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Is death by cyanide the same as suffocation?
Reading this description of cyanide poisoning — http://indianapublicmedia.org/amomentofscience/how-cyanide-kills/ — makes me wonder if death by cyanide is equivalent to suffocation. Is it?

In suffocation or asphyxiation you are actually deprived of breathing oxygen. As a result, the arterial blood oxygen concentration decreases (hypoxemia) which is detected by the chemoreceptors of the carotid body and aortic arch. This induces a neuronal response in the medulla that increases the respiratory rate. Simply put, you get panicked. Prolonged suffocation may lead to seizures, cardiac and respiratory arrest and eventually death.
Cyanide poisoning is an example of histotoxic hypoxia resulting from tissue poisoning by $\rm CN^-$ ions. Unlike other forms of hypoxia where the concentration of oxygen is less in tissues, in cyanide poisoning, the concentration of oxygen is perfectly normal in both the extra- and intracellular fluid. It is the cell that is unable to utilize the oxygen present in/around it. As a result the arterial blood doesn't lose much oxygen during its course to the tissue as the oxygen gradient is not quite steep, resulting in an increase in the $\rm HbO_2$ concentration in the venous blood as well.
Thus your skin gets cherry red, not blue like in the case when you are deprived of breathing oxygen, which occurs due to an increase in the concentration of deoxygenated hemoglobin in the blood.
Here is what happens at the molecular level.
The $\rm CN^-$ ions diffuse into the mitochondria. They have high affinity to the ferrous ion of the mitochondrial enzyme cytochrome c oxidase involved in the electron transport chain (ETC), one of the phases of cellular respiration where $\rm ATP$ is generated from $\rm NADH$ and $\rm FADH_2$. And it is this process that actually requires oxygen. The inhibited cytochrome c oxidase is of no good in transporting electrons, thus no $\rm ATP$ molecules are generated. The oxygen molecules waiting for those electrons remain empty handed resulting in the increase in the concentration of molecular oxygen. Remember, ETC occurs in almost all living cells except a few like RBC which get their major share of ATP from the highly inefficient anaerobic glycolysis. Also, $\rm ATP$ is the energy currency of our body and is required in a wide variety of bodily processes like osmotic balance, nerve impulse transmission, muscle contraction etc. With no $\rm ATP$ your heart and respiratory muscles can't contract, your medulla can't regulate breathing, your kidneys can't concentrate urine and the list goes on. Death is imminent if a high concentration of cyanide gets into your blood.
The symptoms of panic like tachypnea and tachycardia (that result due to low oxygen in blood) are not usually seen unless the victim himself knows he is poisoned. The end effects like cardiac and respiratory arrest, seizures and coma, however, are similar to those of suffocation.
For further read:
The Mechanism of Cyanide Intoxication and its Antagonism

@mindwin it is always recommended to put citations in answers, not only to back-up claims, but also to provide sources for further reading

I'm not a doctor, so I'm not 100% sure about the physiological differences, but on a molecular level there is one:
Cyanide blocks the complex IV of the oxidative phosphorlytaion, which will directly stop cells from consuming oxygen and producing energy needed to survive. This is mechanistically different from suffocation, where there is not enough oxygen in your blood stream to sufficiently power oxidative phosphorlytaion to produce energy (meaning complex IV could work, if it just had more oxygen).
During suffocation - or low blood oxygen - the body can react to the lowered oxygen supply (by increased breathing):

In humans, hypoxia is detected by the peripheral chemoreceptors in the carotid body and aortic body, with the carotid body chemoreceptors being the major mediators of reflex responses to hypoxia. This response does not control ventilation rate at normal pO$_2$, but below normal the activity of neurons innervating these receptors increases dramatically, so much so to override the signals from central chemoreceptors in the hypothalamus, increasing pO$_2$ despite a falling pCO$_2$

The mechanism for these oxygen sensors doesn't seem to be known, so we can't be sure if cyanide would also trigger them, but I think it's rather unlikely. I would also guess that the reflex reaction to low blood oxygen (triggered by these sensors) can additionally induce panic, which would likely not happen in cyanide poisoning. Other symptoms like dizziness, which are a more direct effect of neurons shutting down (or having not enough energy) should be similar.
Edit:
The time it takes you to die is likely to be different as well. Cyanide acts fast - once it is in the cells - but depending on how you 'take' it, it could be similar to suffocation (although, you still might not directly notice the effects).

