text:
Interplay of neuritic and synaptic growth
Let me try to give a picture of my understanding of neuritic and synaptic growth and their interplay.
Pick two neurons in corresponding areas of opposite hemispheres which are connected by a synapse (and a rather long axon).
Both neurons were originally born at approximately the same time t during brain development in a given distance d, without already having neurites.
They necessarily have a latest common ancestor (stem cell), which doesn't have to be the same parent cell, but maybe the same grandmother or great-grandmother cell.
Now several processes start with different delays and at different speeds:

the two neurons wander away from each other
they specialize thus expressing specific "markers" on their membranes
their axons grow
their dendritic trees grow

Case 1: If neuritic growth is fast enough, the two neurons can meet and build a synapse early (recognizing each other by markers they have in common due to their common ancestor). While wandering away from each other, the neurites have to grow accordingly.
Case 2: If neuritic growth is too slow, and the neurons wander away from each other too fast, the growth of axons and dendrites at least has to be guided somehow (by glia cells or by molecule gradients?) such that later they have a chance to find each other. Finally they recognize each other by markers expressed eventually during specialization.
I could imagine that both cases do occur purely, but even that they can be somehow intermingled.
Question: Is this picture essentially correct or flawed? (A yes/no answer would suffice!)

Furthermore, I am looking for a concise presentation of (resp. gentle
  introduction to) these processes (and maybe others?) and their
  interplay that lead to specific synaptogenesis.

Not an expert on this but Case 1 is mostly wrong. Have you read this: https://en.wikipedia.org/wiki/Axon_guidance. Also, interhemispheric connections are rather rare, at least in the cortex.

What do the commissural fibers connect? (See https://biology.stackexchange.com/questions/65351/development-of-the-commissural-fibers)

The Wikipedia article describes Case 2. But does it explicitly rule out Case 1?

I cannot believe that all neurons have to be at their final positions before synaptogenesis starts. It  must be (in my humble opinion), that at least some neurons already connect during their travel to their final positions, so there must also be axon growth just by lengthening, not only guided. But of course I may be wrong.

For example, it might be the case that some "pioneer" axons connect rather early to their target neuron, then follow it (during its travel) by lengthening, and thus help somehow to guide the following axons (somehow like the emigrant trails led by pioneers in North America in the 19th century), which connect to their targets only later.

That may happen to some extent (that's why I said mostly), but it's highly unlikely, based on first principles: if it was extensive at all, it would prevent neural migration. Don't confuse "pioneer neurons" and their axons with how you used the term, as they project after they have arrived at their target area.

My comments are here to help you revise your question, so please refrain from starting a conversation in the comments unless something I said is not clear. Your last three comments could be incorporated in the question, IMHO.

Let us continue this discussion in chat.

Short answer
Both short and long-distance synapse formation can occur.
Background
Short-distance connections can be made between adjacent cells (Van den Pol et al, 1988). Your 'common ancestor part' is a bit obscure to me. In the end, every cell is born out of a single one :)
Long-distance connections can also be made. For example after neuroneogenesis either during development or even in the adult brain, whole neurons can migrate from their origin to a new part (Kaneko et al., 2017), or axons can grow to find a new target distally, for example after neural injury (Purves et al., 2001).
References
- Kaneko et al., J Neurochem (2017); 141(6): 835-47
- Purves et al. (eds), Neuroscience (2001), 2nd ed. Sunderland (MA): Sinauer Associates
- Van den Pol et al., J Comp Neurol (1998); 399(4): 541-60

But the OP is asking about connections that are formed when cells are very close to one another with axons that later stretch as the neurons migrate to their target area. Can that happen in vivo in the case of neurons so far as to be in different hemispheres?

@vkehayas - I don't see that particular question framed as such in the question


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How do castes evolve in eusocial species?
I have been reading about eusocial species and have some questions. What is the basis for caste differentiation? Is it entirely genetic? Does the queen have the code for soldiers, workers etc in her own genes, so only a mutation to the queen results in change of the whole colony's castes? As a related question, how do different castes evolve?
It seems to me that if only one individual in a colony is reproducing, the rate of evolution must necessarily be much slower because any genetic change in the queen would affect all castes, which is likely to have some negative effects.

please rephrase: prevent stagnating evolutionary. casts just have a group fitness impact, I don't understand what you mean.

I think this is a great question (and if I have time I'll attempt an answer later) but it had some issues, so I've attempted to rewrite it more clearly. If you feel it no longer reflects what you wanted to ask please revert it; I won't be offended :)

(I'd also suggest adding some more information about the reading you've done so far.)

@arboviral: Thanks for the edit, As far as I understand the edit, it still represents my intend. And what I read so far... well, the linked wiki article.

Does a fertile queen have the code for soldiers/workers in its own genes, so only a mutation to the queen results in change of the whole coloniy's castes?

Yes.

But how that would protect them from just going extinct due to one unfavorable mutation to a queen?

One unfavorable mutation to a queen could make that queen and her lineage "extinct". It wouldn't necessarily have any effect on the rest of the population (i.e. other queens and their lineages).  There's no difference here between eusocial and other species.

that's totally right, although you may add that the queen can be inseminated by many males and the nuptial flights may have individuals of a wide range genetically. a proportion of the new queens may have the defective gene omitted or complemented via egg fertilization.

Ants are eusocial and close relatives of bees and wasps. Ant and bees use Haplodiploidy. it is a sex-determination system in which males develop from unfertilized eggs and are haploid, and females develop from fertilized eggs and are diploid.
Young queen ants leaving the nest can have one or 10 or 20 fathers. The new queens and workers are not necessarilly clones, and defective genes can be omitted in workers and queens.
the queen may be inseminated by more than 15–20 males, it's polygynous, versus mono androus (andros being male in greek).
Some queens can mate with different species of ant and hybridize.
A nuptial flight of 10 queens in the first year and 1000 queens in the 10th year, all those individuals will have different genetics, because they all come from different fertilized eggs. The males are drones and all the same.
It can vary by species of ant, the queens can be all the same: in the ant Cataglyphis cursor, the queens are produced by parthenogenesis but workers arise from fertilized eggs, suggesting that genetic variation is vital for the worker
caste (Pearcy et al. 2004).
Here is an attempt to unify the literature on ant caste development and evolution with a single theoretical framework, drawing on recent advances in evolutionary developmental biology.
They say that ant populations contain a balance little to big ants, a range of sizes, whereby queen like features, ovaries, wings and light receptors between teh eyes called ocelli, appear in steps as the larvae grow. Ants molt and the develop from small workers to large queens progressively.
If you check an soldier ant, she has a large head, it's almost as big as a queen's, although the body stays small. in the next stage of caste size, the body grows into nearly a queen, else with wings too.
If there is a lack of one caste, more of a particular kind are replenished.
To read the paper faster, search for keywords, for example hormones, they say:

Two endocrine hormones, juvenile hormone (JH) and ecdysone, are important regulators of developmental timing in insects. Pupation (and the cessation of larval growth) is triggered by ecdysone, and the action of ecdysone is inhibited by JH (Hiruma and Kaneko, 2013). Thus, treatment of larvae with JH or JH analogs leads to prolonged growth and larger size, as long as necessary nutrition is present. JH removal and/or ecdysone treatment leads to premature pupation and smaller adult size (Hiruma and Kaneko, 2013). This endocrine regulation of insect size has been demonstrated in Coleoptera and Lepidoptera, and is also supported by experiments in ants.

Some of the small ants have the potential to become queens, and when there is lots of food, more of the small ones will grow and make many queens that can fly on a hot day.

In M. rubra, larvae do not have the potential for queen development under normal conditions (Brian, 1979). However, larvae that are forced to diapause just before pupation reorganize their endocrine organs and delay pupation after growth is resumed (Brian, 1979). If sufficient nutrition is available, these totipotent larvae attain a large size and develop into queens

You may laugh by reading the effective genetic ant population mathematics at the end of the first citation. it is completely professor level, with a maths formula, which demonstrates that it's extraordinarily complex and variable effective genetic population distribution and gene expression.
If someone can say more about eusocial gene determination it's quite a difficult topic.

I would be curious why someone downvoted this?!

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Evolution and different number of chromosoms? (a non-biologist)
I understand that a species becomes a different one slowly and in a continuous way. However, the different number of chromosomes is bugging me. Chimpanzees, for example, have 48 chromosomes whereas humans have 46.
I have few guesses which haven't satisfied me at all:

The species are not that different, despite of their different
number of chromosomes, and capable of breeding. The offspring is
somehow healthy and is also capable of breeding. But doesn't that
make the offspring sterile?
The other possibility is, at some point multiple offspring in a
    population formed with, say, 46 chromosomes and the breeding took
    place among them. Even though it doesn't sound impossible to me, what are odds really?

Can someone provide an insight to a non-biologist?

It depends on which chromosomes are extra... For example, neanderthal and humans have different numbers, and it's the X and Y chromosome for them that differs. so only female humans which mate with a male neanderthal could have a viable chromosomal balance. The chomosomes can work in sets of three technically, they are called trivalent chromosomes. https://biology.stackexchange.com/questions/15727/examples-of-animals-with-different-number-of-chromosomes-that-can-interbreed

I'm not sure how the evolution of populations works out, but it's well known why humans have 23 chromosome pairs rather than 24 -- our chromosome 2 is the result of a fusion of two ancestral chromosomes, which remain separate in the great apes.  See for example https://www.ncbi.nlm.nih.gov/pmc/articles/PMC52649/

Possible duplicate of Evolutionarily speaking, why do humans have 46 chromosomes

You formulate guesses but what is the question you are trying to address? Does the post Evolutionarily speaking, why do humans have 46 chromosomes answers your question? I am voting as unclear for the moment.

I think you are overthinking the problem. Think of chromosomes as parking lots and genes as cars. Just because there are different numbers of parking lots, doesn't mean cars no longer need parking spaces - they have to park somewhere! In the specific example of humans versus chimps, two "parking lots" were joined together so there are technically less parking lots, but there is still enough room for all the cars. Perhaps I've stretched this analogy too far...

