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Why are oceans said to have "low productivity" in terms of photosynthesis?
80% of the world's photosynthesis takes place in the ocean. Despite this, oceans are also said to have low productivity - they cover 75% of the earth's surface, but out of the annual 170 billion tonnes of dry weight fixed by photosynthesis, they contribute to only 55 billion tonnes. Are not these two facts, which I have come across separately, contradictory? If oceans fix 80% of the total $\ce{CO2}$ fixed by photosynthesis on earth and release 80% of the total $\ce{O2}$ released by photosynthesis on earth, they should have accounted for 80% of the dry weight produced as well. Is there any way to reconcile these facts? In any case, if 80% photosynthesis occurs in oceans, that hardly seems low productivity - then why are oceans said to have low primary productivity (a host of reasons are also given for this - that light is not available at all depths in oceans, etc.)? A large amount of photosynthesis taking place should mean a large productivity!

It'll help if you can provide where you found those two statistics (80% of the world's productivity takes place in the ocean and 55/170 million tonnes of dry weight is produced by the oceans)

Actually both were my [high school level] textbooks. But here is a reference for the 170 billion tonnes figure.

BioNumbers suggests that the 170 and 50 Gt values are roughly correct, as measured by the papers cited.

First, we have to know which are the most important criteria for photosynthesis to occur; these are: light, CO2, water, nutrients.
docenti.unicam.it/tmp/2619.ppt
Second, the productivity, you are talking about, it should be called "primary productivity" and it is calculated, dividing the amount of carbon converted per area (m2) by the time.
ww2.unime.it/snchimambiente/PrPriFattMag.doc
So, thanks to the fact that oceans occupy the larger area of the world, the marine microorganisms can convert lots of inorganic carbon into organic (principle of photosynthesis).
A big problem in the oceans is availability of nutrients; these tend to deposit or react with water or other chemical compounds, even though the marine photosynthetic organisms are essentially found on the surface, where, of course, light is present. This reduces as a consequence the  photosynthetic productivity potential of oceans.

You should provide some references to support your answer.

If oceans fix 80% of the total CO2CO2 fixed by photosynthesis on earth
  and release 80% of the total O2O2 released by photosynthesis on earth,
  they should have accounted for 80% of the dry weight produced as well.

First, what is meant by "O2 released"? Does it mean "O2 released from the oceans into the atmosphere, where it contributes to a growing surplus"? That can't be the case since the amount of O2 in the atmosphere is pretty constant, and there is evidence that it is significantly lower than in Jurassic times.  Overall the global O2 sinks must balance the O2 sources, or if anything must slightly exceed them, resulting in the current gradually increasing atmospheric CO2 levels at the expense of O2 levels.
So by "released" we have to just mean "released by the process of photosynthesis, at the point of its operation".
Oceans fix 80% of the total CO2 fixed by photosynthesis, yes, but they also unfix it at a similar rate. For every algal cell that's photosynthesising, there's one that's dead or dying and being consumed by bacteria (which consume O2), or that's consuming oxygen itself in order to keep its metabolic processes operating at night. So the NET amount of O2 released by the oceans is something close to zero.
Now we have to ask what we mean by "productivity" in this context. If a molecule of CO2 gets fixed due to algal activity but then almost immediately gets unfixed again, does that count as "productivity"? But, blink and you'd miss it! Even if you don't blink, it's hardly likely to be measurable. The dry weight of the algae at the end of the of the process is the same as at the beginning. so if we define "productivity" as "increase in dry weight of algae" then the productivity is zero.
For algal photosynthesis to have an enduring effect on global CO2 or O2 levels, the fixed CO2 has to become incorporated into something less fleeting than algae. Something like cod or hake, which as a bonus can be harvested and placed on tables. "Productivity" usually refers to the power of the oceans to replenish the stocks of these things post-harvest, and that is indeed low when compared to the ability of the land to produce repeated harvests.
It would be a different story if we were to regard algae as potentially suitable for mass harvesting, so that their ability to grow like wildfire in the presence of fertilizer runoffs from the land was regarded as "productivity" rather than as a profound nuisance. But this is not the case.
In other words, we tend to define "productivity" in terms of what is useful to us as a species, and algae are generally not useful.


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Adaptation by standing genetic variation and fitness variance
I've read a couple of paper on Fisher's Fundamental Theory of Natural selection that states:
$W(t+1) = W(t) + Var_{W}(t)$
Given a population with some degree of genetic variability, and assuming that no new mutations can appear, eventually the most fit strain will be fixed (discarding the effect of drift). The FFTNS allows to predict, given the mean fitness at any point and the fitness variance, the mean fitness of the population in the next generation.
However, can we predict the variance on fitness for the new population?
Given the possible complexity of the problem, the situation I'm focus have specific conditions, but I would also like to know the general answer. But in my case:

Individuals reproduce asexually
Random mating
Diploids
Expanding population with recurrent bottlenecks (we can approximate to Wrigth-Fisher population with certain effective population size)

More generally, given only the initial mean fitness and variance of the fitness can we predict the trajectory of the mean fitness during adaptation? If not, what do we need more? Number of strains present? Or only the full composition of the population allow for such prediction?
Thanks in advance

Welcome to Biology.SE. Your question is a possible duplicate of How does Natural Selection shape Genetic Variation?. You might also have a look at this post to understand Fisher's Fundamental Theorem of Natural Selection

Thanks for point that out! I will read with more attention, but I still think that it is not clear in that post whether, given only the mean fitness and fitness variance of a population, one could predict the future mean fitness and how. One of my conditions is saying that the G matrix is unknown (population composition is unknown).

The evolution of the G-matrix is exactly what you are interested in if I understand your post correctly. Once you read the other post, you might want to ask your question in reference to this particular post.

Although I understand the point of the G-matrix, what I was looking for was a way to predict mean fitness without direct access to the G-matrix... Given only the measured fitness variance of the population and assuming no new mutation, no recombination, no migration, can we predict future fitness variance (and by the FFTNS the mean fitness) of the population.

Given the measured fitness variance of the population you can construct a G-matrix (if you have sex-specific variance and cross sex covariance estimated, it would be a 2 x 2 matrix) and perform the prediction using the multivariate breeders eq. $\Delta \bar{z} = G \beta$ where $\Delta \bar{z}$ would be the change in fitness, $G$ is a 2 x 2 matrix as above, and $\beta$ is the sex-specific selection coefficient, thus fitness after selection would be $z + \Delta \bar{z}$. Price equation is also likely very useful.

Thanks a lot!! Can you point out a reference for constructing the G-matrix from the variance in fitness alone? By the way, if the species is asexual, then G is a 1*1 matrix right? And how does G changes for every generation?

Asexual would be complicated, not something I've considered before, so I'm not sure how that would affect it off the top of my head. Just a note, you may also want to consider the effects of non-genetic variance in fitness and how that impacts selection (see Hansen and Houle's papers on the concept of evolvability)

Sure! Although I want to start with a simple model, without external complications... It's funny, I had always the felling that asexual populations would be easier to model than sexual!! :)

Given the asexual condition in my question I think that the linked question does not answer it, so can the "This question may already have an answer here:" be removed?

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Are there lifeforms that have more than 2 sexes?
Are there any lifeforms on earth that have more than male and female biological sexes?
If so, are all three mates required for reproduction or is there something else going on?
If not, why not? There are species that have one sex and there are species with 2 sexes. I get some of the basics of why there are two instead of one, but would those benefits not be even greater if there were three sexes?

NOTE: I am of course only talking about sexual reproduction. I have no intention or desire to talk about transgender or LGBT issues nor am I wanting to make any points on the issue. This is solely a question about sexes in biology and not human social constructs.

Also, I am a computer programmer, not a biologist. Please forgive me for not knowing any of the terminology.

I'm not sure. Could you explain why it would? Again. I am not talking about social structures as much as I am about genetic reproduction. As far as I'm concerned, to have more than 2 genders (let's say three for example), either all three would need to be involved with the reproduction of offspring like we have with male and female humans. [ A + B + C = new life form ] or any of them can mate with any other and still somehow produce offspring [A + B --OR-- B + C --OR-- C + A = new life form].

Do you mean case where it takes 3 individuals for reproduction to happen? Or any two individuals from different sex would do? In the second case, the definition of sex (or gender) might become quite tricky.

Is there precedent for either case?

“There are species that have one sex” — No, by definition. There are sexless species. There are no species with a single sex.

@MakPo Yes, there’s precedent for the three-parent baby but it didn’t evolve naturally.

@KonradRudolph - I just read through the linked article. While it's really cool, it really isn't the same thing. I am really only wanting to know about naturally occurring sexes. In the article, there was one male parent and two female parents. It's really not the same, at least for my purposes.

@KonradRudolph - "There are sexless species. There are no species with a single sex." That brings up an interesting point. What is the difference between asexual and ?mono-sexual (if that's a thing)? There are simple multi-cell organisms that reproduce via mitosis (I think that's right) and there are some creatures where the female is able to produce offspring without a male (parthenogenesis). In in all of the cases of parthenogenesis, the species still have males, they are simply not always involved. Are there cases of species where they are 100% parthenogenesis and 100% females at birth?

@KonradRudolph there are single sex species but they are pretty rare, the new mexico whiptail is an example, it is a hybrid species both parent species have males but they do not, and they cannot reproduce with the males of the parent species. but the are capable of parthenogenesis oddly the females still have to "mate" with each other to trigger ovulation even though no genetic exchange occurs.