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Do all body organs grow in proportion during the period of physical development?
It is obvious that during childhood and puberty, the human body grows uniformly or proportionally so that a child's arm length, for example, is shorter than an adult's arm length but is proportional to a child's leg length.
What I'd like to know is whether the same is true for internal organs, or are there any organs (even external but perhaps less obvious) that do not grow in dimensions when the rest of the body grows and develops (I am talking about physical growth).

Careful: what you claimed to be obvious ("during childhood and puberty, the human body grows uniformly or proportionally") is not what happens! Actually, that's what led the pre-renaissance painters depict child Jesus in the Madonna paintings as a strange, miniaturised adult. Human body grows disproportionately during childhood.

I suggest reading this wikipedia article Allometry

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How can tree branches grow upwards against gravity?
I saw this tree in front of my room with those branches, and I asked myself why they didn’t grow downward in the direction of gravity since that would be easy for them? And I came to the conclusion that they are seeking sunlight. Is there any research which explain how they can do that?
I found that this mechanism is called Gravitropism (Tree Branches grow against gravity, while roots grow into the soil in the direction of gravity) but I didn’t find a clear explanation.

This review paper might help answer your question: http://www.plantphysiol.org/content/120/2/343.full
It seems that starch-filled organelles called amyloplasts sediment in the cell according to the pull of gravity, and in doing so this gives the cell some form of basic up-down polarisation.  If my memory serves correctly, this can then cause changes to the growth of the cell in the branches, meaning the side of the cell opposite the amyloplasts grows slower and the side closest the amyloplasts grows faster, causing the upwards curvature of the branches seen in your tree.

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Why high quality DNA should be between 10 and 20 kb?
On this website, they are saying that, when using a gel electrophoresis to assess DNA quality, :

High quality genomic DNA should give a major band of 10-20 kb on the
  gel.

Why is that so? I thought it could be because of the size of the chromosomes, but chromosome X in humans is 156,040,895 bp, which is far from 10-20kb. So why is that threshold of 10-20kb? Is DNA breaking usually in chunks with that size?

The website specifically talks about DNA samples intended for sequencing. The DNA in these samples was/is/will be extracted from cells and this extraction procedure leads to fragmentation (breaking into chunks). Since the expected average chunk length will greatly depend on the extraction process, I guess its reasonable to assume that 10-20kb can be expected from the most common protocols.
Much larger or much smaller fragments will also cause problems with the sequencing. (This is again method dependent, but generally true with varying fragments sizes that can be sequenced with the different available methods)


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How to use a published phylogenetic tree?
I would like to know how should I use a phylogenetic tree from an already published article, to put it on my own article so I can analyze the evolution of a trait. Is there any software I can use, or do I only have to "edit" the tree with a traditional image editing software?
I've seen that using trees from other authors is a common practice. Many times they summarize the trees. But no paper seems to tell you how they did it.
Thank you!!

Have you looked at the supplementary material?

Can you explain what you mean be "use" the tree? Do you mean just getting the tree into a usable (e.g., Mesquite) format? Or do you mean do you have the right to use a published tree?

If you'd like to reproduce the image, contact the publisher. If you'd like to reference the data in your analysis to publish, cite the author appropriately. If you'd like to obtain the raw data so you can do something with it, you can do what @Remi.b notes and check the supp. materials for a table or something, or you can contact the author, and cite the author.

Thanks Remi.b and CMosychuk.
My answer is more in the way that says CMosychuk, I mean that I would like to take a tree from the paper "A" and include it on my own paper "B". The tree from "A" will be modified to adapt to my analysis, for example by changing fonts, size, and adding images representing characters in some taxa. I do not mean to modify it on its structure, nodes, or distances.
I do not know how to explain it better.

I don't know how generalized this is, but some journals require the authors to deposit the trees in a database, like treebase. In this case, papers should indicate the accession numbers of their trees.
You then need the appropriate software to load the tree, manipulate it and print it, for instance ete.


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What is the most basic organism to respond to Classical conditioning (capable of learning)?
I have been doing some reading of Classical conditioning which is considered to be an indication of animal's ability to learn...
Before this I considered insects to be machine like - devoid of any sort of 'thinking' just doing things that evolution 'made' them to do to survive...
However I have found that cockroaches and even fruit flies could be conditionally trained...
Which made me wonder What would be the least complex species that respond to classical conditioning?
I have also read this question about single-celled organisms capable of learning and I don't think that this 'cuts it'... this is nothing more than chemical response... however classical conditioning is different and in my opinion certainly does indicate ability to learn...

It's not clear what you mean by "first"? Earliest in evolutionary time?

