy is not involved

, then the two parents must necessarily be carrier (both of them) as long as at least one of their children express the disease.
Note, by the way that some of the above assumptions are too strict and could be partially released.

This question does not require any complicated bayesian statistics (or any statistics at all) or any use of Hardy-Weinberg rule. If a children expresses a purely recessive disease, then (s)he is necessarily aa, where a is the recessive allele and A is the dominant allele(s). It means that both parents must have at least one a. Because, no parents express the disease, both parents are necessarily Aa (or aA)

Suppose assumption #2 is untrue for this particular disorder. Then, what statistic would I want to look at?

We can reduce assumption #2 to "if no individual can express the disease without being aa". If this assumption hold it is fine, you are sure that both parents were carrier. I edited assumption #2. Other assumption can eventually be further reduced or specified.

I still don't understand. Mutations cause the alleles, and a recessive allele can only express itself if a dominant allele is not present. Thus, if we're talking Mendelian genetics, then it is biologically impossible for assumption #2 to be false. I suppose I'm getting something wrong, though, aren't I?

I don't really understand what you misunderstand! Assumption #2 says that if an individual is sick (express the disease), then this individual must be aa. We can imagine a case where there are some Aa individuals that would express the disease if they smoke a lot for example. All the assumptions are probably assumptions you wanted to make to start with.

Why dont hemophilia follow these steps? The father has no diagnosis of hemophilia and the  mother can only be a carrier yet show no symptoms of a hemophilac. The child could only be a male with no x chromesome from the father because he recieved two y's from the mother, even without any family history of hemophilia the mutation is said to be spontaneous or inherited and the new adult version where it comes out of dormancy in males of 40 years of age for the first time.

@moonman239 I think assumption two is just stating that the disease is only genetically determined and that the dominance is complete. One can not get the disease by exposure to an environmental factor for example.

@Remi.b is that a correct interpretation of two?

@rg255 yes it is correct. I guess I did not need to state these assumptions as every body make them implicitly in introductory courses to genetics and now it is confusing the OP :) I merged assumption #1 and #2 hopefully that may help.

What if the allele that causes the disorder is not purely recessive? Does such an allele exist in the human population?

Yes they exist. Often the relationship of dominace is not perfect. Some disease are even caused by dominant alleles such as Huntington's disease for example


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Species Identification: Snake, New Mexico
The snake is about one and a half inches in diameter at its widest, a half inch at the head, and about two feet long. I found it in central New Mexico. It's hard to see the head in the pics, but it wasn't triangular or any bigger than the body/neck

did you notice whether the snake was a fast mover?

@rg255 yes, very fast

Coachwhips seem to be noticeably fast

You can tell from the head that it is definitely a coachwhip. They have big eyes compared to most snakes.

It's difficult because the image quality is low, but there are some key features that can be made out which suggest it to be a Western Coachwhip, or "Whip snake", Masticophis flagellum testaceus.
There is not a huge number of species in New Mexico, and most have quite clearly different patterns and coloration, which brings it down to just a couple of species. With respect to colour and pattern, the main candidates are Western Coachwhip, New-Mexico Ridge-Nosed Rattlesnake, Mojave Rattlesnake, and Prairie Rattlesnake.
We can rule out the rattlesnakes because of the shape of the pupil; like most poisonous snakes, the rattlesnakes all have a "cats-eye" pupil, while in the second picture of yours it's fairly clearly a round pupil, which is a feature of the Western Coachwhip.
The slender head is a very telling feature that suggests Coachwhip.
The length is also about right (I'm going to suggest though that the one in your photo is perhaps more than 2 feet/60 cm - it looks bigger to me using the surroundings as relative measures); Coachwhips are in the region of 1-2 metres (3-6 feet) when fully grown.
The range is also perfect for the Western Coachwhip, though Sonoran Coachwhips are also found in southern areas of New Mexico. However, you list this as central New Mexico, so that virtually rules them out.
It seems, given that your picture is in the daytime, that it is diurnal (unlike many species in New Mexico which are nocturnal).

I'm bad at estimating length, thinking back, it's very possible it was closer to 3 feet or a little more

From the picture on your link to nmherpsociety.org, it's definitely the Western Coachwhip. I didn't even know we had these snakes here. Thanks for the research and the answer!