There exists something like multiple sexes in fungi, but it's a bit complicated.
First of all fungi don't actually have anything that represents the two classical animal sexes, phenotypically their reproductive cells are all equal (they have isogamic reproduction).
However there can be certain alleles in some fungi species (sometimes multigenic, sometimes not), that restrict sexual reproduction to other fungi with a different variant of that allele, these alleles are therefore called mating types. It is however important to note, that almost all fungi can also reproduce asexually (by basically cloning themselves).
In general all of the mating type systems always require only 2 individuals to (sexually) reproduce, it just can't be 2 individuals with the same type.
In their simplest form mating types resemble the male/female sex we often see in animals: for some fungi (e.g. yeast) there exist exactly 2 forms of the mating type allele (called a and $\alpha$), so basically they have '2 sexes' (though genetically/biologically the difference is MUCH smaller).
There are however also much more complicated mating type systems:
Some species of the Basidiomycota or Agaricomycotina groups have a tetrapolar mating type, which is composed of 2 independent alleles (with 2 variants per allele this would already results in 4 different 'sexes'). Additionally they can have many more than 2 forms for each of the alleles (up to hundreds), which leads to (ten-)thousands of different mating type combinations (or 'sexes').

@KonradRudolph Yeah I was adapting the to the terminology the OP used  - with the changes made to the questions I'll change gender to sex in this answer as well, since that is the better word in this context. Generally though fungi have neither a gender nor a sex, which is why the word mating type is used instead.

It depends on just what you mean by "required", but insects such as bees and ants sort of meet the criteria.
First, the double helix of DNA is inherently binary, so at the lowest level you need two and only two individuals for sexual reproduction.  However, the actual process in the world may require more types.
Take bees for instance.  There are basically three types of individuals in a hive: one female queen, which lays eggs, male drones which fertilize a queen (or try to), and then die, and neuter workers, which feed the queen, raise the eggs & larvae, and determine whether a particular egg will become a new queen or drones.
So for bees, only two types of individuals actually participate in sex, but all three types are required for the hive to survive and reproduce.

That very well just might be what I was looking for. Is the third type biologically different in that it is missing the sex organs of the other two? It's not just a situation where they are not aloud to breed due to enforced celibacy or something? By "neuter workers" are they born able to reproduce but castrated at birth or are they born neutered?

"First, the double helix of DNA is inherently binary, so at the lowest level you need two and only two individuals for sexual reproduction." - I'm not sure I follow. You don't get one DNA strand from your father, and one from your mother... While it seems excessively complex, there's no reason not to have three copies of each chromosome, one from each of three parents.

@gilleain - Why would that be beneficial? It would mean reproduction would take more participants, decreasing the possibility of pregnancy occurring. That is unnecessarily complex when two will do. "You don't get one DNA strand from your father, and one from your mother..." Well, basically kinda you do... You get one chromosome from mother, one from father.

@anongoodnurse I agree it wouldn't be beneficial! It is unnecessarily complex, but there's nothing theoretically binary about it. A chromosome is a double helix (plus chromatin, etc) so you get 2 strands from the mother and 2 strands from the father

@anongoodnurse It’s potentially beneficial in the same way that sexual selection reproduction is beneficial over asexual reproduction, in that it further increases diversity. Furthermore, it may even prevent specific issues with binary sexual reproduction, by decreasing the probability of recessive disease phenotypes. Of course there are diminishing returns and it’s unlikely to offset the vastly increased complexity of the three-way meiosis.

@KonradRudolph - It would not be beneficial if it decreased reproduction rate, which is a mighty important consideration.

@anongoodnurse We agree that on balance it’s probably a terrible idea. But it does have distinct advantages, they’re just outweighed by disadvantages. (Then again, consider that the three-parent baby actually does exist, albeit with a quite different mechanism than discussed here. So under specific circumstances, at least, we happily accept the hardships.)

@gilleain: Multiple copies of chromosomes is a step up from what I meant by DNA being inherently binary.  The molecule is a double helix, and in reproduction it (simplifying considerable) it splits apart and each strand is duplicated.  For chromosomes, having more than two of each (https://en.wikipedia.org/wiki/Polyploidy ) does happen, particularly in plants, where artificially inducing it is one way of breeding stronger varieties.  But there are still two parents...

@jamesqf yes, but the fact that dna has two strands is completely separate from the fact that sexual reproduction involves two parents. you don't get a strand from each parent, polyploidy or otherwise.

@jamesqf - fwiw, a small %age of female worker bees (they are not neuter scientifically speaking, I don't believe) can lay eggs, but only produce male offspring. Only the queen, who has mated, can produce male and female offspring. Tomato/tomahto...

Yes in many different way. No for a species in which all three are required at once.

there are species that have more than one type of male or female, each with drastically different body plans, this is called Alternative mating strategy. (African cichlid fish, cuttlefish)
Bacteria with up to 7 sexs are known to exist, each sex can mate with any of the other 6 but not itself. Tetrahymena thermophila technically these are called mating types.
Worms which have males, females, and hermaphrodites exist. Auanema rhodensis this is probably the closest you will find.

But there are no species that have three sexes that all need to participate. Part of the issue is logistics it is just harder to get three animals together than two, and there are far more ways to split a genome in half than into thirds for exchange and evolution is often a lazy tinkerer. There is also an issue with mitochondria since they mutate faster and differently they do not do as well with genetic exchange than nuclear DNA. it is better for a mating creature to only use mitochondria from one parent, a logistically that makes for two gender one with one without. There is also a statistical issue that three genders are not stable and drift can turn them into two genders rather easily.

I have trouble seeing 1 as different sexes. They are male or female with a different strategy I think. I like the other examples though.

As you describe, needing three sexes comes at an extra cost. And there is no benefit. Evolution makes short work of such a trait.

It depends on how you define sex, Alternative mating strategy is the most common of the options, but I agree it is probably the furthest from consideration.

There are some single celled organism that are considered to have more than 2 sexes but biologist generally call them mating types rather than sexes. One good example is Chlamydomonas. They use flagellas for mating and once their chromosomes is mixed in the fused cell, the cell undergoes meiosis to produce the next generation of haploid daughter cells. (See this Quora post).
A mushroom Schizophillum commune has two mating type genes, with one having over 300 possibilities and the other 64. This leads to a documented 23,328 distinct mating types. A S. commune individual would be capable of reproducing with just under 23,000 of these types. (See this Reddit post for a detailed discussion on this topic).
Clam shrimp have a male as well as two varieties of hermaphrodite, which either self-fertilize or mate with males but cannot mate with each other. The protozoan Tetrahymena thermophila has seven distinct "sexes" that can hook up and swap genes (See here).
See this biology.SE question and this worldbuilding.SE question for more information.

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What is the best way to analyze non-quantitative mass spec hits from an immunoprecipitation pull down?
I am studying a nuclear protein and want to come up with a list of potential proteins that it interacts with. From the nuclear fraction of 293T cells, I did an IP (immunoprecipitation) to pull down my protein and submitted whatever I pulled down for a mass spec analysis. I also did an IP with a non-specific antibody as a control. I got a huge list of hits, and I'm not sure how to prioritize them. I can manually remove the hits that also came down with the non-specific antibody, those are obviously just sticky proteins. I looked around Pubmed for ways to prioritize non-quantitative mass spec hits, but I'm not sure if any of them would work in my case. All of them require multiple mass spec repeats - I can do that if I need to, but would like a way to look at my initial data more intelligently.

The title refers to quantitative data but your question seems likely to be describing shotgun proteomics (where peptides are selected for MS/MS based on their intensity) which is not necessarily quantitative. Could you clarify this so that the question can be answered correctly? Also, the facility that has performed the analysis is likely to offer a basic consult on data interpretation.

@Michael_A its suppose to be quantitate. I apologies for the typo.

If they are available, talk to the people who analysed your data. Using their knowledge is intelligent.
I will assume two critical steps are completed. First that your results have been searched correctly. I will also assume that the peptide and protein identifications have been filtered to provide a false discovery rate of 1:100 at each level.
You can remove all the proteins that were identified in your affinity purification control. Another option is to use the Contaminant Repository for Affinity Purification (the CRAPome) which provides a formal framework for removing contaminant proteins. It is a nice resource if your data are compatible.
The remaining proteins are what you have to work with, this is the

list of potential proteins that [your protein] interacts with.

Prioritise these proteins based on the biology of your experimental system. If the list is small work through the function of each protein and assess how it fits with the biology you are researching.
To assess the potential functional links between the proteins you can create an in silico network. Markov clustering can highlight the presence of functionally distinct groups of proteins within a network. String, linked above, can do this. Centrality measures can indicate the presence of proteins with the potential to influence the behaviour of the network.
For larger lists you can also assess the function of the proteins in the list by performing a functional annotation enrichment analysis. There are many other things you could do but the primary goal is to keep biology at the forefront of your efforts.
Finally you mention that repeats are necessary. Analysing the data is time consuming. If this was a test run verify that the test was successful and then run the replicates. Time spent analysing incomplete data can be spent completing the data set or ensuring the right data is collected. Quantitative data can be very useful and with care shotgun proteomics approaches can provide quantitative data but the people who run the machine need to be consulted when quantitative data is required.