@kmm Hi kmm, I am looking for the 'most basic' one, but I think that acquiring ability to learn was so advantageous that it will be same ancestor for all of us that got this ability, so evolutionary 'first' should be the same...

C. elegans, with only 302 neurons, is reportedly capable of both learning and memory, e.g. http://learnmem.cshlp.org/content/17/4/191.long so very simple nervous systems are capable of it.  Don't know how you would determine which was first in evolution, as behavior doesn't fossilize well :-)

@jamesqf Wow! Could you post it as answer please I would like to accept it... I am sure that first ancestor is long gone....

When you guys say "the first", I hope you understand that the scala naturae is a completely wrong concept, that should be buried where it belongs: to the dark ages. I, you and a nematode worm have exactly the same evolutionary time, and no one (neither humans or nematodes) are the first.

I changed your question to ask about the least complex as opposed to the first since the "first" doesn't really mean anything (see, for example, here).

While we all have a vague intuition of what is a complex and non complex organism, the term complexity is not well defined. I would guess that the accurate definition would matter little to the purpose of the question though

@Gerardo Furtado: Actually that nematode is argually more evolved than a human (or just about any vertebrate), because evolutionary time should be measured in generations, not years.

@jamesqf Where on earth did you read that?

@Gerardo Furtado: I didn't read it.  It seems a fairly obvious conclusion from the mechanism of evolution.

@GerardoFurtado obviously, the whole idea of "more evolved" doesn't make any sense. However, if you were to use the term, the only reasonable definition for "more" or "less" evolved would be "has gone through fewer or more generations". By that measure, nematodes are indeed "more evolved" for whatever that's worth. Relevant Q&A: https://biology.stackexchange.com/q/832/1306

I don't want to use an argument from authority here, but I will: I'm the author of a university book on evolutionary biology, and I've taught evolution for more than two decades, specially phylogenetic systematics: "more" or "less" evolved make no sense, and talking about generations makes no difference and it's not more reasonable, unless one compares a terminal with its direct ancestors. However, the only certain fact here is that I'm spending more time on this forum than I should... that being said, whatever you guys say is correct. Cheers.

@GerardoFurtado good grief, relax! Please read what we are saying, my comment (and my answer in the linked post) are saying precisely that the whole idea of "more" or "less" evolved is nonsensical. However, if you were to use those silly terms, the only way they might make sense is in terms of generations. And with all due respect, get off your high horse. We're all experts here and have been working for just as long as you have.

I've read what you said, and my opinion is that talking about "generations" makes absolutely no difference to the nonsensical concept of "more evolved or less evolved".

Very simple nervous systems are capable of learning  C. elegans, with only 302 neurons, is reportedly capable of both learning and memory.  There is a fairly large literature on the subject, as C. elegans is a popular research subject - a Google Scholar search gives about 40K hits, e.g. http://learnmem.cshlp.org/content/17/4/191.long
We have to remember that small is not necessarily primitive: the C. elegans nervous system (like every other one in existence today) has been optimized by millions of generations of evolution to do what C. elegans needs in order to survive.
Actual evidence of learning in nervous systems in the distant past is rare.  It's behavior, and behavior doesn't fossilize well :-)  Actual nervous systems apparently don't fossilize all that well, either.  The earliest well-preserved example I could find was this http://www.cam.ac.uk/research/news/520-million-year-old-fossilised-nervous-system-is-most-detailed-example-yet-found from 520 million years ago.  But since learning would give a creature a survival advantage, I'd guess that it evolved fairly early.


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Cell organels during cell reproduction
When one studies cell division, usually the process is explained through what happens with the DNA of the cell, particularly, that in eukaryotes the nucleus dissolves. But what happens to the rest of the organelles? I read here what happens to the ER and Golgi complex, in particular I'm wondering what happens to the mitochondria, in which part does it reproduces? do they make a parallel process? or do they get dissolved?
$%---------
%I started wondering about this because I was reading Lynn Margulis' article _Bacterial Bedfellows_, and it baffles me that in such little time an organism can just coexist with an attacker and turn it in a _good relationship_, how ever it's not clear to me how cell reproduction might work in those cases.$

During mitosis the cellular organelles that have their own genetic information reproduce independently. Other organelles like the Golgi complex disintegrates and then form all over again in the daughter cells. Other organelles that are smaller and more numerous like ribosomes are divided between the two cells. Meiosis is the same thing only that there is crossing over in the nucleus of the cell.

So mitochondria reproduces at the same time as the rest of the cell?