Speciation doesn't happen from one generation to another, it is a slow and continuous process, and for each changing that is kept by natural selection, there are millions of changes that resulted in less functional phenotypes and were negatively selected, and another million of changes that were lethal hence soon aborted (e.g. a mutation that causes an embryo to die even before a fruit or animal can get any development). So it might be possible that many chromosome number changes are taking plane in many organisms, but they  never will estabilsh in their populations. On the other hand, some numerical changes (and all the genetic processes that follow any change) may result in a good fit, and the individuals survive, establish and reproduce. But keep in mind that it is a slow and continuous process.
Theoretically, if among Chimpanzees, multiple offsprings outcome with 46 instead of 48 chromosomes:

In a theoretical scenario: They could be able to reproduce only among themselves (the 46-chromosomed-individuals) and, with time, accumulate some differences in relation to the 48-chromosomed-Chimpanzees, and them they would be named as another species.
In a theoretical scenario: In some conditions, they might be able even to reproduce with 48-chromosomed-Chimpanzees (e.g. if this numeric change resulted from fission of one chromosome, and when the two gametes meet, the two half chromosomes of one parental pair with the whole chromosome of the other one... That is not probable for animals, but happens a lot in plants)
If you are asking if they 46-chromosome chimps would crossbreed with humans... well, I believe they have accumulated too much differences in their genotypes and thus would no be compatible even if they have the same chromosome number. It happens that having the same number is not the most important factor allowing or preventing species to crossbreed. There are many barriers to hybridization, e.g. the lack of biochemical recognition between egg and sperm resulting in no embryo formation... in cases that embryo is formed, it may not develop, it may develop poorly, or it may develop but the offspring comes out compromised and live shortly. Another example that chromosome number does not prevent crosbreed is the mule, which is the offspring of a female horse (64 chromosomes) with a male donkey (62 chromosomes). That's because even having different chromosome numbers, they are still quite simmilar in a genetic perspective.

All that sayd, the odds that Chimps would loose two chromosomes, stablish in the population and reproduce with humans are really really really low... I would say that's impossible. But simmilar phenomena are possible and even quite common in plants (just so you know that it exists)
If you want to learn more about chromosome number changes, I recommend this link: https://www.ncbi.nlm.nih.gov/books/NBK21229/
(Modern Genetic Analysis. Griffiths AJF, Gelbart WM, Miller JH, et al. New York: W. H. Freeman; 1999.)

I think your answer is wrong and unclear -1. Wether your answer answers the question is hard to tell as the question is unclear as well (not your fault). Here are a few critics. Evolution really takes place in a slow and continuous way this is rather wrong! What do you call numerical changes? I don't understand the sentence if among Chimpanzees, multiple offsprings outcome with 46 instead of 48 chromosomes. You seem to think that chimpanzee are humans's ancestors which is wrong. the odds are really really low for Chimpanzees the odds for what?

I'm surprised how poorly I seem to have expressed myself...when I say that evolution is a slow process, I mean that it does not occur from one generation to another... By numerical changes, I mean disploidy... And I don't see what in my answer made you think that I believe chimpanzees are humans's ancestors, but if you got this impression I clearly expressed myself poorly... Thus it's important to remark that humans and chimpanzees share ancestors (as we do with all the extant life, by the way).

I'll edit this answer tomorrow, thanks for pointing out so many things to improve

No worries, misunderstanding is not so uncommon. You are making a hypothetical scenario where chimps lose a chromosome pair and this feel weird to me given that the reason for why there is a mismatch between human and chimpanzees chromosome number is due to a fusion in the human lineage (Ijdo et al. 1991). Btw, welcome to Biology.SE!

Yes, this feels very very weird... But I got from his question that he was asking about the odds of multiple chimps loosing one pair, establishing in the community and reproducing  among themselves... And this is a crazy hypothetical scenario for chimps... But things like this do happen in life... It's even very common in plants... And also, do you think humans would really match chimps if they loose 2 chromosomes? I think they now have too much differences, numeric compatibility wouldn't be enough for them to reproduce and have fertile offspring.. (Btw, thanks! =])

Well, I'll have to disagree with you: evolution does happen from one generation to another! That's the very definition of it!

@GerardoFurtado, maybe you can help me improve this answer, Professor... what I mean is that the fact tha in a population one individual was born with a small difference, that doesn't mean a new species has evolved

Sure, speciation is a very complex process. But the technical definition of evolution (which is not synonymous with speciation) is, in an oversimplification, a change in the allele frequency in a gene pool... and that does happen in just one generation!

Absolutely. I guess since the question mentions "one species becoming another one", I took speciation as evolutionary process and used the world evolution improperly. Thank you, Professor.

I think it is probably worth noting that humans did not evolve from chimpanzees as the question and answer imply. In fact, the most recent anthopoid ancestor of both chimps and humans had a diploid karyotype with 50 chromosomes, according to Stanyon et al. (2008) in the journal Chromosome Research.

I never said that humans evolved from Chimps! They only have common ancestors

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Does evolution violate the data processing inequality?
The data processing inequality (DPI) states that if $X\rightarrow Y \rightarrow Z$ is a Markov process, then $I(X;Y) \geq I(X;Z)$.  We can think of $X$ as a random variable representing some complex functionality that is unrelated to the organism's reproductive fitness, e.g. high intelligence in humans.
If $f(Y) = Z$, and $f$ is a standin for evolution, then evolution can only increase mutual information between $Y$ and $X$ if $f$ contains information about $X$.
However, evolution only contains information related to reproductive fitness.  Therefore, $f$ does not contain information about $X$, since $X$ is unrelated to reproductive fitness.
According to the DPI, $f$ should decrease the mutual information between $Y$ and $X$.
This means that the process of evolution should eliminate all functionality that is not directly related to reproductive fitness.
Yet it seems many organisms have very complex functionality that is not related to reproducing.  Ironically, the higher up the food chain we go the less reproductive the animals become.  So, based on this argument, much of the upper echelons should not exist.  What am I missing here?
UPDATE:
Here is a simple program in python that illustrates the point.

Measure fitness by number of 1s in the bitstring, more 1s the more fit it is.
Set a random bitstring to be a phenotype of interest, P.
Set another random bitstring to be the organism being evolved, O.
Iteratively evolve the organism by flipping a random bit, and then keeping the new bitstring if it is more fit, otherwise rejecting it.

As long as there is no correlation between the phenotype and the fitness function, then evolution cannot turn O into P.

from random import random

P = [int(random() > 0.5) for i in range(100)]
O = [int(random() > 0.5) for i in range(100)]

print "Matches between O from P", sum([o == p for o,p in zip(O,P)])

for i in range(1000):
    j = int(len(O) * random())
    old_fitness = sum(O)
    O[j] = (O[j] + 1) % 2
    new_fitness = sum(O)
    if old_fitness > new_fitness:
        O[j] = (O[j] + 1) % 2

print "Matches between O from P", sum([o == p for o,p in zip(O,P)])

I didn't understand all the maths, however, you have to give examples of "complex functions not related to survival and reproduction" ... All biological functions are either very useful to survival and multiplication, else they are relics of previously apt designs, which are vestigial or modified. ... Also, you will see that mammals can have small bloodcells without DNA nuclei, and small veins, that means they can miniaturize and be metabolically apt. Mammals radiated into bats, whales, moles because of their big "dormant" genome. Birds and lizards, with small genomes and bloodcells, didn't.

Your paragraph beginning "However, evolution is not purposeful" is gibberish. There's no connection between the first sentence and the second. I can't tell if you simply misunderstand evolution or if you've made some logical fallacy in your assumptions, but I suggest you focus on that and explain why you think this makes sense.

All of this in a neutral, respectful tone: ".. if $f$ contains information about $X$. -- $f$ doesn't "contain" anything; it's just a mapping. Also, $f(Y) = Z$ doesn't say anything about $X$, and, it's quite erroneous to just throw in evolutionary processes like that, most especially without even attempting to provide a definition of $f$, other than "$f$ is a standin for evolution".

"According to the DPI, $f$ should decrease the mutual information between $Y$ and $X$." -- though this may be true of Markov chains in general, when applied to biology, it falls apart. Not all evolutionary traits undergo divergent changes, and, it could be that, due to the environment of the organism, $X \rightarrow Y$ could be reinforcing a lack of change between states, and thus, entropy between the two variables is minimized over time, not maximized.

Overall, it's great that you're attempting to describe biology within such a probabilistic context, as that way of modeling can be fairly dependable depending on the question(s) being asked. The problem though is that the probability & mathematics that you're studying is far too complex to accommodate such superficial logical leaps as the ones you're attempting to make. That being said, I am VTC due to OP being too broad (however, I think it could also fall within being primarily opinion based, since your proposed conclusions really aren't based on anything concrete).

@iayork I've attempted to fix the problem paragraph.

You are misinterpreting the meaning of that inequality and confusing information and entropy (there are other logical errors but this one is the first and most obvious, and makes all the others unimportant by comparison).
$I(X;Y) \geq I(X;Z)$
is referring to the mutual information between X and Y compared to the mutual information between X and Z. Essentially "knowing X, how much can I reduce my uncertainty about Y or Z". Those quantities say nothing about the actual magnitude of entropy or complexity in X, Y, or Z, except for placing a lower bound (i.e., you can't have more information about X from Y than the total amount of entropy in X or Y). Entropy in Z could potentially be much greater than entropy in X, but the inequality is just saying you can't get any more information about Z from X than you can from Y.
Interpreting X, Y, and Z as DNA codes, this inequality is perfectly consistent with one part of the evolutionary process that you seem to be thinking about: the introduction of changes into the genetic code (mutation). $I(X;Y)$ in this context would be a measure of how similar the genomes of X and Y are. If Y evolves from X and Z evolves from Y by purely random processes (we are omitting selection and other processes here, which is of course an incredibly important part of evolution as well), then you would expect that inequality to hold: X and Y would be more similar to each other than X to Z. Because evolution is not strictly a random process, however, you could actually get cases where for small parts of the DNA the inequality would not hold. That is because selective pressures do contain information. At the whole genome level this would be probabilistically impossible, however.
You could actually use these measures as a rough way of estimating relatedness (though there are better purpose-built measures for doing so). Essentially, if $I(X;Y) \geq I(X;Z)$ you could conclude that it is likely that X and Y are more closely related species than X and Z.
If you want to view X, Y, and Z as phenotypes, there is really no difference. Decreases in mutual information with X from Y to Z doesn't mean a loss of functionality as you imply, it only means that X and Z are more different than X and Y.