You can look for the most abundant proteins in your sample. Although, as you say, the LC-MS analysis of your IP was non-quantitative, you can still try to get some quantitative estimation. To elaborate, you can use for example sequence coverage, no. of PSMs for each protein, no. of peptides ID'ed for a protein, share of spectrum ID, etc, as proxies for abundance.
There exists rough correlation between abundance of a protein and all these quantities. If a protein is more abundant you are more likely to have more number of peptides ID'ed from it, more no. of PSMs assigned to it, it would have higher sequence coverage, etc. Different people use different things. I have often used no. of PSMs normalised by length of the protein as an estimation for the abundance of that protein.
As others mentioned, discuss with the people who analysed your data. As a rule of thumb, I would filter my data first on 1% FDR at the PSM level, then at the Peptide level and then at the protein level. Then I would throw out all the proteins that were not identified by at least two unique peptides. Then I would compare the proteins ID'ed in the negative control list and remove the common IDs. Then sort the remaining list on no. of PSM for each protein. This would give an estimate of the more abundant proteins in the IP sample. To give an example, your bait protein (protein against which you did the IP) should be the most abundant protein in your sample. Proteins after this could then be assumed to be interactors of your bait.
Do remember that this is not a proper quantitative way of measuring protein-protein interactions by affinity purification coupled to LC-MS. But, it is a useful start. I always used preliminary information from such an analysis to design better ones. Also, read about reciprocal IPs to confirm interactions.

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Using UV to kill bacteria in shoes
I see that UV-C is the best to kill bacteria generally. We are interested in using to kill off odor in shoes.
What illuminance is needed to kill most bacteria with UV-C?
Thanks!

Welcome to Biology.SE. Only the last of the three questions relates to biology. The others are questions of material physics.

Do people still use the foot-candle in the USA? The standard unit of illuminance is the lux. Note that once you know the illuminance on the target, finding out the illuminance at a given distance is quite basic (and is a question of physics/math). I would recommend you restrict your whole question to something like "What illuminance is needed to kill most bacteria with UV-C?".

Close vote retracted and +1.

The wavelength of UV-C most effective at provoking mutagenesis in DNA is 260 nm, which has been shown to kill Cryptosporidium parvum at doses below 10 mJ/sq cm.
http://www.ncbi.nlm.nih.gov/pubmed/12834745
In units of lux, 10^5 lux of sunlight has been shown to kill 99.9% of Aeromonas salmonicida after two hours of exposure.
http://www.sciencedirect.com/science/article/pii/S0043135499001591


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Can we digest food as well as herbivores
I heard some guy say that we can't digest plant food as well as herbivores. Which seems weird to me seeing as how humans can survive without any nutrient deficiencies besides b12 on only plants but we would pretty much just die of nutrient deficiencies on a carnivore diet. Can someone show me how we can't digest plant food as well as herbivores?

Hi and welcome to Bio.SE! This is an interesting question, but it remains quite broad at the moment. Could you narrow down which plant food you mean. For example, we can eat onions but they are somewhat toxic to horses, yet most grasses would probably cause us to vomit whilst cows can't get enough of the stuff! More context is key to making this an answerable question.

Humans do not have microflora that can hydrolyze cellulose, but plant-eating herbivores do. One advantage of that though is that the cellulose helps move food through your gut and aids digestion. Herbivores have fermentation chambers in their alimentary canals that contain mutualistic bacteria and protists that can break down the cellulose for them; some of the microorganisms also use some of the sugars from the digested cellulose to produce nutrients vital to the animal, such as vitamins and amino acids. Also, herbivores have longer alimentary canals relative to their body size, due to the fact that plant matter is harder to digest because of the cell walls.
Here is an excerpt on herbivore teeth structure, taken from Campbell Biology, 10th Edition.

"Herbivores, such as horse and deer, usually have premolars and molars with broad ridged surfaces that grind through tough plant material. The incisors and canines are generally modified for biting off pieces of vegetation. In some herbivores, canines are absent" (Reece et al. 906).

References:

Reece, Urry, Cain, Wasserman, Minorsky, and Jackson. Campbell Biology. 10th ed. N.p.: Pearson, 2014. Print.


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General anaesthesia and brain cell damage
Do we lose brain cells when we undergo prolonged surgery under general anaesthesia?

You are asking two distinct questions. You should decide which one you want answered.

These are conditions which can cause decreased oxygen supply to brain.I have asked so in that context.Want to know about both situations

Surgery, sneezing, strangulation. You ask a lot of anyone trying to research an answer. It's your question but I would vote to close as overly broad.

Okay .I understood.I just related these situations.Sorry for the inconvenience it created for answering

I think this question is fine now. The system won't let me change "loose" to "lose" or "anaesthesia" to "anesthesia." This would be an improvement...+1.


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What is the difference between endomysium and sarcolemma
They both are lining of muscles so how can we differentiate these two? Please answer in simple terms.

What's an endomyceus? When I search google it says 'endomysium'. Am I still new in the field or is the spelling wrong?

Sorry,it is endomysium

Homework questions and trivial questions about basic biological concepts are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Check this other image too from google. A single muscle cell or fibre has been magnified to show the sarcolemma and other contents like eccentric/peripheral nuclei as well as sarcoplasm. It's not the best image but hope this is ok.

If you have more information to add to your answer, please use the edit link (between share and delete just below the text of your answer). Please do not create a new answer unless it is substantially different from the first. Finally, you must cite/link to the sources of all images you use in answers (and questions). It helps to provide context, may give additional sources of information, and is just scientific common sense - you always cite your sources.

Just to illustrate Gerardo's answer, this picture is provided. The endomysium as you see is a layer of connective tissue which surrounds the individual muscle fibres (cells) (in between one muscle cell and the next) but each muscle cell in particular is lined or covered by a plasma membrane called the sarcolemma.


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Is there an ecological scenario where terrestrial insect larvae can show food choices?
I have been going through literature on insect food choices. I plan to study the effect of prior experience on food choices in both adults and larvae of the red flour beetle, Tribolium castaneum. There are plenty of studies that focus on larval and adult experience having an effect on adult preference. I would like to look at how larval experience changes larval choice, but only if it has some ecological relevance. However, I could not find a single study that provides an ecological relevance to larvae making food choices.
This appears to be due to the fact that larvae are usually sessile, and since adult females are the ones making the oviposition choices, therefore most studies seem to assume that the choices of the larvae don't matter. (Preference Performance Hypothesis)
Larval food choice might be ecologically relevant under conditions where females make "mistakes" during oviposition, say if the environment is spatially/temporally fluctuating. But if they show limited dispersal (or slower dispersal than adults), then does their choice really matter?
Does anyone know of any examples (published or unpublished) where insect larval food choice is ecologically relevant? It would help me out a lot to design my study.
Thanks in advance!

Welcome to Biology.SE, and congratulations on a great first question! One suggestion: the 'ecological relevance' criterion is a bit unclear - could you clarify what you would or would not consider to meet this criterion?

@arboviral
I see, I'm sorry for being vague. Well, the criterion for 'ecologically relevant' would be -

The larval choice actually occurs under natural conditions.
There are life-history or evolutionary consequences to this behaviour.
EITHER of these criteria would be sufficient to call it 'ecologically relevant'. It would be fantastic if it were both.

The diamondback moth (DBM), Plutella xylostella L. (Lepidoptera: Plutellidae) is one of the most important pests of cruciferous crops in the world.. A strain capable of complete development on sugar pea (Pisum sativum L. var. macrocarpon) has recently appeared. A recent study (Henniges-Janssen, Heckel & Groot (2014), "Preference of Diamondback Moth Larvae for Novel and Original Host Plant after Host Range Expansion"; link) compared the feeding preferences of L4 larvae reared during previous larval instars on cabbage and pea. Pea-reared larvae of this strain preferred peas, while cabbage-reared larvae preferred cabbage. L4 larvae of the original strain preferred cabbage irrespective of their previous diet. I don't think this example has been shown to occur in the field, but the two plants are both fed upon by these caterpillars in the wild.
There is also evidence that larvae of Cydia pomonella (codling moth), a marjo agricultural pest of orchards with a near-global distribution, learn to avoid apple flavoured with saccharine if they have previously encountered saccharine-flavoured noxious plants (Pszczolkowski & Brown, 2005); this probably meets your second criterion for ecological relevance more closely (evidence for learning to avoid odour/flavour cues encountered in a toxic plant, thereby increasing survival) but it's less relevant to a real-world field situation than the first example.
I also found an article on associative learning in insects here that may include some useful examples.

Thanks, @arboviral! The references helped! Unfortunately, I have not yet found examples for the first criterion for 'ecologically relevant'. I guess the second will have to do until someone actually observes larval choices occuring in the field and characterizes conditions leading to that.


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Can human eys/the brain be trained to see with bidirectional monocular vision?
Most people have a dominant eye, and while it uses its non-dominant eye in tandem with the dominant eye most of the time, the brain, being an expert in eliminating redunant information, ignores the images received from the non-dominant eye.  However, with special training or practice most individuals can force the brain to temporarily switch to receiving images from their non-dominant eye, even to receive images from both at once, resulting in a blurred chamelion-like or image.
Some individuals however, have a non-dominant eye so weak, that not only does the brain ignore the images it sends, the eye it self no longer moves in tandem with the dominant eye.  This is known as strabismus or Lazy eye.
My question is, if the eyes are capable of not moving in tandem in those people, why can't we all train our eyes to move independently, and couldn't we also train our eyes to focus on two different images (on opposite sides) at once?