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When was the first exception to Mendelian genetics discovered?
In addition to the question in the title, I'd like to know, how scientists reacted to the exceptions?

Before Mendel? e.g. Galton. When Mendel was rediscovered by de Vries et al. they immediately found that Mendel's phenotypes weren't quite Mendelian.

The first exception to Mendelian genetics was probably discovered by Mendel.  As a followup to his pea experiments, Mendel used hawkweed, in which his rules do not seem to apply due to some unusual aspects of hawkweed development; see Apomixis in hawkweed: Mendel's experimental nemesis for details.
Mendel eventually abandoned his biological experiments, and though the main reason was probably his increasing other responsibilities, his thousands of apparently-unsuccessful experiments with hawkweed may have contributed.

I would say that first exception might be White gene in Drosophila Melanogaster, described in 1910 by Thomas Hunt Morgan and Lilian Vaughan Morgan. At least, is the first exception we study in genetics since sex linkage its so fundamental. These experiments established the chromosomal theory of inheritance.

Thomas Hunt Morgan, an embryologist who had turned to research in heredity, in 1907 began to extensively breed the common fruit fly, Drosophila melanogaster. He hoped to discover large-scale mutations that would represent the emergence of new species. As it turned out, Morgan confirmed Mendelian laws of inheritance and the hypothesis that genes are located on chromosomes. He thereby inaugurated classical experimental genetics.
After breeding millions of Drosophila in his laboratory at Columbia University, in 1910 Morgan noticed one fruit fly with a distinctive characteristic: white eyes instead of red. He isolated this specimen and mated it to an ordinary red-eyed fly. Although the first generation of 1,237 offspring was all red-eyed but for three, white-eyed flies appeared in larger numbers in the second generation. Surprisingly, all white-eyed flies were male.
These results were suggestive for hypotheses of which Morgan himself was skeptical. He was at the time critical of the Mendelian theory of inheritance, mistrusted aspects of chromosomal theory, and did not believe that Darwin's concept of natural selection could account for the emergence of new species. But Morgan's discoveries with white- and red-eyed flies led him to reconsider each of these hypotheses.
In particular, Morgan began to entertain the possibility that association of eye color and sex in fruit flies had a physical and mechanistic basis in the chromosomes. The shape of one of Drosophila's four chromosome pairs was thought to be distinctive for sex determination. Males invariably possess the XY chromosome pair (Morgan used a more cumbersome notation) while flies with the XX chromosome are female. If the factor for eye color was located exclusively on the X chromosome, Morgan realized, Mendelian rules for inheritance of dominant and recessive traits could apply.
In brief, Morgan had discovered that eye color in Drosophila expressed a sex-linked trait. All first-generation offspring of a mutant white-eyed male and a normal red-eyed female would have red eyes because every chromosome pair would contain at least one copy of the X chromosome with the dominant trait. But half the females from this union would now possess a copy of the white-eyed male's recessive X chromosome. This chromosome would be transmitted, on average, to one-half of second-generation offspring—one-half of which would be male. Thus, second-generation offspring would include one-quarter with white eyes—and all of these would be male.
Intensive work led Morgan to discover more mutant traits—some two dozen between 1911 and 1914. With evidence drawn from cytology he was able to refine Mendelian laws and combine them with the theory—first suggested by Theodor Boveri and Walter Sutton—that the chromosomes carry hereditary information. In 1915, Morgan and his colleagues published The Mechanism of Mendelian Heredity. Its major tenets:
• Discrete pairs of factors located on chromosomes like beads on a string bear hereditary information. These factors—Morgan would soon call them genes—segregate in germ cells and combine during reproduction, essentially as predicted by Mendelian laws. However:
• Certain characteristics are sex-linked—that is, occur together because they arise on the same chromosome that determines gender. More generally:
• Other characteristics are also sometimes associated because, as paired chromosomes separate during germ cell development, genes proximate to one another tend to remain together. But sometimes, as a mechanistic consequence of reproduction, this linkage between genes is broken, allowing for new combinations of traits.
Morgan's experimental and theoretical work inaugurated research in genetics and promoted a revolution in biology. Evidence he adduced from embryology and cell theory pointed the way toward a synthesis of genetics with evolutionary theory. Morgan himself explored aspects of these developments in later work, including Evolution and Genetics published in 1925, and The Theory of the Gene in 1926. He received the Nobel Prize in Physiology or Medicine in 1933.

quoted from: http://www.genomenewsnetwork.org/resources/timeline/1910_Morgan.php
see more: http://www.esp.org/foundations/genetics/classical/thm-10a.pdf

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


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Do two compatible tRNA codons bond together?
Can two tRNA with complementary anti-codons link together?  For instance UUU with AAA. If not, why not?