"Essentially "knowing Y or Z, how much can I reduce my uncertainty about X"." -- This is an incorrect interpretation, given the context of a Markov chain. In a Markov chain, as you may or may not already know,  only immediately future events are attempted to be predicted from the current state of the system. And so, when utilizing mutual information inequality, the verbiage would be, "Given X, how much can I say about Y? And, given Y, how much can I say about Z? And then, because X implies Y implies Z, can X say anything about Z?" The perspective of comparison is always forward moving.

"Those quantities say absolutely nothing about the actual magnitude of entropy or complexity .." -- This statement is inaccurate. $X, Y,$ and $Z$ must be measurable variables/functions, and so, $I(X;Y) = \sum_{y\in Y}\sum_{x\in X}p(x,y)lg(\frac{p(x,y)}{p(x)p(y)}) = H(Y) - H(Y|X)$ does contain entropy information, where H() is entropy function. See this diagram as well.

"Interpreting X, Y, and Z as DNA codes, this inequality is perfectly consistent with evolution. " -- This is not true either. In a Markov chain, the future state of the system must purely be dependent upon the immediately local, current state of the system, and nothing else. In this sense, evolution does not match well with an ideal Markov chain, since evolution of genes is governed by many forces completely external to the interval of DNA code; i.e., a forest fire will occur regardless of the DNA makeup present within the organisms subject to experiencing the fire.

You really misread my answer. To your first comment: "Essentially "knowing Y or Z, how much can I reduce my uncertainty about X" is talking about information theory; there is no directionality to Shannon information. To your second point, you missed the next statement: The information sets a lower bound on the entropy, but that's it. Look at the equation you just wrote: I(X;Y) = H(Y) - H(Y|X). I(X;Y) can be zero even if H(Y) is very large, as long as H(Y|X) is similarly large.

For your third comment, again, I'm not talking about Markov chains or their connection to evolution, I am talking about the inequality the OP was using. I didn't say Markov chains are a good model for evolution, I said that the inequality is consistent with evolution. I open my answer making it clear that I don't intend to dissect all of the logical missteps in the question, but rather I focus on one upon which the rest of it falls apart.

The very definition of the inequality is under the assumption of a Markov chain.. if you're not providing a response that takes into account the imposed upon constraints of a Markov chain, then your answer is not relevant to the OP.

I think that it is a weaker argument to protest that evolution does not follow Markov-like behavior, because that inequality DOES describe evolution in most contexts, it just doesn't mean what OP says it does. The current state of DNA is all you need to predict the probability of the next state of DNA after a mutation. It doesn't matter what the DNA looked like 1000 years ago. That's the part that makes it Markov-like.

Let us continue this discussion in chat.

Thank you for taking a shot at answering my question and illustrating where I went wrong.  My critique of your answer is it misunderstands how I use the variables $X$, $Y$, and $Z$.  Only $Y$ and $Z$ are DNA strands.  $X$ is a phenotype attribute.  So as long as $f$ does not contain information about $X$, then the attribute will be removed by $f$.

@yters You are totally misunderstanding the math here. It isn't that the attribute will be removed by f, it's that the mutual information between X and Z will be less than between X and Y. If you really want to define things the way you are, then the correct interpretation is that when the DNA changes (i.e., goes from Y to Z over evolutionary time) it gives you less information about the phenotype X. This is obvious because in actual biology, it is the DNA Y and Z that gave you the phenotype X. Of course when you change Y to Z then Z will not give you the same X as Y did.

I think this is missing the elephant in the room, namely that you need to have selection (natural or otherwise) for evolution to happen (in a reasonable time). And selection (unlike mutation) is not a local operation on the DNA strands as required by the data processing inequality. Selection tosses out some individuals carrying certain strands in relation to others carrying different strands. The "comparison" performed by selection is not a local post-processing operation (as required by DPE to apply) on a single strand/individual; it takes two or more things to compare them...
The more relevant math for evolution is the Price equation, which partitions the change in fitness in that due to selection and transmission causes (like mutation, recombination etc.) If there's no selection, you're left just with the transmission causes. And in your case the single-individual/strand post-procession would be just mutation. What your math is saying is that not much evolution is likely to happen by mutation alone. (Also, you are taking evolution to mean an increase information/complexity rather than in fitness, but that is a lesser sin. An elephant with 500 legs isn't necessarily the most fit in many environments.)

Given your stated interest in ID, I have the feeling you're dressing up with math a common misconception/argument used by ID proponets, namely that complexity is unlikely to occur via evolution; usually the ID propoents jump to that conclusion by misrepesenting (or misunderstanding) the evolutionary mechanims (as you have done here). Your question reminds of this common ID argument:

Assume that, at each mutational step, there is equally as much chance for it to be good as bad. Thus, the probability for the success of each mutation is assumed to be one out of two, or one-half. Elementary statistical theory shows that the probability of 200 successive mutations being successful is then (½)^200, or one chance out of 10^60. The number 10^60, if written out, would be "one" followed by sixty "zeros." In other words, the chance that a 200-component organism could be formed by mutation and natural selection is less than one chance out of a trillion, trillion, trillion, trillion, trillion! Lest anyone think that a 200-part system is unreasonably complex, it should be noted that even a one-celled plant or animal may have millions of molecular "parts."
The evolutionist might react by saying that even though any one such mutating organism might not be successful, surely some around the world would be, especially in the 10 billion years (or 10^18 seconds) of assumed earth history. Therefore, let us imagine that every one of the earth's 10^14 square feet of surface harbors a billion (i.e., 10^9) mutating systems and that each mutation requires one-half second (actually it would take far more time than this). Each system can thus go through its 200 mutations in 100 seconds and then, if it is unsuccessful, start over for a new try. In 10^18 seconds, there can, therefore, be 10^18/10^2, or 10^16, trials by each mutating system. Multiplying all these numbers together, there would be a total possible number of attempts to develop a 200-component system equal to 10^14 (10^9) (10^16), or 10^39 attempts. Since the probability against the success of any one of them is 10^60, it is obvious that the probability that just one of these 10^39 attempts might be successful is only one out of 10^60/10^39, or 10^21.
All this means that the chance that any kind of a 200-component integrated functioning organism could be developed by mutation and natural selection just once, anywhere in the world, in all the assumed expanse of geologic time, is less than one chance out of a billion trillion. What possible conclusion, therefore, can we derive from such considerations as this except that evolution by mutation and natural selection is mathematically and logically indefensible!

Which has been (easily) debunked before:

This is a rather simplistic attack on evolution by mutation and natural selection. The way that he is calculating the probability actually does not take into account natural selection. What he is calculating is the chance that 200 random beneficial mutations happen sequentially without any bad or neutral mutations happening between the beneficial mutations. Natural selection will select and preserve the beneficial mutations and select against and eliminate the bad mutations. Once a beneficial mutation has become fixed in the population, any offspring produced that changed this would be selected against. His example also has no basis in a known biological system. His model essentially has an organism that reproduces only one offspring and then dies. All biological systems known to me the organisms on average have more than one offspring, allowing multiple chances for unique mutations to happen for selection to act on. Even using his unrealistic model slightly modified to have more than one offspring with adding in Natural Selection and having it take 2000 generations for a single beneficial mutation to fix in the population it would take ((2000 generations) * (200 fixed mutations)) = 400,000 generations to get the 200 fixed mutations, which with a generation time of 0.5 seconds would take about 2.3 days. If we use his numbers of one mutation per generation with a 1/2 probability of being beneficial, which would equal to a fixation rate of beneficial mutations about once every two generations much more generous than my 2000 generations. We do the same calculation with these numbers we get (2 generations) * (200 fixed mutations) = 400 generations, which is about 3 minutes.
tl;dr: The guy is an idiot.

For a more academic discussion of this argument see "There’s plenty of time for evolution". The gist of that paper is

The fact is that with the parallel model, i.e., taking account of natural selection, the number of rounds of mutations that are needed to change the complete genome to its desirable form are only about K log L, instead of the hugely exponential K^L which would result from the serial model.
where L is the length of the genomic “word,” and K is the number of possible “letters” that can occupy any position in the word

For a broader treatment of information theory issues in ID vs evolution see Elsberry and Shallit; an older version of that paper can be found freely on teh interwebz.

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


text:
Question About the Physiology of Seizures
Absence seizures usually occur in children between ages 4 to 14 (Hopkins Hospital). Spontaneous remission occurs in 65–70% of patients during adolescence (Medicine Central).
My question is what takes place biologically that allows you to 'grow out of them?' Is it synapse pruning in the brain or something? I have looked everywhere online but can't seem to understand the physiology of how one grows out of seizures.

@anongoodnurse - absolutely not - but, migrating a question should be done on the basis of being explicitly offtopic. In this case I am not doubting the expertise on Health; rather I am questioning this being offtopic here.


text:
Binucleate cells of transitional epithelium (bladder)?
Working through Histology slides of the transitional epithelium (urothelium) of the urinary bladder, I noticed that the dome-shaped cells at the top of the transitional epithelium are frequently binucleate.
In doing research, I found that the top cells of the transitional epithelium are 'often binucleate and usually polyploid'

Why is this?
  What purpose does this serve?
  Is the binucleate feature consistent enough across slides to be used as a common identifying feature to recognise transitional epithelium from the urinary tract? Is the absence/over-abundance of binucleate cells characteristic of certain diseases?

I also see prominent granules (of glycogen, I presume?) in these cells.

Is this glycogen? & What purpose does this serve?

Also, I'm having difficulties recognising transitional epithelium in slides. Does anyone have any tips to share on how to easily recognise transitional epithelium as such (common features to look out for, etc.), especially in distinction to pseudo-stratified epithelium, which often looks similar?

At what magnification you are seeing slides?

Magnification of x540 @JM97

please don't ask more questions in a single post, its against the site's guidelines.