I edited your post to remove the alien reference. While I, and maybe others may think it's funny, many users of this forum will disapprove and possibly downvote your question. They do have a point in not wanting the forum bloated with humor. [This comment to be removed.]

@bpedit well couldn't you have least edited it, not simply remove it?  I wanted to know if people with strabismus could see like chameleons.

What are your sources on this information? Note that stereoscopic vision is lost entirely with only one dominant eye doing the work. I.e., ...couldn't we also train our eyes to focus on two different images (on opposite sides) at once? is the very basis of binocular vision. I quite frankly don't understand your question.


text:
Are these principles worth being validated?

Odunayo's principle of inhalation states that provided a given amount of water is ingested, inhalation through the nostrils will be excluded due to the presence of oxygen in the water.

From the above theory, I was drinking water and it suddenly hits me that when drinking water, it'll be impossible to breathe. So.....
Q1. My principle is based on the fact that why it's impossible to breathe while drinking water is because of the presence of oxygen in the water, Is this true?

Odunayo's principle of immortality states that provided the injuries to the heart and brain remain excluded, an organism will be unable to experience immediate blackout with the aid of determination by that organism although weakness and other symptoms related to it may persist.

I actually came up with this principle when wondering if when a person is shot apart from the heart or brain, will be able to survive much longer than how an ordinary person would due to that person determination to stay alive.
Q2. Is that true or is it simply due to the place the person was shot,(still, apart from the brain and heart and when no treatment is involved in such scenario)
Q3. If the second principle given above is true, could it also be applicable to animals?
Q4. Which of the principles given above is worth being validated and how can it be improved, if there is any room for improvement?

I know this question is a bit primarily opinion-based, but i'm not sure where to post this question except from here, since it's a biology related question.

Odunayo is actually my late colleague's name, I named the principle from him. And the principle was made up by me,(a 16yr old kid)

No matter how much an individual wants to live, an untreated traumatic injury that is causing loss of blood will lead to loss of consciousness and eventual death unless something is done to treat the condition. A body (human or otherwise) requires a certain amount of oxygen to be delivered to the brain per minute in order to survive. Go lower than that limit, and the brain shuts down. Stay lower than that limit for a certain amount of time, and recovery is impossible. It's as simple as that. You need to stop watching quite so many movies and crack open a few books.

Additionally, it's not very scientific (I understand you're only 16) to make up pompous-sounding "principles" just to ask about them on a website. If you have a question, ask it, according to the rules discussing what is on-topic and what is not. Pay attention to the advice given in How to Ask a Good Question as well. We encourage curiosity, but not lying.

I don't know who this Odunayo is, but the reason you can't breathe while drinking water (or swallowing anything else for that matter) is that your epiglottis closes off your trachea to make sure you don't aspirate the food/drink which could cause infection or drowning. This has absolutely nothing to do with the oxygen content of either.
Other organisms that do not use the same orifice to eat/drink and breathe, such as invertebrates with a trachea or book lung system would not be subject to these limitations; you could say the same for the gills of fish.
These "principles" sound meaningless from any scientific standpoint, though there are some studies that support a true effect of "will to live" in some terminal patients, though it's hard to separate cause and effect and impossible to do a true randomized experiment. There is no evidence that "will to live" has any effect on outcomes related to acute trauma like a gunshot - these studies are mainly focused on elderly patients with chronic illnesses.

Thanks for your answer, so, I guess you've shown to me that my first principle doesn't actually have a scientific background. What of the second principle, from your answer, you clarified that the second principle could be supported in some cases(that is, 50% proved)

I never said anything was 50% proved, I said there is some support that terminal patients who have a strong will to live may possibly live longer than others who don't. The biological explanations for this are very unlikely to involve any sort of "mental power" but maybe something more along the lines of differences in cortisol levels. This isn't the same thing as surviving a severe trauma - the Hollywood "just stay with me!" refrain, for example, is totally bogus. If EMTs ask patients something like that they are just trying to judge their level of injury, not actually provide treatment.

@BryanKrause as far as I know, the whole "will to live" thing applies to people late in life who still want to do things, remain active, be involved in family, community, and decisions about their care, etc. etc. These active participants tend to live longer than neglected elders in nursing homes with little to know family or social interaction, often previously-deceased spouses or significant others, and little desire to remain in this world. You might want to clarify that a bit in your answer. I've never read of, for example, gunshot victims who just want to [...]

[...] hold on for little Jonny back home, and have the will to live, vs. a depressed gunshot victim who welcomes the circumstance and just wants to die in peace. That sounds 100% Hollywood. An injury is an injury, and while there is certainly medical evidence of some people being able to control certain aspects of their physiology, including heart rate/blood flow, breathing, body temperature, etc., two in other ways identical average Joes who get the same traumatic injury will die pretty much at the same time, regardless of the "will to live" of one over the other.

@MattDMo yes I think in my comment I made that clear, and in the answer I said terminal patients. Even in those cases, the science is a bit unclear. There are clear statistical trends for increased death rates following holidays, for example, but it isn't really known if that is because people are "holding on" for the holidays or if there are stresses caused by the holidays that hasten death in the following days to weeks. Nonetheless, I will clarify my answer a bit.


text:
How do cells determine what size to grow to before dividing?
How do cells determine size to grow to before dividing?

Have a look at this review.

All eukaryotic cells have 'checkpoints' during their cell cycle (1)1. They will only commit to cell division or the next phase of mitosis until all requirements have been fulfilled. The cell needs to have enough energy and the right external stimuli before it starts the irreversible commitment to cell division. The proteins effecting these changes are the cyclins and the associated CDK's. These proteins integrate a wide array of signalling inputs (e.g. DNA duplication complete or no major DNA damage) and steer the proteins actually duplicating the DNA and the other machinery needed to split a cell. You can learn more about these proteins and their signals by googling 'restriction point'
If you interfere with cyclin D modifying proteins you can get very large or very small cells. One of the best understood proteins involved is WEE1 from fission yeast. If you knock this one out, you get very small cells (2).
In mammalian cells the size of the spindle during anaphase also seems to be crucial in splitting cells equally (although some divisions are asymetrical)(3).


text:
Why are de novo genetic mutations usually NOT inherited?
I am told de novo genetic mutations (germ mutations in either parent's sperm or egg cell, or the newly fertilised egg) are not usually inherited, and do not contribute to heritability.
It would seem to me that, intuitively, a de novo mutation would be passed from the affected individual (assuming they survive and are fertile) onto offspring, just like any other inherited mutation. But apparently not.
Why is this?

A germ line mutation will be passed to the offspring only if (1) the individual reproduce (2) the individual reproduce after the mutation has occurred in the germline, (3) the spermatozoid that is transmitted is descendent from the individual cell who had the mutation, (4) the right of the two chromosome is being transmitted (last point applies only if the mutation occurred before the meiosis).

@Remi.b  That sounds like a pretty good argument, can you write up an answer based on it?

The statements at the beginning of your question seem to be separate issues; I think @Remi.b answered the first part but didn't address the second: "do not contribute to heritability" - this statement might refer to the fitness of the parent to reproduce, which is determined by that parent's phenotype, and not the genotype of the gametes, which is the only thing affected by a germ-line mutation (unless there is a corresponding phenotype effect in the gamete such as reduced sperm motility, or the mutation is lethal, which would clearly affect heritability).

A germ line mutation will be passed to the offspring only if

the individual reproduces
the individual reproduces after the mutation has occurred in the germline. Indeed if the mutation appears in the testes 5 years after the individual has reproduced then the offspring will never carry this mutation. Note that female mammals make a big storage of ovules early in life while mammal males do not. As a consequence the number of new mutations transmitted to offspring is age-dependent in males but age-independent in females. See this post for more info
the gamete that is transmitted is descendent from the individual cell who had the mutation. There is of course many lineages of gametes and their pattern ancestry will affect what fraction of gametes carry a given mutation.
the right of the two chromosome is being transmitted (last point applies only if the mutation occurred before the meiosis). Of course, there is always segregation who decreases the probability of a new mutation to be transmitted by half.

Of course, there are also all the mutations occurring outside the germ lineages (somatic lineages) which won't be transmitted but you specifically asked for germ line mutations.


text:
How to Calculate how many times an enzyme would cut a plasmid
I'm a little confused as to how to figure out the formula needed to figure this out.
I have a plasmid that is 7.3Kb and am told that it is cut with an enzyme of 4bp. For some reason I thought that the formula needed to figure this out is:
(1/4)^4 x 7300
But it gives me such a low number that I don't think it's right so I'm just a little confused.

Do not work from formulae people give you. Work from logic. You will find it here, among other places.

There are $4^4$ 4-cutters, which means that given a 4 cutter, you expect it to cut once every 256 bases on average. $7300/256 = 28.5$, so you expect 28 or 29 cut sites in the plasmid. This is identical to what you calculated.


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

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

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

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

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

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

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

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

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

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


text:
Evidence that Attention Deficit Hyperactivity Disorder (ADHD) is caused by too much cellular ATP?
The question is pretty simple — it's just a theory that I remember my biology teacher mentioned long ago and for years now I've wondered about it without ever asking.
Some people with attention deficit hyperactivity disorder (ADHD) report "energy bursts" with the feeling of needing to explode while sitting still. Further, they report that movement, like vibrating the legs, can help suppress this feeling.
Is there any reason to think that symptoms like these might come from too much ATP inside cells?