@Ashafix has given an answer to your question which is technically correct, although it relates to artificial conditions rather than cellular ones. Perhaps this is what you are interested in. However I wonder whether you were thinking about such interaction competing with the interaction of the tRNA anticodon and mRNA codon in the cell. If so, you should make that clear so that we can provide an answer addressing that point.

Yes, tRNA can form dimers. For example it was shown that E. Coli tRNA GCC forms homodimers, i.e. two identical molecules interact with each other. In this case the dimerization occurs between the anti-codon loops (what was probably meant with UUU and AAA).
References:

Sequence and structure of naturally-occurring tRNA transcripts and site-directed variants are significant barriers to forming oligomers beyond dimers.
(Harold S. Bernhardt, Warren P. Tate, Advances in Bioscience and Biotechnology, 2013, 4, 1-16 ABB)
Anticodon-anticodon interaction induces conformational changes in tRNA: yeast tRNAAsp, a model for tRNA-mRNA recognition.(D Moras, A C Dock, P Dumas, E Westhof, P Romby, J P Ebel, and R Giegé, Proc Natl Acad Sci U S A. 1986 Feb;83(4):932-6)

A naturally occuring mutation, A3243G in human tRNA(Leu(UUR)), causes dimerization via a motif which is not in the anti-codon loop.
Reference:

Wittenhagen LM1, Kelley SO., Nat Struct Biol. 2002 Aug;9(8):586-90.,
Dimerization of a pathogenic human mitochondrial tRNA.

Link-only answers are generally not acceptable on Stack Exchange sites. The link may change or become unreachable in the future, and without a summary of what the link contains this answer would be useless. Please summarize what is in the link (don't just copy and paste) and use the link solely for reference. If you remove the link and the answer cannot stand on its own, it is not a good answer.

Thanks for the info! I will update the answer later. I thought that giving a reference to a published scientific article would be safe even if the link is dead.

The reference is fine, and while I only skimmed the article it looks like it may be useful for the OP. We (as in the Stack Exchange community) don't like link-only answers as the link may change or die, but also because it requires you to go to another site and attempt to interpret the research (in this case), which may not be possible for some readers  given the level of their scientific education. Just summarizing the abstract should be fine. One question though - it seemed like the paper only talked about dimers, and couldn't find multimers. You may want to change your answer.


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Mechanism by which water flows through xylem
I was doing a Cambridge iGCSE past paper when I came across the question:

Describe the mechanism by which water flows through the xylem

I thought the correct answer would revolve around the xylem being composed of dead cells, thus allowing water to use capillary action to flow upwards, but it wasn't.
Instead, the mark scheme referred only to transpiration causing tension and so forth, not even mentioning capillary action.
Is capillary action not a valid answer? And if not, why not?
Thanks

See http://www.sparknotes.com/biology/plants/essentialprocesses/section1.rhtml capillary action is just a part of the valid answer.

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NO,for capillary action 2 things are of importance 1) the radius of capillary tube[R] ,2)the tension force between molecules at surface of liquid [T] (for water=72.8 dynes/cm= 728 X 10^-6 N)
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height to which the fluid will rise due to cap.effect, H=(2T cosα)÷(ρgR)
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[ρ=density of liq,here water =1000kg/m³]
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numer.=constant(for given liq) denomin.=variable R
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so if capillary was in effect for trees 100s of meters tall the deno. wud have to be small while the ρg is a fixed value here for water = 10000 units the R wud have to be impossibly small

WHAT HAPPENS IS the transpiration of water droplets from the stomata causes a suction as no air can enter to fill in for the water lost the water as to rise up taking more of it from the soil

Could you add sources to your used formulae and reasoning?