Upvoting because these easy-to-see features of dome-shaped cells go seemingly unexplained in all major histology textbooks. My PubMed searches have not been helpful so far. Specifically, are the dual nuclei the result of an incomplete mitosis, or do cells fuse together into a syncytium?

This might help: https://www.nature.com/articles/s41598-018-19690-7  They had occasional multinucleated cells, but couldn't find a good literature reference for how many to expect (in mouse).  General discussion - https://en.wikipedia.org/wiki/Binucleated_cells

In other stratified epithelium, it is the basal cells that replicate to replace the cells lost in the top layers.  In transitional epithelium, which is also a stratified epithelium, the most superficial layer of cells are replaced or  turnover occurs because of mitosis of the superficial facet cells themselves.  In this case it is not unusual to see dividing cells in its last stage of division as a large cell containing two nuclei, which soon that cell will be 2 cells.

Welcome and thanks for your contribution. Can you add sources to your answer? I have to banner it for now. Ping me once you referenced your answer and I'll remove that banner.

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


text:
How do you read the histone code?
I took it upon myself to research how methylation/acetylation affects histone tails via post-translational modifications. However, I find myself confused about how to "read" this histone code, specifically for the Euchromatin.
My problem is that there are both acetylations and methylations. Does that mean that the methylation of lysine 4 will cause that portion of the chromatin to be condensed, but the acetylation of the lysine 9 and so on will cause that portion to be decondensed?

The "histone code" is not like the genetic code where one codon in an ORF always is translated to a single amino acid. It's closer to something like GC content or CpG islands: a single instance doesn't tell you anything, but enrichment over some finite window may be biologically significant.
You may want to review the basics, starting with the Wikipedia page on the histone code. In particular read the paragraphs at the end:

Every nucleosome in a cell can therefore have a different set of
  modifications, raising the question of whether common patterns of
  histone modifications exist. A recent study of about 40 histone
  modifications across human gene promoters found over 4000 different
  combinations used, over 3000 occurring at only a single promoter.
  However, patterns were discovered including a set of 17 histone
  modifications that are present together at over 3000 genes.[13]
  Therefore, patterns of histone modifications do occur but they are
  very intricate, and we currently have detailed biochemical
  understanding of the importance of a relatively small number of
  modifications.


text:
SNP vs common SNP
Wikipedia citing Nature defines SNP to be a one where each (thus the lowest frequency) allele exceeds some percentage threshold in the population. But I see a lot of papers and books calling such an entity a "common SNP" rather than leaving it unqualified example 1, example 2. Are they using a different/simpler definition of SNP?
Another book says that "SNPs most commonly refer to single-base differences in DNA among individuals" with no qualification on frequency. So I'm guessing those two sources that define "common SNP" use this broader definition of SNP. Would anyone venture a guess which definition of SNP is more prevalent? There's no discussion on the topic of the definition itself on the talk page of the Wikipedia SNP article...

I think the convention is that a point mutation with a frequency of 1% or more of the population is a 'Single Nucleotide Polymorphism' and anything lower would be 'Single Nucleotide VARIATION'.
So regardless of the frequency, any point mutation would be a 'Single Nucleotide Variation'. At higher (more significant) frequencies, we call it a 'Single Nucleotide Polymorphism'. Some may choose to name an SNP of high frequency (for example with a frequency of 15% or more of the population) as a 'common SNP'. In reading, texts will usually give you the percentage for the SNP and their naming choice should make sense. There is no fixed systematic number at which an SNP becomes 'common' or 'rare', since anything less than 1% won't count as one.


text:
What happens if you intake pure magnesium?
We know that body needs a certain amount of magnesium. Why are magnesium supplements in the form of magnesium oxide, magnesium citrate, etc?

Note that this is true for all the trace metals; your body uses magnesium ions, not elemental magnesium. The free metal is not found naturally, it's far too reactive.

Elementary Mg isn't available normally in the environment, only when it's chemically reduced in the lab and stored in the absence of oxygen or other oxidative sources.

I would think pure magnesium would react with the stomach's hydrochloric acid, producing magnesium chloride and hydrogen gas.  Probably not a good idea to perform the experiment on yourself, though.

Because like a lot of material we need the ion not the pure form. Pure sodium is explosive metal and pure chlorine is horribly toxic gas but change them into their ionic form and they are essential nutrients, sodium chloride, table salt.
In the case of magnesium however the problems one of reactivity and absorption. If you swallowed a solid lump of magnesium, not much will happen, the molarity of stomach acid is fairly low, it reacts too slowly to get significant amount of magnesium (or hydrogen) out of it before it passes. Your body just is not equipped to break down solid magnesium since it does not occur naturally often. We can only absorb it in it's ionized state.
More importantly we take in some ion combinations better than others, this is called bio-availability and is influenced by a number of factors. Magnesium oxide for instance has very low absorption rates and basically just passes through without doing much, while magnesium glycinate has a fantastic absorption rate, some combinations can actually be mildly toxic like magnesium sulfate. This is a reoccurring issue with dietary supplements many do not contain bioavailable forms of the mineral they list, which is how people can end up with deficiencies even while taking supplements for that mineral.

Thank you so much! I've heard magnesium is good for IBS. The question is, which form of it. You said magnesium glycinate has a fantastic absorption rate, so it seems like the perfect choice?

once it is absorbed it is basically all the same, but different compounds are absorbed at different rates.

you said magnesium sulfate could be mildly toxic. I'm wondering if different combinations have different mechanism of action?

Magnesium sulfate is a fairly powerful laxative,  that is what I was referring too.


text:
How is a substance classified as a vitamin?
From wikipedia

A vitamin is an organic compound and an essential nutrient that an organism requires in limited amounts.

There are many essential nutrients to an organism. Glucose for example. However, not all of them are classified as vitamins. Is there a clear, non-arbitrary definition of vitamin? If not, who decide what ought to be called a vitamin?

I completely rewrote your question. I removed one of the two questions (which you might want to ask on a separate post). I think the question is good but you already got a close vote but it needed a lot of reformatting and needed is scope to be reduced. Feel free to roll back if you don't like my edit.

@Remi.b  Hm, I posted an answer to the original two-part question just as you edited it.  If we keep the question in this new form, feel free to edit the answer ...

Thanks for changing my question. I'm not native English people, so my english skill is not up to scratch. Before edited, I asked two questiom - 1. Why vitamin D is classfied even it can be naturally synthesized.

And Why vitamin A B C D E K are classified and named as 'Vitamine'

@jong-hyunYeo Vitamine is an abbreviation for vital amine. When vitamins were first being defined and categorized, they were termed as such because originally all vitamins contained an amine. Eventually though, they broadened the classification criteria of vitamins, and so the e was dropped, as it no longer applied.

1) Vitamin D is a bit of an umbrella term that actually refers to a whole group of related molecules. One of these, vitamin D$_3$ (cholecalciferol) is formed spontaneously from ergosterol in the presence of UV radiation, which happens in the skin when exposed to sunlight. Cholecalciferol is then converted to calcitriol, the active form, in the liver. Here is some information on the metabolic pathway.
2) Actually, if you consider the definition carefully, only a few molecules are essential for human growth and nutrition, in the sense that they cannot be replaced with something else, and are required in small amounts. For example, the majority of amino acids can be synthesized by the body from other amino acids, and are therefore nonessential. The remaining amino acids are essential nutrients because there is no synthesis pathway -- but they are required in large amounts and not considered vitamins. This distinction between "large" and "small" might sound strange, but it is important since it tells you if the nutrient is consumed for energy/growth (like amino acids) or has some "supporting" role, such as antioxidants, cofactors for enzymes, or hormones (like the vitamins).
That said, it is sometimes a bit fuzzy if a nutrient is essential or not. Vitamin D is a borderline case: it should perhaps not be called a vitamin, since it can in fact be synthesized by most adults in adequate amounts. However, vitamin D deficiency can occur if one does not get enough exposure to sunlight, and this can cause the disease rickets. Some researchers have suggested that this is one factor behind evolution of lighter skin in northern human populations, since dark skin pigment reduces UV radiation needed for vitamin D synthesis.

Thanks for your answer.I usally takes some supplements for my immune system  and I wonder why some supplements are not classified as Vitamine - Especially Coenzyme Q10 and Omega-3-fatty acid. Your answer give me more clear view than my thoughts.

You're welcome! Btw, coenzyme Q10 is not an essential nutrient; omega-3 fatty acids are essential, but not considered vitamins since they are required in larger amounts.

Please keep reading the Wikipedia article, it clarifies substantially in the next several lines, for example (emphasis mine):

An organic chemical compound (or related set of compounds) is called a vitamin when the organism cannot synthesize the compound in sufficient quantities, and it must be obtained through the diet

and also:

By convention the term vitamin does not include other essential nutrients, such as dietary minerals, essential fatty acids and essential amino acids

Glucose, as an example, is something that is both used in relatively large quantities by humans, and can be synthesized by humans (from carbohydrates and other energy sources).

Wikipedia actually has a really good definition of an essential nutrient:

An essential nutrient is a nutrient required for normal physiological function that cannot be synthesized by the body, and thus must be obtained from a dietary source. Apart from water, which is universally required for the maintenance of homeostasis, essential nutrients are indispensable for the metabolic processes of cells, as well as the proper physiological functions of tissues and organs. In the case of humans, there are nine amino acids, two fatty acids, thirteen vitamins and fifteen minerals that are considered essential nutrients.

For vitamins, this appears to be a definition by exclusion: everything that is an essential nutrient but not a mineral, amino acid or fatty acid is considered a vitamin. Specifically:

Vitamins are organic molecules essential for an organism that are not classified as amino acids or fatty acids. They commonly function as enzymatic cofactors, metabolic regulators or antioxidants. Humans require thirteen vitamins in their diet, most of which are actually groups of related molecules (e.g. vitamin E includes tocopherols and tocotrienols).