That's an interesting hypothesis - however, I am not aware of any evidence that this is the case. Importantly, there can be a lot of difference between cellular access to energy, like ATP, and the perception of "energy" or liveliness.
Here is a paper that actually suggests the opposite: that ADHD could be caused by a neuronal energy deficiency because of differences in astrocyte responses to catecholamines (astrocytes are non-neuronal cells in the brain that, among other functions, regulate metabolism in the brain including access to glucose). Importantly, though, this remains just a hypothesis, not a well-established theory.
ADHD is thought to impact the parts of the brain that are important for attentional control, inhibiting responses, and motivation. Based on that perspective, an alternative explanation for the symptoms you describe is that a sensation occurs that doesn't really require a behavorial response, and for a neurotypical individual this sensation is quickly suppressed (attentional control by not focusing on this sensation, inhibiting your response to shake your leg) without any real conscious effort. Instead, with ADHD, it is difficult to direct focus away from that sensation and mental resources need to be directed towards trying to hold still. The relief from moving around comes from letting the activity progress and not trying to suppress it any more, not because there was a literal excess of energy in the sense of ATP.

References:
Barkley, R. A. (1997). Behavioral inhibition, sustained attention, and executive functions: constructing a unifying theory of ADHD. Psychological bulletin, 121(1), 65.
Todd, R. D., & Botteron, K. N. (2001). Is attention-deficit/hyperactivity disorder an energy deficiency syndrome?. Biological Psychiatry, 50(3), 151-158.

I have no expertise in ADHD whatsoever, but basic biochemistry shows that this is not possible. A cell can't really have "too much ATP", and ATP does not by itself change how cells behave.
ATP is just a carrier of energy, an intermediate that stores energy extracted from nutrients like glucose and delivers it to energy-demanding processes like neurons firing action potentials ("work"). The amount of ATP stored in any cell is very small compared to the rate of production and consumption, so ATP is a short-lived molecule --- a cell's ATP store turns over (is consumed and renewed) in a few minutes. Therefore the amount of ATP does not really matter for energy metabolism; it is the rate of ATP production / consumption that matters.
Now, the rate of ATP metabolism is controlled by the demand for energy (how much work has to be done), not by how much nutrients are available. When cells need to do work --- for example, you start to run and muscles begin to contract --- the rate of ATP consumption increases. In response, the rate of ATP synthesis is increased by "burning" (oxidizing) nutrients more quickly, so that the system balances. Similarly, when a neuron starts to fire action potentials, its ATP consumption increases, and in response the cell generates more ATP by burning sugar. In contrast, ATP turnover cannot be increased by having too much nutrients. If this was true, cells would start doing work randomly as soon as they encounter nutrients, regardless of whether its needed or not, just to dispose of the generated ATP. Think about your legs starting to kick wildly as soon as you have a meal ...
In summary, the need to do work causes ATP turnover, not the other way around. Of course, having too little nutrients available does limit the amount of work that cells do, but that's a different question. Also, there are many signaling / hormonal mechanisms that alters behavior in response to nutrients. Eating a meal triggers reward centers in the brain, for example (hence, "comfort food"). But these systems are not directly related to ATP metabolism.


text:
Do Schwann cells have Na+/K+ ATPase pump?
I was studying "Action Potential" and this question crossed my mind.
Another question is that, "Why does the action potential not occur in Schwann cells, or if it does, how does it occur?"
I know that many animal cell membranes have this pump, but I was not sure about this one.

Yes. Although utilizing the action potential is not in their function, Schwann cells do have Na/K ATPases. In fact all animal cells do. It contributes to the resting membrane potential in neural networks, with regards to Schwann cells, and prevent differences in osmotic pressure from disrupting the cells.
As for your second question, action potentials do not occur in Schwann cells as there is nowhere for this "impulse" to travel to. A localized depolarization is not an action potential. Papers such as this, and this suggest that voltage-gated ion channels in Schwann cells serve complex and specific purposes such as inducing myelin formation.

Please do add some references.

"All three α-subunit isoforms are expressed in the CNS but to varying extents in different regions and cell types. The α1 isoform appears in glia, Schwann cells, choroid plexus epithelium and some neurons." link

Sorry put simply yes. Schwann cell, also called neurilemma cell, any of the cells in the peripheral nervous system that produce the myelin sheath around neuronal axons. Schwann cells are named after German physiologist Theodor Schwann, who discovered them in the 19th century. As such of it function an action potential is needed.
The principal primary active transport system in neurons, as in most other animal cells, is a P-type pump that concurrently extrudes Na+ and accumulates K+. For brevity, we will refer to it as the Na,K-ATPase. Depending on their functions, different tissues have vastly different requirements for pumping Na+ and K+. Transport by Na,K-ATPases is specifically inhibited by cardiac glycosides, such as ouabain.
http://study.com/academy/lesson/the-myelin-sheath-schwann-cells-nodes-of-ranvier.html
enter link description here

The purpose of the Schwann cells is to promote saltatory conduction whereby the action potential, in the neuron, "skips past" the Schwann cell to initiate an action potential at the next node between Schwann cells. The diffusion of ions in the short distance between Schwann cells is faster than the contiguous propagation of the action potential.

@Martin Anderson, -1 as you haven't answered the question of whether schwann cells have Na,K-ATPase pumps. I don't believe they do as it is unnecessary for their function (which bpedit outlines above). If you edit the answer I'll change the downvote to an upvote.

-1. You seem to have just pieced together unrelated facts about Schwann cells and copy-pasted citation text without reference to the question at all. Consider deleting your response.


text:
How do poiklotherms survive at different temperatures even though enzymes work at specific temperature?
Since enzymes have an optimum temperature at which they are able to catalyze the reaction best and increasing the temperature above optimum can even damage them, how do poikilotherms survive as they change their body temperature according to environment unlike homeotherms. Also wouldn't their metabolism stop with increased temperature?

Instead of viewing poikilotherms as having the same temperature as the environment, view them as lacking an internal thermoregulatory system. Poikilotherms indeed suffer from not having the ability to regulate their internal temperature.
Homeothermy is ecologically advantageous, allowing optimal functioning at a range of temperature. Poikilotherms, therefore, are more restricted in their habitat range, have to depend on external mechanisms for maintaining temperature (eg: Hibernation, Shade-loving lizards, burrowing in desert animals) or simply die due to environmental change (eg: poikilothermic fish are the earliest to die from a thermal runoff into a water body).


text:
Unknown larvae in grey cocoon
Location: Germany
While cleaning the windows today, I realized some dirt falling off the top of the window frame. By looking further, it seemed to be some kind of cocoon. (The first picture is very bad, I'm sorry)

Those cocoons were about 2-3cm long. There was a total of 6 cocoons.
Two were damaged by falling down.

The last picture shows the inner part of the second picture I think. The larvae(?) was about 0.8cm to 1cm long.
Not sure if it matters, but the window is an attic window, located at the third floor.
Do you have any idea, what kind of larvae it is?

This is a neophyte that has been recorded in Europe since 1979:
Sceliphron curvatum, in German also known as orientalische Mörtelwespe. Unusually large considering what else is buzzing around, but mostly harmless.
The nests, or rather individual larvae cells, are made of mud and while there are about thirty species in the genus, only Sceliphron curvatum is found in Germany - there‘s no other wasp or other insect in Germany that builds similar nest cells, especially the size is a good indicator. Your description of nest location in a window frame is typical, curtain folds or (vertical) nooks in furniture, e.g. shelves are also welcome. Our specimen picked a hiding spot behind a few books a few years ago.
Because of their size, there are usually some articles about them in the low-news summer media lull, describing baffled citizens and their “discovery”. A few less sensational descriptions, photos and further information can be found here (sorry, in German).
Nice find!

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


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How to color based on b-factor for all the frames in one object in Pymol?
I load a protein.pdb file into Pymol. This file has multiple frames (or states), and with different b-factor values at different frames at the PDB file b-factor columns.

After running the spectrum b command, the colouring is only based on the last state of the object.
So can I colour the frames differently using their corresponding b-factor values? In that case, I can see the colour changing throughout the frame playing.
In case someone wants to create a PDB of multiple frames, you can do like this:
MODEL        1
ATOM ......
ATOM ......
ENDMDL
MODEL        2
ATOM ......
ATOM ......
ENDMDL

Do you have a PDB ID one could use to reproduce this?