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What would kill you first water or cola?
After discussing this with some colleagues, I devised the theory that you could drink more coca-cola in a single sitting than you could water, without killing you.
Defining the volume it would take for one of the liquids to kill you as the 'x volume'.
Thus the hypothesis goes that the x volume for water would be lower than that of coke.
This is based on the notion that water would affect the body's water potential significantly more than the cola solution. For instance, the large volume of water would diffuse, via osmosis, into your blood and this would reduce the water potential of the blood, which would in turn diffuse into your cells which would in turn damage the micro environments and prevent proper enzymatic activity in all aspects of the cell cycle: which would have devastating affects on the brain function. Given enough water: something that can be read about here (water intoxication).
Coca-cola on the other hand which has an acidic pH -- though I'm not entirely sure of it's water potential -- would not have the same disturbance on somatic cells in the body due to the acids and sugars. However, although the large consumption of cola may have longer term effects: would the x volume of coca cola be higher than that of water?

What is the duration of a "single sitting"? There are many other additional factors. You may die of some other effects due to the cola consumption. Without additional details this question cannot be answered.

The LD 50 listed on the wikipedia page you link to is 90 mL/kg, which would be about 6 liters for a 68 kg (150 lb) person. This is consistent with at least one report, where someone died from drinking 7 liters of water in 1.5 hours.
The mechanism by which water kills people is by lowering the amount of ions (chiefly sodium) in the blood. A condition called hyponatremia.
Coke contains four relevant looking ingredients: Water, sugar, phosphoric acid, caffeine. Coke also has carbonic acid from the carbonation, but I'll assume we're either talking about uncarbonated Coke, or that the carbonation does not contribute to toxicity (perhaps a bad assumption).
Before worrying about whether the water will kill you, let's verify that the caffeine and sugar won't kill you first.
It seems unlikely that the caffeine in the coke would kill you before the hyponatremia. The concentration of caffeine in coke is about 0.1 mg/mL, and the LD50 is > 150 mg/kg, so for the same 68 kg person, it would take about 100 L of coke to get a lethal dose of caffeine.
The sugar in coke is more deadly, but still not as bad as pure water. There are about 0.11 g sugar per mL of coke. The LD50 of sucrose is apparently around 30 g/kg. So it would take about 2 kg of sucrose to kill our 68 kg person. That is about 18.5 L of Coke.
The concentration of phosphoric acid in Coke is about 5 mM which is about 0.5 mg/mL. The LD50 is about 1530 mg/kg. Which works out to about 212 L of Coke to kill by phosphoric acid.
Now that we've ruled out some other possibilities, lets get back to whether coke will kill you faster or slower via hyponatremia than pure water will.
Take another look at the the nutrition information for Coke. Notice that Coke actually contains some sodium, about 0.13 mg/mL in fact. A drink called "Powerade Isotonic"  which claims to have a proper electrolyte balance contains sodium at 0.28 mg/mL.
So given that (A) what kills you first from drinking too much water is hyponatremia. (B) Coca-cola contains a non-trivial (but still less than many electrolyte drinks) amount of sodium. and (C) other potentially toxic components of Coca-Cola, such as acid and caffeine, require much higher doses to be toxic. It seems reasonable to conclude that Coca-Cola has a lower acute toxicity than distilled water.
Caveats:
I did not consider osmolarity. There could be some effect here that I'm overlooking.
I did not consider the effects of carbonation (soluble carbonic acid).
For people with certain medical conditions, such as diabetes or caffeine sensitivity, Coca-Cola may be toxic at much lower doses than for other people.


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What is the relationship between stroke volume of blood and ventricular end-diastolic volume?
I do know what each term means. That is, i know that stroke volume is: the volume of blood pumped by each contraction of a ventricle, while ventricular end-diastolic volume is: the volume of blood in the ventricle just before systole. However I can't relate the two in terms of, say, graphs or in the mode of action of the heart between this period(s).

I'm not sure what you're asking. Both are simply volumes of blood. They are different because not all of the blood in the ventricle is ejected. It sounds like you're asking about the cardiac cycle, not volumes, but I'm not sure. (The red line is the graphic "relationship" between the two.)

Thanks! I did see this diagram before on Wikipedia but i might have overlooked the label of ventricular volume. Thanks again!

The simplest relationship is "EDV=SV+ESV", "EF=SV/EDV" (EDV: end-diastolic volume, SV: stroke volume, ESV: end-systolic volume, EF: ejection fraction)