I think the reason why food like glucose is excluded from this list is because no particular form of food is necessary in and of itself: as long as you're consuming carbohydrate or fatty acid, the human body can produce energy through carbohydrate catabolism or fatty acid catabolism. So it isn't one particular nutrient that's necessary, just "anything that can be used as an energy source".


text:
Land recultivation? Land revegetation? Land reclamation? Land rehabilitation?
I'm translating a Russian text about the recultivation (рекультивация) of land formerly used for open-pit mining. The process of 'land recultivation' in Russia involves three general stages:

Preparatory stage: a feasibility study, justification of investment, development of working documentation.
Technological stage: engineering operations that involve large-scale movement of soil, removal of machinery and buildings, etc.
Biological stage: seeding of trees and plants, soil improvement operations, irrigation & drainage work, etc.

It is said that the last two stages can last for "years or even decades".
Which English word should I pick? Recultivation, revegetation, reclamation, or rehabilitation?
Example sentences (I retained the original "recultivation" here):

All too often a coal mining company implementing a recultivation project in this region limits itself to the use of simplified technological solutions that fail to take into account the need to preserve biodiversity. The range of plants used at the biological stage of recultivation is limited to five tree species, which depletes the genetic resources of the region's ecosystems and exacerbates the existing invasive species problem.

P.S. The authors of the text do no imply that the land should be used for agriculture - to the contrary, their goal is to improve biodiversity.
P.P.S. Here is a newspaper article about this "recultivation" of open-pit mine land in Kuzbass: source (in Russian)
P.P.P.S. I've just discovered that the English-language title of the Russian national standard GOST R 57446-2017 that comes into force on 1 December 2017 translates the term as land reclamation. However, those who translate Russian documents into English are not always correct.

I think the word choice depends on the ultimate intended use of the land, e.g. recultivation would be appropriate only if it's intended to grow crops.

@jamesqf - growing crops is out of the question - their goal is biodiversity restoration. Maybe I should pick revegetation then.

I'd say that rehabilitation would be the best choice for intending to improve biodiversity.  Simple revegetation would be what's done by the coal companies in that quote.  I think reclamation would be a generic term that includes all the others.  But I'm commenting as just an ordinary English speaker, not a professional in the field.

@jamesqf reclamation is the term I see most often in English texts about this subject. However, I'm no native speaker, so can't really judge it.

Reclamation can be used in this context, but I think in this situation the most appropriate word would be "remediation", from the Latin word remediare which means "heal" or "cure". It is most often used in the sense of fixing environmental problems such as pollution or contaminants.
https://en.wikipedia.org/wiki/Environmental_remediation
A Google search suggests this is a widely used term in the mining industry for the situation you describe.
https://www.google.co.uk/search?q=remediation+mining
It does depend exactly which stages you're attempting to describe, though. From http://www.miningfacts.org/environment/what-happens-to-mine-sites-after-a-mine-is-closed/:

The terms reclamation, remediation, rehabilitation, and restoration
  are all used to describe mine closure activities that attempt to alter
  the biological and physical state of a site. [11] The terms are
  sometimes used interchangeably, and are closely linked, but refer to
  distinct steps in the preparation of the site for another use: [11,
  12]
Remediation: The cleanup of the contaminated area to safe levels by removing or isolating contaminants. At mine sites, remediation
  often consists of isolating contaminated material in pre-existing
  tailings storage facilities, capping tailings and waste rock piles
  with clean topsoil, and collecting and treating any contaminated mine
  water if necessary.
Reclamation: The physical stabilization of the terrain (dams, waste rock piles), landscaping, restoring topsoil, and the return of
  the land to a useful purpose.
Restoration: The process of rebuilding the ecosystem that existed at the mine site (where applicable) before it was disturbed. The
  science of mine reclamation has evolved from simple revegetation
  activities to a discipline which involves using native plants to mimic
  natural ecosystem development over an extended period of time. [13]
Rehabilitation: The establishment of a stable and self-sustaining ecosystem, but not necessarily the one that existed before mining
  began. In many cases, complete restoration may be impossible, but
  successful remediation, reclamation, and rehabilitation can result in
  the timely establishment of a functional ecosystem.

See also this publication by USGS:
Finger, Church, and Guerard. Potential for Successful Ecological Remediation, Restoration, and Monitoring, Integrated Investigations of Environmental Effects of Historical Mining in the Animas River Watershed, San Juan County, Colorado, 2008; U.S. Geological Survey Professional Paper .

Thank you! Based on the definitions you provided, I'd pick rehabilitation because the bulk of my document is concerned with restoring the steppe/meadow ecosystem at the spoil tip sites.

Can reclamation include rehabilitation? I'm getting tangled in all this.

Reclamation is about the physical geography of the site, rehabilitation is about the ecosystem (I think). I'm not sure if rehabilitation and bio-/phyto-remediation overlap though!


text:
How do we know we have to use the mouth for eating and drinking?
I have a question that I am very curious to: how do we know we have to use the mouth for eating and drinking? Because we have multiple openings where, if we didn't know better, could put food and drinks in. So there must be someone who started with eating via the mouth and started to teach their children.
I spent many hours on the internet, but did not find any answer.

It's an instinct, there's no teaching involved. You're better off asking about the biology of this instinct.

The people who fed themselves through their other orifices died out, leaving only that minority who used that crying orifice. As they survived, it was taught to subsequent generations. Now it seems everybody does it that way.

Excuse me, I heard that this kind of logic is prevalent in the knowledge of sects and cities where artwork and nudity is banned. People become very confused... I also would not breathe with my head if no one told me. I would breathe with my armpits or something. You don't have to... If you put a some small foods in the other way round, and you stay upside down, you can regurgitate it and it will still be digested backwards through your digestive tract... try it at home one day. so you don't have to use your mouth if you dont want to. the world is an illusion anyway. why listen to reason?

Food doesn't taste good when you put it in your ear. It does when you put it in your mouth. So every baby who experiments with stuffing food into places, will quickly find that it's much nicer when put in the mouth. Not really much to it.

Quite frankly we don't, eating is instinctual, only later as we grow up do we learn why we do it. It is reinforced with learning later but that is a minor effect. Eating is one of the most basic of animal instincts.
The association "hungry > eating > not hungry" this could reinforce the behavior, but the instinct is present first. infants will learn eating stops hunger long before their brains have have even developed the capacity for abstract thought, and they will latch and feed long before that.
No human "figured out" or "started" eating, eating existed before brains existed. And every single organism between that first feeding organsm and you and me ate. Eating was hardwired into the genome long before parental care existed.

There are several reflexes that are hard-wired and present in newborns. The root reflex and suck reflex are two of them, among others. An infant doesn't have to know how to feed, it will automatically do that.
Once it is feeding through the mouth, the growing baby will have no reason to change its habit when starting on solid foods. Besides, its parents will start to spoon feed the baby by presenting food to the mouth. The parents will do the best they can to comfort the baby when its crying because of hunger. Stuffing the food in the wrong place won't aid that purpose.


text:
How does heart rate change when entering N1 sleep?
I would like to know how the heart rate changes as a person enters N1 (NREM 1) sleep from a wakeful state. The focus is on entering N1, and it would be great to have time-series data to see the pattern of the decrease, but a  textual description of the decrease would be good too. Most importantly, by how much does heart rate decrease from resting to N1, and how quickly does it fall?


text:
Do similar adaptations result in similiar genetic code?
Sometimes organisms within the same species evolve similar adaptations to similar living conditions without interbreeding.
Let's say we have two human populations which need to adapt to a colder climate, albeit one lives on the Northern hemisphere whilst the other one on the Southern hemisphere. Both populations develop hairy skin. Would the gene encoding the hairiness of the skin look similarly in both populations? Would this gene be at the same locus at the same chromosome in both populations?

Do similar adaptations result in similiar genetic code?

It can be the case but it is not necessarily the case. You sure can have the same mutation happening and raising in frequency in two independent lineages but you may well also have different mutations leading to similar adaptations in different lineages.
Example
As you talk about humans, let's take an example from humans. The ability to digest lactose (milk) at adult age has evolve several times independently. I just copy-pasted from this answer of mine

Gene LCT
Mammals have a gene (called LCT C/T-13910) coding for the lactase enzyme, a protein able to digest lactose. Lactose is a disaccharide sugar found in milk.
Expression of LCT
In mammals, the gene LCT is normally expressed (see gene expression) only early in development, when the baby feeds on his/her mother's milk. Some human lineages have evolved the ability to express LCT all life long, allowing them to drink milk and digest lactose at any age.
Today, the inability to digest lactose at all ages in humans is called lactose intolerance.
Three independent mutations
Tishkoff et al. 2007 found that the ability to express LCT at an old age has evolved at least three times independently. Indeed, they found three different [SNPs][6] (stands for Single Nucleotide Polymorphism; it is a common type of mutation), two of them having high prevalence in Africa (and people of African descent) and one having high prevalence in Europe (and people of European descent). The three SNPs are G/C-14010, T/G-13915 and C/G-13907.

In this example we can know that the ability to digest lactose at adult age evolved at least 3 times independently. It is quite hard to tell whether it had evolved more than three times. It is indeed possible that the mutation G/C-14010 had occurred in two independent lineage but it would be hard to disentangle them today if the two lineages are not clearly geographically isolated (and in humans, very few populations are really isolated from the others).

That's exactly what I suspected, just wanted to make sure. Thank you for your answer, I really like that you included a real-world example I can stick my nose deeper into :D


text:
Why are bees eating the wax?
I left outside a piece of wax few weeks ago and each day I saw lots of bees "eating" it. Why do they do this when they can create new wax? (it seems a really hard work considering how little was taken in the course of few weeks).

I do not have an answer but it is a very cool observation and photo; thanks for posting it.

Recycling?  One would think that it's more efficient to re-use old wax than to make new.  Was your wax beeswax, or something else?

@jamesqf It is fully natural beeswax that I solar melted from their old combs. I use it to seal tree cuts.

I'm not a bee person so I can't answer, but I'm curious could it be possible that the bees are treating this loose piece of wax as though it's actually part of their normal hive?  Like they are trying to do normal activity just in the wrong location?  I'm not sure, but I think it could be possible if they are getting the correct chemical signals from the wax.  But...no idea.