The PDB downloaded from the PDB website usually has only one frame. But my PDB comes from molecular dynamics, which has multiple frames. You can simply add a line of "MODEL        1" before the content, then add another line of "ENDMDL" at the end, and repeat this multiple times to create a PDB with multiple frames

Well, didnt find a wat to do it in PyMol (even with  spectrum b, blue_white_red, minimum= 0 , maximum=40, byres=1 on split_states test I get same colors on all the 4 models even if the b factors of the 4 models are different).
Ended up using on my test.pdb  hosted here https://file.io/Y37LZ3El6UyR with Biopython mini-script to split test.pdb into 4 models pdbs with code:
import Bio
print('\n\n------------------------------------------------')
print('\n  Biopython Version : ',  Bio.__version__)
print('\n\n------------------------------------------------')

from Bio.PDB import PDBParser
from Bio.PDB.PDBIO import PDBIO

parser = PDBParser(QUIET=False, PERMISSIVE=True)
struct = parser.get_structure('test', 'test.pdb')
print('\nstructure : ', struct ,';  struct.id :',struct.id,   ';   len(structure) : ', len(struct))

for i in range(len(struct)):
    io=PDBIO()
    io.set_structure(struct[i])
    io.save(struct.id+str(i).zfill(4)+".pdb")

and assembled movie out of the four models uploaded as 4 independent objects in PyMol, colored by spectrum b, blue_white_red, minimum= 0 , maximum=40, byres=1,  as described in Exercise 2: Scene based Movie in PyMOL Moviemaking Tutorial.


text:
Can VMD change its cartoon representation for secondary structure according to trajectories?
I am using VMD to visualise the secondary structure of protein.
The trajectories are from my Gromacs simulation. Firstly I use File - New Molecule... to load the protein.gro file. Secondly I use File - Load Data into Molecule... to load my protein.xtc trajectories.
Then I use Cartoon to visulise the structure. As I drag the time frames, all the secondary structures (e.g. alpha-helix, beta-sheet) keep the same. But I am pretty sure some of them are changing, as I look into the Timeline analysis for secondary structure.
So how to use VMD to see the secondary structures at different time frames?
Thanks a lot for @Stefan's help! It finally works! So follow Stefan's guide, and replace the molid with the number under the ID in the VMD Main.

I see this was asked first on bioinformatics.SE: https://bioinformatics.stackexchange.com/questions/3432

yes, because no one answer it.

And could you please tell me, where is rule that I cannot ask a repeated question in two sites? @marcin

@lanselibai it is all over the place, check this answer by the cofounder of SE for instance.  And it's not a rule per se, but its generally preferred that you tailor your questions to the audience of the site you're posting on.

I understand the necessity to ask only in one place. But because there is not a clear boundary line regarding my VMD software issue, I feel it can fit both sites. So, it would be better if there is an explicit definition of where my question should be posted.

As Martin pointed out, VMD doesn't update secondary structure content over the course of an MD trajectory. You can easily do this in VMD by using the SSCache script:
http://www.ks.uiuc.edu/Research/vmd/script_library/scripts/sscache/sscache.tcl
I believe it ships with the newest versions of VMD, actually, but I'm not exactly sure; even if not, you can easily source it:
Extensions > Tk console (in the console, type source Downloads/sscache.tcl (or where ever you've saved the script)). Once you've sourced the script, the easiest thing to do would be to load your topology and trajectory and (in the Tk console) issue the command start_sscache molid, although I advise having a look at the examples and options in the script.

thank you very much. Both source Downloads/sscache.tcl and start_sscache molid could use. However, as I move along the time frame, I could not see any secondary structure (SS) change. I was using Extensions - Analysis - Timeline- Calculate - Calc. Sec. Struct. to visualise the SS, so I know the SS is definitely changing. So I wonder if the sscache is adopting the same algorithm as Timeline (which is STRIDE) for SS?

'molid' in this example is just a substitute for your system's ID; you can see it under ID next to the number of atoms in the VMD main window. If your system is called 'myMolecules,' you issue start_sscache myMolecules in the Tk console (you have to issue source Downloads/sscache.tcl, of course)


text:
What is the meaning of "E-value" in the BLAST search?
After reading many pages, I still do not understand the definition. Can someone use simple words to explain me that?
https://en.wikipedia.org/wiki/BLAST
This expectation or expect value "E" (often called an E score or E-value or e-value) assessing the significance of the HSP score for un-gapped local alignment is reported in the BLAST results.
If a lower E value means closer results to the query sequence, what is its difference to "Sequence Identity Cutoff"? http://www.rcsb.org/pdb/search/advSearch.do?search=new

You can find the definition here:

the number of hits one can "expect" to see by chance when searching a
  database of a particular size.

Also read some of the background information given to understand the meaning:

It decreases exponentially as the Score
  (S) of the match increases. Essentially, the E value describes the
  random background noise. For example, an E value of 1 assigned to a
  hit can be interpreted as meaning that in a database of the current
  size one might expect to see 1 match with a similar score simply by
  chance. The lower the E-value, or the closer it is to zero, the more
  "significant" the match is. However, keep in mind that virtually
  identical short alignments have relatively high E values. This is
  because the calculation of the E value takes into account the length
  of the query sequence. These high E values make sense because shorter
  sequences have a higher probability of occurring in the database
  purely by chance. For more details please see the calculations in the
  BLAST Course. The Expect value can also be used as a convenient way to
  create a significance threshold for reporting results. You can change
  the Expect value threshold on most BLAST search pages. When the Expect
  value is increased from the default value of 10, a larger list with
  more low-scoring hits can be reported.

If you want to understand the calculation I would highly recommend to read the BLAST course
Update
Identity is not the same as the E value
I would try to explain this as easy as possible so let's suppose a sequence:
query sequence: ATGCCGTGC

When you BLAST this (of course your sequence is much longer), you can get the sequence ATGCCGTGC, which will result in 100% identity (NOTE most of the time when you have 100% identity, you have the right sequence but I just picked 100% to make the difference clear. When you have lower percentages of identity the E value is much more important. So when you have 70% identity in different matches e.g. it is important to look a the E value to decide which match is the "right" one for your purpose), now you probably would think that's nice that's the sequence I was looking for. However this would be a mistake! Maybe this sequence is present many times in the database and this is just a random match, this is the point were the E value comes in. Looking at the E value this would be pretty high because you have a short sequence and the chance of matching this in a big database is really high so you can get an E value of let's say: 10. What this means is that you have a chance of finding 10 matches by chance when searching a database of a the current size in other words this match would probably be random! So it's much better to conclude if a match is "significant" based on the E value cut-off than on the identity. Further the choice of the E value is completely yours as said by WYSIWYG♦ as answer to a cut-off question:

E-value refers to the expected number of random hits for a given
  alignment score. Smaller it is more reliable is your match. There is
  no hard and fast rule for e-value cutoff. You can keep whatever you
  want depending on the level of stringency that you require. But you
  should note that for smaller sequences (< 30nt) there is always a
  higher likelihood of random matches. In such cases it is practical to
  relax the e-value cutoff.

Short simple example

Both of these sequences got the same identity but a different E value. What does this mean? Both of the sequences match the same amount(57%) of the amino acids however based on the E value you can say just as you said that the first match is less likely to be a false positive. I want to note one thing: Always take a look at the biological significance of your result. E.g. you extract proteins from a red blood cell and find proteins with a high E value for red blood cell proteins and a low E value for proteins from nerve cells. It's clear that despite the high E value the red blood cells are probably more biologically significant.

I re-edited the question. I feel that "E-Value Cutoff" and "Sequence Identity Cutoff" are the same? Also to clarify, the "hit" means the resulting sequences by BLAST? I think I do not need to know the details of the algorithm. I just want to know how the set the threshhold.

yes the hits are just the result sequences of BLAST, I updated my answer to clarify the difference between identity and the E value @ianselibai

thank you so much! I think I understand most of it. So it reduces the random hits. In that case, the lower of the E-value, the less likely for the "false positive" hits.

It doesn't really reduces the hits but it helps to make a choice about the significance of the hit, just as you said if the E value is low it's less likely that this match is a false positive. So in simple terms: the E value scales your score (based on identity and other factors) so that you can compare this to the other matches. I added a little example in my answer hopefully that will make it clear!

Sure, so for your "Short simple example", I guess, the first one is shorter than the second one?

I just closed the result but that's what you would expect indeed! However there are other scaling factors which can influence this but for that you should read the BLAST course

Sure, I use E-value = 0 to search, still can get hundreds of hits. Thank you for all your help!

If you want to restrict the matches you can try to use other scoring matrices and other parameters.

On the RCSB website, I can only increase the "Sequence Identity Cutoff".

try to use the offical BLAST: https://blast.ncbi.nlm.nih.gov/Blast.cgi But you need to search some information about the paramters if you want to change these

sure, temporarily I will use RCSB


text:
what is the reason for using 70% alcohol (ethanol)l?
For the purpose of sterilization I am using 70% alcohol (ethanol) for a really very long time. but whenever I ask about why actually we are using 70% alcohol till now I did not get a very specific answer. So why actually are we using 70% alcohol for sterilization?

why use ethanol? or why use 70%?

You can probably switch to IPA, too, because it's cheaper. Also note that for disinfection alcohol works fine to blast vegetative microbes on surfaces but for effective eradication alcohol requires at least 60 seconds of wet contact time to really do its job!

accepted answer with a negative vote...interesting : first time to witness that scenario...