It's unclear how costly wax production really is, here are a few resources with some guestimates and studies:
http://www.honeybeeworld.com/diary/articles/fdnvsdrawn.htm
http://www.beesource.com/forums/archive/index.php/t-260700.html
http://www.bushfarms.com/beesharvest.htm#expenseofwax
But doubtless wax is costly to make. So it seems totally reasonable that your bees are actually collecting wax. But my guess, if they were doing this in October, is they drawn by the smell and were poking around for something besides wax per se, like sugar or pollen bits in the wax.
I just saw honey bees buzzing around a compost pile on a warm day in January, focusing on orange peels and used coffee grounds. They would masticate both grounds and peels with their mandibles, but to my eyes weren't actually collecting anything (they didn't bring it to their mouths with their tongues nor pack anything on their corbiciculae). I suspect they will pick at lots of things when there's not a strong pollen or nectar flow, maybe for medicinal reasons or the like, or perhaps more "for something to do."


text:
Why does sequence of amino acids presented on the Catalytic Site Atlas from a given protein differs from the sequence on the RSCB Protein Data Bank
I wanted to compare the amino acid sequence of enzymes for this project I'm working on and need to compare them at their catalytic site. For that, I went to the Catalitic Site Atlas to get the information on the catalytic site, but since they don't offer an easy way for me to download the structure data programmatically I downloaded it from the RSCB PDB by downloading the fasta sequence. When checking for the catalytic sites it wasn't matching what the CSA was telling me and that's when I realized that they are different files. Take for example the 3nos, the CSA presents the following sequence:
MGNLKS...
While the PDB presents the following sequence:
PKFPRV...
Why aren't they the same sequence if it's the same protein?
Sorry if it's a noob question, I'm not a biologist, just a computer scientist who happens to like bioinformatics.
Important info:
The CSA data comes from here while the PDB data comes from here

Please [edit] your question and give us the exact links you used to download. The simplest explanation is that you are not actually looking at the same protein, but we can't be sure unless you show exactly what you are comparing. For instance, your RCSB link shows two sequences but no information about what species they are from, what isoform, nor whether they're the entire protein. In fact, they look like protein fragments (most proteins start with an M). My guess is that you are looking at the entire sequence in one site, and a subsequence in the other but I can't be sure.

There you go, sorry about that

Crystallography results (pdb files) almost always contain a truncated sequence.
Both ends of a protein are often flexible (even in a crystal) and don't result in enough data for a good fit. The corresponding residues are removed from the model and the sequence, and you're left with only the residues that show a defined electron density.

One sequence is partly contained in the other (highlighted).
So the CSA sequence is (FASTA format, truncated):
>sp|P29474|NOS3_HUMAN Nitric oxide synthase, endothelial OS=Homo sapiens GN=NOS3 PE=1 SV=3
 MGNLKSVAQEPGPPCGLGLGLGLGLCGKQGPATPAPEPSRAPASLLPPAPEHSPPSSPLT
 QPPEGPKFPRVKNWEVGSITYDTLSAQAQQDGPCTPRRCLGSLVFPRKLQGRPSPGPPAP
 EQLLSQARDFINQYYSSIKRSGSQAHEQRLQEVEAEVAATGTYQLRESELVFGAKQAWRN...
taken from http://www.uniprot.org/uniprot/P29474 for convenience.
While the PDB one is :
>3NOS:A|PDBID|CHAIN|SEQUENCE
PKFPRVKNWEVGSITYDTLSAQAQQDGPCTPRRCLGSLVFPRKLQGRPSPGPPAPEQLLSQARDFINQYYSSIKRSGSQA
HEQRLQEVEAEVAATGTYQLRESELVFGAKQAWRNAPRCVGRIQWGKLQVFDARDCRSAQEMFTYICNHIKYATNRGNLR
SAITVFPQRCPGRGDFRIWNSQLVRYAGYRQQDGSVRGDPANVEITELCIQHGWTPGNGRFDVLPLLLQAPDEPPELFLL...
The Uniprot entry mentions 3 different isoforms due to alternative splicing, so perhaps that is what is going on here. Here is the output from a sequence alignment (using https://www.ebi.ac.uk/Tools/psa/emboss_matcher/):

#=======================================
#
# Aligned_sequences: 2
# 1: NOS3_HUMAN
# 2: SEQUENCE
# Matrix: EBLOSUM62
# Gap_penalty: 14\
# Extend_penalty: 4
#
# Length: 240
# Identity:     240/240 (100.0%)
# Similarity:   240/240 (100.0%)
# Gaps:           0/240 ( 0.0%)
# Score: 1294
#
#
#=======================================

NOS3_HUMAN        66 PKFPRVKNWEVGSITYDTLSAQAQQDGPCTPRRCLGSLVFPRKLQGRPSP    115
                     ||||||||||||||||||||||||||||||||||||||||||||||||||
SEQUENCE           1 PKFPRVKNWEVGSITYDTLSAQAQQDGPCTPRRCLGSLVFPRKLQGRPSP     50

NOS3_HUMAN       116 GPPAPEQLLSQARDFINQYYSSIKRSGSQAHEQRLQEVEAEVAATGTYQL    165
                     ||||||||||||||||||||||||||||||||||||||||||||||||||
SEQUENCE          51 GPPAPEQLLSQARDFINQYYSSIKRSGSQAHEQRLQEVEAEVAATGTYQL    100

NOS3_HUMAN       166 RESELVFGAKQAWRNAPRCVGRIQWGKLQVFDARDCRSAQEMFTYICNHI    215
                     ||||||||||||||||||||||||||||||||||||||||||||||||||
SEQUENCE         101 RESELVFGAKQAWRNAPRCVGRIQWGKLQVFDARDCRSAQEMFTYICNHI    150

NOS3_HUMAN       216 KYATNRGNLRSAITVFPQRCPGRGDFRIWNSQLVRYAGYRQQDGSVRGDP    265
                     ||||||||||||||||||||||||||||||||||||||||||||||||||
SEQUENCE         151 KYATNRGNLRSAITVFPQRCPGRGDFRIWNSQLVRYAGYRQQDGSVRGDP    200

NOS3_HUMAN       266 ANVEITELCIQHGWTPGNGRFDVLPLLLQAPDEPPELFLL    305
                     ||||||||||||||||||||||||||||||||||||||||
SEQUENCE         201 ANVEITELCIQHGWTPGNGRFDVLPLLLQAPDEPPELFLL    240

This answer is correct, I just wanted to add that the correct sequence numbering is preserved in the PDB file in the DBREF record (which you can see by opening the PDB in a text editor):
DBREF  3NOS A   66   492  UNP    P29474   NOS3_HUMAN      66    492
In plain English, the sequence presented in this file (3NOS chain A) corresponds to residues 66 - 492 of the associated UniProt (UNP) entry (accession: P29474).


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What species of tree is this?
We have this cute little tree in our front yard (Denver CO):

Unfortunately we have to get our water main replaced and this tree lies right in the path of destruction. Anybody know what species it is? And, in your opinion, is it worth saving?

Please add your location (country, state) and if possible where the tree comes from (wild or planted), that will make it much easier to id.

I am in Denver CO. The tree is planted. Its a residential area.

Looks vaguely apple-ish to me, but with a cultivated tree, it may be hard to tell (especially as other fruit trees also look similar). Take a look at the base of the trunk - is there any indication that the top portion has been grafted onto a different rootstock? If so, it's a strong indication it's a fruit tree, though without some sort of tag, telling which variety it is may be difficult/impossible.


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What kind of Brazilian Arthropoda is this?
It looks like a Diplopoda, but I've never seen anything like that. A friend took those pictures in the Brazilian Cerrado (Goiás state, Brazil) these days (October, start of rainfall in Spring). It was inside a country house, she already found it dead.
She said it has about 3 cm (~1.2") long. We can see it's not so small as a Symphyla or Pauropoda. Looks like it has 12 pairs of legs.

Similar to Allothereua maculate and Scutigera coleoptrata.

I was fooled by the red marks in its back, that made me believe they were each pair of marks in a segment. Looks like they're distributed in one pair of red marks for each 2 segments. Maybe that's a mimic of some similar Diplopoda (which usually have such colored marks, see for instance Rudiloria)?
Looks like it's some species of Scutigera or some related group.


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Enhancer elements in prokaryotic DNA?
I know that in terms of post-translational modifications of genes, prokaryotes and eukaryotes differ highly because of the lack of introns in prokaryotic DNA.
With this said, do prokaryotic DNA sequences contain enhancer elements other than the UAS(upstream activating sequence)?
In addition, are enhancer elements like promoter-proximal elements and enhancer elements encoded directly within the DNA? Or are they proteins that attach themselves to the strand of DNA in order to enhance transcription?

do prokaryotic DNA sequences contain enhancer elements

Yes: https://www.ncbi.nlm.nih.gov/pubmed/1776167

other than the UAS(upstream activating sequence)

The Gal4/UAS system is borrowed from yeast, a eukaryote https://en.wikipedia.org/wiki/GAL4/UAS_system

In addition, are enhancer elements like promoter-proximal elements and enhancer elements encoded directly within the DNA?

Yes. Enhancers are usually considered to be encoded directly within the DNA; e.g.: see the following recently published historic perspective on the discovery of enhancers by its discoverer, Walter Schaffner : https://www.ncbi.nlm.nih.gov/pubmed/25719310
Sidenote: Enhancers have originally been discovered in a virus, and thus neither in prokaryotes nor eukaryotes

Or are they proteins that attach themselves to the strand of DNA in order to enhance transcription?

Enhances (often / ~always) exert their function though proteins. https://en.wikipedia.org/wiki/Enhancer_(genetics) Note that this doesn't necessarily affect the definition of enhancers.


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What is the likelihood of a single human gene to the same gene from the other human?

The human genome comprises 3,234.83 Megabases and contains ~ 19,000 genes. It has been estimated that the genomes of humans are 99.9% identical. How likely is it that any single gene might vary from one individual to another? Assume an average length for a gene of 3 kilobases.

Is it still 0.01%, the same as for the whole genome? Why then we have the number of genes in this exercise, together with an approximate length?

Assumptions
Let's assume that we can perfectly align all human genome and therefore calculate such statistics of identity.
Let's assume that the probability of identity of 99.9% is the same for neutral sequences than for coding sequences. This assumption is most likely wrong but there is no other way to answer the question with the data that are given to us.
What is the question exactly?
Your homework question is a little unclear unfortunately. I don't know what is meant exactly by

How likely is it that any single gene might vary from one individual to another?