Alcohol and water both vaporize completely, leaving no residues. 70% ethanol has been found to be most effective in killing microbes. Higher or lower concentrations are not so effective in killing microbes.
As amir from the university of Karachi states:
70% percent of alcohol is ideal to a stronger solution. Pure alcohol coagulates protein in contact. Suppose the pure alcohol is poured over a single celled organism. The alcohol will go through the cell wall of the organism in all direction, coagulating the protein just inside the cell wall. The ring of the coagulated protein would then stop the alcohol from penetrating farther from the cell, and no more coagulation would take place. At this time the cell would become inactive but not dead. Under the favorable conditions the cell would then begin to function. If 70 percent of alcohol is poured to a single celled organism, the diluted alcohol also coagulates the protein, but at a slower rate, so that it penetrates all the way through the cell before coagulation can block it. Then the entire cell is coagulated and the organism dies.
https://www.researchgate.net/post/Why_is_70_ethanol_used_for_wiping_microbiological_working_areas [accessed Jul 14, 2017].
Martin Luther from Halle Witternburg states: The effectivity of ethanol as e.g. desinfectant or antiseptic agent depends on the concentration of ethanol-water-mixture: An ethanol percentage of 50-80% destroys the cell wall/membrane of bacteria by denaturing their proteins and dissolving their lipids (effective against most bacteria, fungi and some viruses; ineffective against bacterial spores). Therefore, the ethanol has to pass the bacterial membrane/wall to get into the bacteria - if you use 100% ethanol instead, the bacteria get 'sealed' and they will survive... An other mechanism is the high osmotic pressure of ethanol/water-mixtures; and the 70% has the highest one.
Here is an interesting experiment using alcohol water ratios:
https://www.youtube.com/watch?v=h3iUy4Wg8lg

you can perhaps try the alcohol-protein reaction by mixing it with an egg. a bit like some scotch whisky.

your answer was a little bit convincing but now i am thinking that which are the proteins which gets denatured and form the coagulation in the bacterial cell? these proteins are the plasma membrane proteins(extrinsic and intrinsic proteins) or the proteins in cytoplasm ?


text:
Why doesn't cellular, replicative senescence (or the hayflick limit) constrain the normal development of an organism?
The wikipedia article on cellular senescence states:

Cellular senescence is the phenomenon by which normal diploid cells cease to divide. In culture, fibroblasts can reach a maximum of 50 cell divisions before becoming senescent. This phenomenon is known as "replicative senescence", or the Hayflick limit.

My question is, if many cells in diploid organisms (e.g. humans) have an inbuilt limit of the number of cell divisions, how is it that a human can develop from a single celled zygote to a organism comprised of many 10's of trillions of cells - if many cells can only divide 50 or 60 times?
Wouldn't the cells "use up" their available telemeres during development? or is it a simple mathematical relationship, that whilst yes, existing cells are "burning up" their telemeres as they divide during development, but because the number of cells are increasing exponentially they develop all the tissue mass the organism needs before hitting the hayflick limit?
e.g. if cell numbers are doubling during each division phase, it only takes 30 doublings to achieve a billion cells, after 40 doublings you have a trillion cells.
i.e. after 40 or 45 doublings it has developed all the tissue mass of a mature organism, and still has some telemeres left over for additional tissue generation during the organisms lifetime?

Read about telomerase - the Wikipedia article you mention talks about it specifically as a mechanism for getting around the limit - but yes, you can also get an awful lot of cells with 50 or 60 divisions; 10^18.

One cell divides into two. Each of those divides into two. Each of those divides into two... Etc. If this happened 50 times, you would get 2^50=1,125,899,906,842,620 cells. That's plenty and then some.

Yes this article expresses it as a formula: $ Nt = N_0 2^{tf} $ where Nt is number of cells at time t,
N0 number of cells initially, t is time (days), f is
frequency of cell cyces per unit time

You pretty much have answered your own question. It is a math problem. Cells are burning up their telomeres during fetal development onward but the cells are multiplying exponentially in number.
But biology is a bit messy, embryonic stem cells do have telomerase activity and their telomerase are maintain. So the clock doesn't start counting down immediately.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360127/
Temporal wise hES cells are around 4–5 days post fertilization, at which time they consist of 50–150 cells. https://en.wikipedia.org/wiki/Embryonic_stem_cell.
So you don't quite start with an n of 1 cell. But of an n of 50-150 (in humans)... before you start to see telomere shortening. With that head start those 50 doubling can make a lot more cells. By my guestimate with excel ~1.69E17 cells ~320 tons. More than enough you to last a life time.)

Thanks,  the links you provided were useful. I also found an article on the maths behind cell division It would be interesting to come across an article which specifically addressed the "race" between tissue mass created through cell division and the hayflick limit. But I guess we need to figure that out ourselves, and then as you mention there is always the fact that biology is a bit messy :)


text:
conversion from cpm/mg to mg
I 've an essay about wheat sprout extract, there's a graph about protein content in first 4 day of wheat sprout. so under the graph there's this text

Phosporylation by endogenous kinases of the macromolecules contained
  in 1 g of the aqueous wheat sprouts extract. Results are expressed as
  cpm/mg of protein±SEM at 4 different days of germination. 0 are
  unsprouted seeds

so my problem is to know how many mg (milligrams?) is content for 1 g of protein
in few words I need how many mg of protein is content in 1g of products, a conversion from cpm/mg to mg ... is possible?
cpm = counts per minute

What is cpm (counts per minute)? It does not seem like a common abbreviation.

yes sorry counts per minute

I feel like the question isn't written very clearly, and you would get better answers if you can clarify a bit. Unfortunately I can't quite get what you are trying to accomplish so I'm not sure how to make helpful edits. The graph you are displaying is about phosphorylation levels, not content, so maybe that is part of the confusion? I.e., the graph seems to be already normalized to protein content, so from just this information you know nothing about the total protein content on various days, just the relative levels of phosphorylation.

yes, thanks for clarification, the problem is this:

yes, thanks for clarification, the problem is this: I found this info in a experiment sheets about content protein in a wheat sprout, so in the documents, that I found that I have to eat this sprouts during second day of germination because have the max level of proteins, but I can understand how many proteins of I have... If this comment is also unclear please write me thanks

@LXG But that paper just shows there is more phosphorylation at day 2, nothing about the quantity of proteins.

So you're saying that with this data is just impossible to find the quantity of proteins for 1g or percentange ? and you're saing that the 4 day I have more proteins content that in the seconds ? thanks

E. Cpm to fmol/mg:  Enter the specific radioactivity as cpm/fmol, the number of cpm counted, and the protein content of the sample in mg. The result is the number of binding sites in fmol/mg protein.
here is a guide of conversions.
The measure is a relative measure, and it can't be very precise as a discrete measure without knowing the precise measurement conditions, i.e. is it mixed every 5 minutes or every 1 minute, is it dissolved in 1 liter or 100ml? CPM denotes the reactivity and not the weight. You are more likely to get a Mol/L rating associated with a CPM, and two vials with the same CPM rating can have different Mol/L and Mg/L depending on their reactivity.
So, if your paper gives you a comparative measurement, and if it gives you a specific measurement at some stage you should be able to multiply it and figure out the numbers for the various days.

ok i've tried but no luck I can't convert 299,000 cpm/mg in 1g to mg can U help me? thanks maybe this can help : Figure 2 shows the phosphorylation by endogenous
kinase of the macromolecules contained in
1 g of the aqueous wheat extract from seeds
sprouted for four days:
1day163900±17911 cpm/mg of protein;
2day 299,000±35,834 cpm/mg of protein;
3day 120530±11940 cpm/mg of protein; 4 day

Perhaps try a pharmacy forum perhaps, someone who has done a thesis in applied biochemistry can probably say it better. also the chemistry forum, i will have a go tomorrow if you send a comment, my eyes are blurry at the moment!


text:
What is the space between -10 promoter sites and start sites (+1)
Between the transcriptional start site of a gene and the -10 promoter region there is always a space of around 10 nucleotides, what is this space function and purpose?
Do you see the space between operator and promoter.. that is what I am referring to, even without an operator it is usually still there
Also, if I want to insert a specific promoter into a vector backbone, how much space should be between the promoter -10 and +1 transcription start site? Is it always 10 bp?

Please [edit] your question and clarify what you mean. Are you referring to the transcription start site  or the translation start site? I guess you mean the former, but it isn't very clear from your question.

I would say that you are referring to the kozak sequence
https://en.wikipedia.org/wiki/Kozak_consensus_sequence

Transcription start site

By "start site", do you refer to the "start codon"?
I think the spacing you are referring to is the 5' UTR.

The 5′ untranslated region (5′ UTR) (also known as a Leader Sequence or Leader RNA) is the region of an mRNA that is directly upstream from the initiation codon. This region is important for the regulation of translation of a transcript by differing mechanisms in viruses, prokaryotes and eukaryotes

Have a look at the wikipedia article for more information about its roles.
The 5' UTR is typically 3 to 10 nucleotides long in prokaryotes but can be much longer (up to several thousands of nucleotides) in eukaryotes. On which species did you notice this spacing of about 10 nucleotides?

I think the OP is referring to the transcription start site, not the ATG. Otherwise, their mention of a promoter doesn't make much sense.

No, the 5' UTR would include the -10, -35, Shine-Dalgarno and other operator motifs. The OP is specifically asking what the ~10 base pairs between the -10 box and the actual start codon are for.
As far as I'm aware, as a molecular biologist, the site merely serves as a spacer to allow the relevant enzymes to dock with the nucleic acids correctly. You have to bear in mind that just because the ribosomes binding site is only 6-8 bases, the actual amount of DNA that it's occluding will be considerably more potentially.

Yes that is exactly what I was referring to, the base pairs between the transcriptional start site which usually includes the 5' UTR and the upstream (-10) part of the promoter. There doesn't seem to be much information around what exactly this section function and purpose is. Even with an operator in a prokaryotic sequence, the space is still there...

@condo1234 OK, but please edit your question and clarify.

The major reason I am asking is say if I want to insert a specific promoter into a vector backbone, how much space should be between the promoter -10 and +1 transcription start site? Does it always have to be -10?