Does it mean

You randomly sample two humans and randomly sample one gene. What is the probability of perfect identity a this gene?

or does it mean

You randomly sample one gene, what is the probability that all humans are identical for this gene?

I will assume it means the first one.
Step by step
I will go by subquestions to guide through the thought process! Try to answer the following questions one by one and you should be able to get to the final answer yourself

Randomly sample two individuals and randomly consider one nucleotide in their genome. What is the probability that this nucleotide is the same?
Randomly sample two individuals and randomly consider two nucleotides in their genome. What is the probability that these two nucleotides are the same?
Randomly sample two individuals and randomly consider n nucleotides in their genome. What is the probability that these n nucleotides are the same?
Randomly sample two individuals and randomly consider n nucleotides in their genome. What is the probability that these n nucleotides are different?
Randomly sample two individuals and randomly consider 3000 nucleotides in their genome. What is the probability that these 3000 nucleotides are different?

What answer did you get? If you got stuck somewhere, please let me know where!
Hints

No point about using a calculator, it will return Infinite or 0 at some point anyway!
Don't worry too much if you're not using all the numbers that are given to you!

Hint: a modestly advanced calculator will easily calculate this without overflowing or underflowing.

I don't know how many bytes modern calculator typically use for a number but I think (might be wrong, you'll correct me) that it takes about 4 kiloBytes to store the inverse of this number (neglecting the decimals)! I have never seen such number being used in computer science but I don't know what data type (and how much RAM) advanced calculator typically use.

Remi, apparently we have completely different calculations in mind.  It seemed to me (and your answer also suggested to me) that the answer would just require a simple exponentiation operation, and the numbers involved would be reasonable.

Too bad we can't give the answer out loud here to further this discussion! If the OP shows effort at trying to solve the issue form my hints, we can further this discussion :)

The answer: 0.25% of genes will be different
How I got the answer is by simulating two genomes using the following code:
lengthGenome=3234.83*10^6
numGenes=19000
lengthGene=3000
fracSim=0.999

trialHolder=1:100
for(trial in 1:100){
    genomeA=rep(0,lengthGenome)
    genomeB=rep(0,lengthGenome)
    genomeA[sample(1:lengthGenome,round((1-fracSim)*lengthGenome))]=1
    genomeB[sample(1:lengthGenome,round((1-fracSim)*lengthGenome))]=1
    startGenes=sample(1:lengthGenome,numGenes)
    equalGene=0
    for(i in 1:numGenes){
      equalGene=all(genomeA[startGenes[i]:(startGenes[i]+lengthGene)]==genomeB[startGenes[i]:(startGenes[i]+lengthGene)])+equalGene
    }
    trialHolder[trial]=equalGene/numGenes
}
print(mean(trialHolder))

To quickly walk through the code you make a genome of the specified length, and then change 0.01% of the genome to be a mutation, and therefore not similar to the other genome at the same position.  Then define the start points of the number of genes specified.  For each gene region, see if the genes look exactly the same (if one does not have the mutation within).  Finally just track the proportion of genes that are all equal.
I ran the code 100 times and averaged the result, it took a little while.  There is likely a more direct, probabilistic way to do this but I imagine the result would be the same.


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What does breathing through the mouth have to do with cracked lips?
https://www.healthline.com/health/mouth-breathing#symptoms3

Symptoms in children
Children who breathe through their mouths for most of the day may also have the following symptoms:
...
...
dry, cracked lips
...

Why can breathing through mouth result in dry, cracked lips?

Breath is humid. Constant addition to humidity to lips and then the drying of that humidity will dry up the lips, similar (but not as quickly) as licking the lips does.

breath varies in humidity and with temperature. lips crack fairly easily. increased airflow can cause dehydration. it's vague guidelines

You may notice waking up with chapped lips at times. It may be because of sleeping with your mouth open. So, of course you breathe through your mouth all night, leaving it exposed to continuous flow of your breath. Continuous airflow around the mouth region can cause chapped lips in many individuals.


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Blue light in a fridge. Is it really beneficial or just marketing?
Recently while visiting a shop with electronics I saw a fridge with a huge advertisment sticker going more or less like this:

There's blue light source in this fridge so there will be less bacteria inside and your fruits will have larger quantities of vitamins.

Can it be true? How can dead (picked, transported and refrigerated) fruit produce more vitamins? How does blue light affect this?
Furthermore I thought that only UV light kills bacteria.
Therefore my question is: how much truth was on that sticker?

Until proven by the manufacturer, I would see this as an unsubstanciated marketing claim.

Fruits and vegetables are generally not dead.  Most fruit contains seeds, which will grow if planted.  (Aside from those bred to be seedless or sterile.)  Many vegetables, e.g. potatos & onions will likewise grow, and sometimes will sprout even in the refrigerator.

Maybe a little bit?
There are two claims here, so let's talk about them individually. I'm not sure how this light is being produced (probably LED), but it'll have a wavelength somewhere between 400 and 500 nanometers.
Reduced bacterial presence:
The intrinsic antimicrobial activity of blue light is well documented. Although the mechanism is not entirely understood and widely debated, the commonly accepted hypothesis is that the blue light triggers the production of reactive oxygen species like singlet oxygen that are highly toxic. However, this has only been observed under high-power light sources, and low levels of light may actually increase bacterial activity. What counts as a high-power source, you ask? The number from this article is $\frac{10mW}{cm^2}$. For a fridge with an internal surface area of >1 meter, such a power source should draw at least 100 W. Given that normal refrigerators use draw 100-200 watts, you'd essentially be doubling your electrical bill for the fridge.
It should also be noted that the above is a best-case scenario. As soon as you add anything to the fridge, you'll reduce the intensity and thus the effectiveness of the light source. Also, the light is unlikely to be on all the time- it probably turns on when you open the door and turns off when you close it. While this helps a lot with power use, it minimizes the effect of the blue light, which is constantly on in experiments.
Larger quantities of vitamins
There's no (reliable) evidence of light of any kind actually creating vitamins, so what the sticker suggests is that it doesn't degrade the vitamins already present as quickly as other kinds of light.
There's a good article here that discusses the stability of various vitamins. It's worth noting that most of these vitamins and essential amino acids are much more likely to be destroyed by cooking than light, which is probably why the fridge focuses its claim on fruits, which are less likely to be cooked.
There's very little research that I was able to find about the effect of different wavelengths of light on the stability of various vitamins, but as a whole I remain fairly skeptical that there's any notable difference. Most experiments that do study degradation of vitamins under light subject pure vitamins to high-intensity light for several days- unlikely to happen in your fridge.
TL;DR:
A claim like this shouldn't be a major factor in your buying decision. The effects of the blue light are probably negligible given the conditions in your fridge, but if you've got two very similar choices this feature could act as a nice tiebreaker. Besides, there's a lot to be said about how cool blue light looks and the confirmation bias present in your purchase.

wooooooowwwwww :O

Light's pulse perturbs the surrounding medium. If the surrounding medium is a living thing, it perturbs the living thing.
The higher the energy of light, the faster the light's pulse; the faster the light's pulse, the shorter the wave-length; the shorter the wave-length, the larger number of compressions ("machine-gun shots") per unit of distance that the perturbation (wave) travels; the larger the number of machine-gun shots, the larger the damage.
Blue light has more energy than green light (which has more energy than red light) but less energy than UV light. Hence, blue light is less efficient than UV light. Some bacteria are more sensitive to light than others; the less sensitive, the higher the energy light is needed to achieve a comparatively same antibacterial effect.
A long-term exposure of bacteria to light---that is damaging to the bacteria but does not kill them all---can lead to a selection of resistant mutants.

https://www.ncbi.nlm.nih.gov/pubmed/29046782

Good question. Asian fridge moguls want to shine blue light on your chopped fruit, mostly, rather than save your life from a hazardous food.
Some research by National University of Singapore studied the effect of visible blue light diodes on some bacteria although not fungi which makes the fruit go moldy (mould propagation in apples is a common bio practical study).
The bacteria studied are not fruit surface bacteria. they are gut and skin bacteria.
The study did not test if fruit last longer in blue light. it just exposed gut and necrotizing bacteria to blue light.
You may get less E-Coli and salmonella, which is weird because you would have a very unwholesome fridge to have a E-Coli danger from it. fruit is not only consumed by bacteria. Salmonella dangers exist inside certain eggs, which is a dark environment. Fruit practically can't transmit major illnesses like S.Aureus, they live in different environments than fruit and are endemic to humans, but fruit do contain a lot of microorganisms necessary for their fermentation and to break them down.
Blue light perhaps increases your appetite too. https://www.sciencedaily.com/releases/2014/06/140602115916.htm
The raw scientific research for it from 2015 is not for funghi or yeasts, and it doesn't penetrate a steak properly, so it's fairly misleading marketing.

And how would the blue light help the salad or make people less greedy?

I found more qualified research which states that blue light can increase your appetite. previously I had read the opposite statement. good comment.  https://www.sciencedaily.com/releases/2014/06/140602115916.htm

That is actually something that makes a little sense to me, as in general, I have always heard that blue makes people "more comfortable". Some people eat more when they are comfortable, while others eat less, though.

"fruit is not consumed by bacteria" Can you support this with a source?

I'll rephrase it.. fruit is not ONLY consumed by bacteria. ask your local fungicide toting farmer. can you support a motion that suggests that fruit treated with antibiotics will not develop fungal and yeast decomposition? if not, the result is the same. The science does not protect fruit from funghi. let's just say that no one puts antibiotics on their fruit to prevent rotting. They industrially use fungicides.


text:
Did Carl Linnaeus ever name a species he never saw?
According to this post Carl Linnaeus named more than 13,000 species which is definitely quite impressive. If we consider a 50 years career it makes about 5 species per week! It would feel impressive that he could actually take time to find, observe and describe that many species.
Apparently Linnaeus named species from outside Europe such as the Wild Turkey (Meleagris gallopavo, Linnaeus, 1758). This surprised me a little bit as travelling accross the atlantic wasn't all that common in the middle of the eighteenth century. Also, the wiki article on Carl Linneaus says:

Boerhaave offered him a journey to South Africa and America, but Linnaeus declined, stating he would not stand the heat.

It made me realize that there are actually many non European species that have been described by Linnaeus such as the Llama (Lama glama, Linnaeus, 1758).
I heard of Linnaeus trip to Lapland and I always pictured Linnaeus as a field naturalist but now I am wondering

Where did he get his specimens from? Did he have an army of graduate students exploring the world for him?
What fraction of the species he named did he really see in the wild?
What fraction of the species he named did he really see alive? (has he ever seen a Llama and a Narwhal?
Did he name species based on other people description but without ever seeing one dead or alive?

Regarding the amount of work of Linnaeus ("If we consider a 50 years career it makes about 5 species per week!"), there is someone that apparently broke that record: Charles Paul Alexander. According to Wikipedia, "He described over 11,000 species and genera of flies, which translates to approximately a species description a day for his entire career."

During Linnaeus' lifetime there was two ways to get in contact with exotic specimens other than travelling abroad: by visiting museums and collections or by receiving the specimens at your home/laboratory✻. Natural history museums were not that popular at Linnaeus time but only some time later, in the nineteenth century (the first natural history museum, the Muséum National d'Histoire Naturelle, was created in Paris in 1635).
That leaves us (or even better, Linnaeus) with the second option: receiving the specimens. According to the University of California, Berkeley:

Linnaeus continued to revise his Systema Naturae, which grew from a slim pamphlet to a multivolume work, as his concepts were modified and as more and more plant and animal specimens were sent to him from every corner of the globe. (emphasis mine)

You could argue that a (dead) llama is a big animal, but one can describe an animal using just its bones, or even just some of its bones. Besides that, it's worth mentioning that Owen received a whole mammoth in UK to study and describe! So, sometimes, size is not a problem.
Answering your second and third questions, a good deal of the animals he described he never actually saw in the wild or alive. Estimating the precise fraction is way more complicated. The same may be said regarding plants, but I guess that the fraction here is smaller: live plants are easier to maintain, seeds are easy to be transported and sown etc. Besides that, botany was Linnaeus' area of expertise. The same link above says...

Linnaeus was also deeply involved with ways to make the Swedish economy more self-sufficient and less dependent on foreign trade, either by acclimatizing valuable plants to grow in Sweden, or by finding native substitutes. Unfortunately, Linnaeus's attempts to grow cacao, coffee, tea, bananas, rice, and mulberries proved unsuccessful in Sweden's cold climate. His attempts to boost the economy (and to prevent the famines that still struck Sweden at the time) by finding native Swedish plants that could be used as tea, coffee, flour, and fodder were also not generally successful.

... which shows us that he dealt with live exotic plants.
Regarding your fourth question ("did he name species based on other people description but without ever seeing one dead or alive?"), the answer is yes, specially for plants and insects: there are several specimens that Linnaeus described based just on drawings or paintings (which may be considered other people's description), without ever seeing the actual organism. Two examples are Dysdercus andreae (an animal) and Porella (a plant).
PS: Not related to this question or to biology, but this is (unfortunately) quite common in sciences: some of Freud's patients, among them his most famous cases (Anna O., little Hans, etc...), he never actually met or even saw at the distance! He "diagnosed" them using just descriptions and hearsay...
✻ According to RHA comment below, there is a third way: sending people to collect the specimens for you.

You have taught me quite a bit today! Thank you it is a great answer +1

Linnaeus actually send students/coworkers to varies places in the world, to collect specimens for him.

Just to add to Gerardo's great answer, there is a lovely paper that describes a specific instance in which Linnaeus described a bird species, Certhia pinus, on the basis of two illustrations (by Catesby and Edwards) as well as a description by Brisson taken from Catesby, without having seen any specimens. Unfortunately, the two illustrations turned out to be based on two different species, which became known as Dendroica pinus and Vermivora pinus. The authors of this paper, Olson and Reveal, clarified this situation by creating a new name for Vermivora pinus: Vermivora cyanoptera Olson and Reveal, 2009.

That's a very nice find.


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What is this tree in Sydney?
My family snapped this picture around Sydney, Australia. Could someone please advise what this tree is? Help! We are smittened with it :)

This is a tulipwood tree, which belongs to the species Harpullia pendula. As an Australian native, they're commonly used as street trees along the east coast.

More information about this tree can be found here.


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What's the best source characterizing proteolysis cleavage sites in the phagolysosome?
I have found MEROPS and TopFIND via the survey paper Quantitative proteomics and terminomics to elucidate the role of ubiquitination and proteolysis in adaptive immunity. These look like a good start, but I'm wondering whether there's anything more specific.
Ideally, I'd like a list of human phagolysosomic enzymes and some sort of statistical characterization of their cleavage sites, such as position-specific scoring matrices.

You can try UniProt to get a list. They seem to give cleavage sites for proteases, though nothing of the statistics you're looking for.

Looking at the first entry on the list, I think those are sites at which the  subject protein is cleaved, not its substrates.

Some of the entries do contain the cleavage site for the protease, but I guess not all of them. Anyways, that list was just a thought I had… it may have been a bad one.


text:
Picture of a camel's red blood cells
I'm an art student in need of a little help. I'm looking for microscopic pictures of camel's red blood cells, I need their shape for an art project.
The pictures I find on Google seem a little sketchy as in "is it reeeeeally camel blood or is it from some other animal?" kind of sketchy.
I have tried looking further on the net and in books, but without any luck so far. I hope there is someone out there who can help, thanks for reading anyway!

Do you expect a camel red blood cell to have a drastically different shape than the red blood cells of other mammals? Why don't you just consider any picture of red blood cell?

@Remi.b They do indeed (as other Camelidae as well).

Instead of using the answer section for comments, please do this in the comments. You can always comment on your own questions. If the answers suits you, it would also be nice if you would accept it. This brings some extra reputation to the person who wrote it and is a thank you.

Unlike humans and most of mammals, which have a biconcave (or "doughnut shaped") RBC, camels have oval shaped (or elliptical) erythrocytes.
The very first result in Google shows this:

That feature (which protects them from dehydration) is not unique to camels, but occurs in other Camelidae as well. This is an image of Llama blood:

Those are reliable sources of images (optical microscopy) of real cells.
However, for your project, I believe a scanning electron micrograph can better show the shape.
This is an SEM of elliptical camel (a) and alpaca, another Camelidae (b and c), erythrocytes:

For comparison, this is the biconcave human erythrocyte:

PS: There is this misinformation that camels' erythrocytes are nucleate. You can read this in several web pages. I have no idea who made this up, or why people keep sharing this wrong information: camels, like any mammal, have anucleate erythrocytes. See the post Do camels have nucleated RBCs or enucleated RBCs? for more information.
EDIT: The way your question is worded it really seems that you're just asking about the reliability of those sources. However, according to your comment below, it seems that you are indeed looking for better images. It's hard finding better ones than those indexed by Google, but since your goal is modelling those cells, here are two papers (about a protozoan parasite of camelids) which has some SEM that may suit you. The images are not high-resolution, but the cells are shown in several angles:

https://www.omicsonline.org/open-access/babesia-cameli-as-a-new-species-infecting-camels-camelus-dromedariusat-assiut-locality-2155-6156-1000700.php?aid=79911
https://www.ecronicon.com/ecmi/microbiology-ECMI-02-000040.php

In both papers the SEMs are at the bottom (just skip the optical ones, they are not good).

Wow I did not expect that! +1 Do you know why an ovale shape reduces water loss? They all "swim" in plasma anyway, it is unintuitive to me that the shape would matter at all. Do you know if the hemoglobin is the same? Would be great to come up with a reference for the claim that camels [..] have anucleate erythrocytes so that we know who to believe.

I believe hemoglobin is the same, 2alpha + 2beta. I'll check this anyway. The elliptical shape doesn't reduce the water loss, but makes the cells better suited for a "thicker" blood (when the blood as a whole looses water).

Ah it all makes sense. We actually already had a post on Biology.SE about the question of whether camels have nucleated RBC. I edited your answer to add it.

Yes this is really interesting.

@canadianer thanks for editing my broken English, I really appreciate that. I just changed the family (Camelidae) back to normal font, we cannot italicise taxa other than species and genus.

Ah, now I’ve learned two new things ;)

@canadianer you're welcome! For bacteria, you can italicise family and below: https://wwwnc.cdc.gov/eid/page/scientific-nomenclature. However, I don't follow that system. To avoid confusion, I used to say to the students: "never italicise family, order, class, phylum, kingdom or domain, and always italicise genus and species". Also, I'm old school: both the ranks and the taxa should be capitalised. That's why I like to write Family Hominidae, not family hominidae.

Thank you so much for the fast answers! I really appreciate that. I was hoping through my question, that I could get a hold on better pictures of the ovale shaped blood cells, than the ones Google have. I'm sorry that I didn't make that clear in the above question. I like the aesthetics of the "pink" ones, do you know where I can find something like those, but in a higher resolution? I may be asking for too much, sorry about that (-:

@HelleP. please check the edit.

Nice answer! It's not relevant to the question, but in case anyone's interested I thought I'd point out that camelids also have weird antibodies (https://en.wikipedia.org/wiki/Heavy-chain_antibody).

@GerardoFurtado Thank you so much ones again! You have been a great help (-:


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Is spliceosomal RNA called snRNP or snRNA?
I have been reading articles by various sources, and they seem to interchangeably call the U1/U2/U4/U6 compounds involved in RNA splicing snRNPs as well as snRNAs.
This confuses me deeply. They must only be one or the other, no?
Thank you in advance!

Another post with no reference supporting your assertion and no evidence of an attempt to solve a trivial question of nomenclature that an internet search would have answered. Please discontinue this practice.

I'm voting to close this question as off-topic because it is a trivial question about nomenclature that is easily solved by an internet search.

snRNA: small nuclear ribonucleic acid
snRNP: small nuclear ribonucleoprotein
snRNA refers to the RNA itself. snRNP refers to snRNA complexed with some protein(s). You could call spliceosomal RNA either depending on the context.

Most small and large RNAs typically exist and function in complex with proteins as ribonucleoprotein particles so the second denomination is more appropriate.