The question itself is unclear. However I guess that the answer, as it is written right now, looks as if it is requesting clarification. It appears more like a comment.


text:
Reading annotations from a plasmid map
Can anyone explain why inside plasmid mapping software the annotations are layered under each other, I am confused as to why there are essentially two layers within the map, for example in the image below.
The bottom red layer is annotated as "DsRed2" and the top yellow is "LacZ-DsRed2 fusion expressed in E. coli". Does this mean that the red layer is inserted into the original LacZ gene or some sort of mutagensis...? Any explanation would be real helpful.

Second Plasmid design

Third Plasmid

Keep in mind that the plasmid map is made by someone, and probably not perfect. They're also made by programs that let you annotate everything everywhere, even overlapping stuff.
In silico, I assume that the DsRed part and the Lacz parts were present, perhaps copied from some other plasmid map including annotation. After that, someone decided it was a good idea to annotate the complete ORF (in yellow).
What I think this means in reality (just guessing from the map, which is just coarse schematic picture): there's a part of Lacz still present in the plasmid (in pink, second lane) which is fused (in frame) to the DsRed gene (red). Together this gives the fusion gene marked in yellow. Also notice the part (terminator?) in pink that's in the third lane.

Thanks for this, I have added 2 more larger images of plasmids since the original was kinda small. The ORF 2 and ORF 3 (blue) in the second plasmid are under the genes (red), does that mean that simply an insert can be placed there? Also there seems to be a third green layer on top, does that mean the terminator and primer are in the same location? And just a last thing, the third plasmid has arrows in reverse, i.e. lacl and amp', what does this mean? thanks!

ORF2 and 3 are probably just there because of the plasmid / annotation software. There's the Ampicillin resistance gene, which is also just one of the ORFs on the plasmid. The place to insert something new would be in the multiple cloning site at the top (with all the restriction sites). Arrows running in reverse mean the gene is on the other DNA strand, "upside down".

If you want to more about the practicalities of a plasmid I'd suggest to look up the manual for the same (or similar) plasmid. Usually the plasmid in your lab is based on a commercial one, or you use a classic plasmid that's also commercially available.


text:
What is the standard electrode potential of human blood?
Healthy humans have a pH of around 7.4 (slightly basic.) But if you hooked up the blood as a battery how much electric voltage would one generate, what is the standard electrode potential?
This seems to me like it should be important for stuff such as transporting ions across the cell membrane.
If I think about it this question basically comes down to if things like iron tend to dissolve $\ce{Fe -> Fe^{2+} + 2e^-}$ (SEP of 0.44)  or precipitate $\ce{Fe^{2+} + 2e^-->Fe}$ in human blood.
Because of important chemicals like haemoglobin I think the SEP should be around 0.44 but differs depending upon whether cells are absorbing oxygen from it or recharging it with oxygen. Maybe this would even vary depending on whether heavy exercise is happening.

@GerardoFurtado Right.  $K_{eq} = e^{\frac{-\delta G}{RT}}$ so the neutral equilibrium and resultingly pH varies with temperature. I just never connected that to acid stuff.

Sorry, I'm just a bit confused.  I thought the electrode potential depended on the oxidation and reduction potentials of the two dissimilar metals, not on the electrolytic medium.  Am I missing something?

@anonymous2 In a Galvanic cell one electrode will dissolve and another electrode will gain a coating. If an electrode is stuck in the human body the electrode would start to gain some kind of coating or start to dissolve. In response, the body would start to deal with the excess of new ions or deal with the loss of ions and maintain homeostasis for a bit until the person starts getting sick.

@StevenStewart-Gallus ah, gotcha.  Thanks for the clarification. :)

I don't think @anonymous2 is confused, I think the question makes no sense. You can't just stick an electrode in the blood, the electrode has to be made of something. Your explanation skirts around that problem: "In a Galvanic cell one electrode will dissolve and another electrode will gain a coating" - what's the electrode that is dissolving and what's the electrode that is gaining a coating?


text:
How does the peptidoglycan layer of a bacterial cell wall help prevent osmotic lysis?
I recently read that penicillin works by damaging the peptidoglycan layers of a bacterial cell wall causing osmotic lysis, which is when the bacteria cell bursts due to osmotic pressure.
I just would like to know how peptidoglycan prevents this. Thanks for any responses!

Peptidoglycan is formed by the linkage of molecules of NAM ( N-acetylmuramic acid) and NAG (N-acetylglucosamine) into a polysaccharide structure.  Many of these structures are then formed into a lattice by crossbridges of polypeptides.  In gram + bacterial cell walls many layers of this lattice are stacked up forming a rigid structure, that is external to the plasma membrane, and provides more resistance to osmotic lysis than the plasma membrane alone posesses.
Penicillin interferes with the final linking of the peptide crossbridges which results in a weaker cell wall that will make it more likely that the cell will undergo osmotic lysis.
Gram - bacterial cell walls are quite different than gram + cell walls.  They do contain peptidoglycan but the peptidoglycan layer is thinner - only one, or very few, layers of peptidoglycan with some structural differences also.  Therefore, gram - bacterial cell walls are weaker than gram + bacterial cell walls.
"Microbiology, an introduction" Tortora, Funke and Case 11th EDition pp 84-86

The bacterium always has a higher internal osmotic pressure (they contain a lot of stuff, and most of the time much more stuff than their surroundings). This pressure is contained by the membrane and cell wall, and when you destroy the cell wall the membrane alone is not strong enough, and the bacterium will spill its guts.


text:
FitzHugh–Nagumo system with diffusion
I was studying the FitzHugh-Nagumo model with diffusion and I quite do not understand the meaning of it.
If we consider the system without diffusion,
\begin{equation}\label{FHN}\begin{cases}
\dot{u}=\mu\left( u-\frac{u^3}{3}+v+z \right), \\
\dot{v}=-\frac{1}{\mu}\left( u-a+bv \right),
\end{cases}\end{equation}
where $u=u(t)$ and $v=v(t)$, then it models the control of the electrical potential across a cell membrane. It models the action potential in neurons, for example. But this happens because in the system there is a stimulus current, $z(t)$. The system with diffusion
\begin{equation*}\begin{cases}
\frac{\partial u}{\partial t} = \epsilon D_u \nabla ^2u+\frac{1}{\epsilon}(u-\frac{u^3}{3}+v), \\
\frac{\partial v}{\partial t} = \epsilon^2D_v \nabla ^2v-(u-a+bv),
\end{cases}\end{equation*}
where $u=u(x,y,t)$ and $v=v(x,y,t)$, models exactly the same but just adding diffusion and removing the stimulus current.

How can it model the same biological behaviour if the stimulus current disappears?
Therefore, which is the exact meaning of this sistem (the second one)?

I've implemented numerically this system, and ploting $u$ in terms of $x$ and $y$ in a specific time, I get something similar to the following images:
https://chemoton.files.wordpress.com/2010/07/fitzhugh-nagumo-type-reaction-diffusion-system-i.png
Where the first image corresponds to $t=0$, the second one $t=10$ and the last one $t=100$.

What does this pattern formation mean? I do not know how action potential (which is modelled in this system) is related with these images...
Does this happen because the activated cells activate the ones in the neighbourhood (since diffusion acts)? Or this is wrong because the system only takes into account one single neuron?

Thank you so much!

The FHN equation describes a dynamical system which is only dependent on time using a system of non-linear ordinary differential equations. When you allow diffusion (of the current) then you'll get a partial differential equation with spatial as well as temporal variable. You will get travelling waves along the spatial co-ordinates. Also have a look at the cable equation.

Thanks for your comment. The system with diffusion also models the behaviour of a single neuron, like the system without diffusion? Or it goes a step further and models a group of them?

It is also of a single neuron. Perhaps you can add details to clarify the premise of your question.

Mmmm... But in the output of the numerical implementation of the system with diffusion (the three images in the link) we observe a kind of pattern formation, which seems to represent that activated cells activate the cells near them.  Therefore, many cells should be taken into account, in this model, or not? If it only models the behavior of a single neuron, what represents the "pattern formation" of the images?

Are you talking about the wikipedia article? I am not sure what exactly you are referring to. Can you add the right reference and also include the diagram that you were talking about. AFAIK, the diffusion is within a cell.

I'm talking about the wikipedia article, right. But I've also included a link with the three images I'm referring to. I wanted to know the meaning of these images: Why do we get a pattern formation and which relation this has with the action-potential.
Thank you for your comments!

Why do you get those patterns? That's the steady state property of some of these reaction diffusion systems. You can read Alan Turing's article on the chemical basis of morphogenesis. All these images denote a 2D space. I presume that the diffusion considered for the FHN model would be 1D (action potential travels along one direction). Moreover, FHN model oscillates and the steady state behaviour of FHN+diffusion would be travelling waves. So none of these plots denote the FHN model.

I've implemented a numerical simulation of the system with diffusion and I also get plots like the ones in the link. I plot "u" (coloured) in terms of "x,y" and the output are pattern formation [x is in the x-axis, y in the y-axis and u is represented just with different colours, not in the z-axis].
I don't quite understant these images because of action potential travels in one direction, as you said. Then I don't know how to connect the meaning of the system with the output of implementing it.

You should first understand the model before simulating it. I cannot be sure what you simulated actually. This is getting into a long discussion. Please ask a precise question. As the question stands it is difficult to determine what it is actually about.

I've changed a bit the question. In fact, what I want to know is the exact meaning of the system with diffusion. Thank you!