Mitochondria can reproduce on their own. I'm not sure how this is controlled exactly, so maybe it happens at a different time point. Also note that DNA replication (or reproduction if you will) does not happen at the same time as cell replication (mitosis/meiosis)

@Nicolai 'Also note that DNA replication (or reproduction if you will) does not happen at the same time as cell replication (mitosis/meiosis)'... In cell cycle, S-phase and M-phase are two distinct phases where the cell divides and DNA replicates receptively. Also the cell cycle almost in all standard text based on the pattern of division is termed Mitosis/Meiosis (not the M-phase). A slight wording issue.


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Can birds raise younglings that are not their own?
For example, if a scientist were to move a chickadee or pigeon egg from one nest to another, would the new bird (second mother) in the new nest incubate or raise the youngling? Or would the new mother reject the egg since it lacks its imprints (like scent for example)?
In other words, can birds differentiate between their offspring and foreign offspring?

You may not realize, but you actually have two questions here.
Question number 1 is this:

Can birds raise younglings that are not their own?

The answer is yes. We call this Brood parasitism, and it occurs in several species of birds.
There is both intraspecific (between members of the same species) and interspecific (between members of different species) brood parasitism. I believe you want to know about interspecific brood parasitism.
By far the most famous examples are the cuckoos (Family Cuculidae). Some species of cuckoos are obligate parasites, meaning that they only reproduce laying eggs in other birds' nests.
It's very funny (for us, probably not for the host) the fact that sometimes the young parasite is way bigger than the host mum:

A Eurasian reed warbler raising a common cuckoo. Source: Wikipedia
Then, we come to your question number 2, which is different:

If a scientist were to move a chickadee or pigeon egg from one nest to another, would the new bird (second mother) in the new nest incubate or raise the youngling?

The answer here depends on several factors, mainly the species involved.
For species that suffer broad parasitism, there is egg-rejection if the parasite egg is somehow different. If you look at the adaptations to parasitism in the Wikipedia link I shared, you're gonna see that "among specialist avian brood parasites, mimetic eggs are a nearly universal adaptation".
However, species that don't suffer broad parasitism are more prone to accept egg transfer (see @bshane comment here).

We cannot infer egg-selectivity in most species (as in the second part of this answer) from the observation of mimetic eggs in brood parasites: not all species suffer brood parasitism, and host species have an evolutionary incentive towards egg-rejection that does not exist for species not involved in a host/brood-parasite arms race. Many species will accept egg transfers, and such 'cross-fostering' is widely used in conservation (e.g., http://www.jstor.org/stable/3809290?seq=1#page_scan_tab_contents and http://onlinelibrary.wiley.com/doi/10.1046/j.1523-1739.1993.07010160.x/full).

@bshane Thanks for sharing this, mate. I just edited my answer. Cheers.

So, in other words, for an inter-specific egg transfer between a non-brood parasitic bird (such as a pigeon) to another, the second mother would probably accept the egg since she lacks any evolutionarily-produced incentive to discern between her own eggs and foreign eggs. But what about if the scientist moved an already hatched youngling to her nest. Would she still accept the transfer? Or can she identify and reject which chicks are not hers?

@orangebull That's a good question. As this is a different problem, I suggest you post another question: that way, you're gonna attract way more attention.


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What kind of bug or insect is this?
One of my friends has seen this insect-like species in water in the mountainous area in Iran (near Qom).

Where (what country / region) was is found?

@Remi.b Iran. near Qom.

Looks like some species of tadpole shrimp. I couldn't tell you what species. There's really no other basis for identification other than these are extremely unique. As you can imagine, they're endemic to a variety of wetland environments. The take home point, however, is it's a crustacean rather than an insect.

what information can be derived when  this crustacean is seen somewhere ?

@M.H I'm not too sure. As you can see, my best candidate for the species happens to distribute over multiple continents and countries.


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How do elk know how long their antlers are?
They fight to compete for females, particularly those with similarly sized antlers. How would an elk know that its antlers are similar in size to another elk's if they can't see how long their own antlers are?
"The stag with the biggest antlers asserts dominance by showing them off and occasionally fighting with them."
Source: Natural Curiosities Ep. 4

Why do you think they can't see how long their antlers are?  I don't know about elk specifically, but most grazers have a very wide visual field.  Also, if they didn't somehow have an idea of their width, they would have trouble going throught the forest: picture one trying to run between two trees that are closer together than the width of the elk's antlers :-)

For comparison humans can't see what hat they're wearing. Elk have a wider field of vision but I doubt they have a field of vision tall enough to actually see their antlers, which extend very much behind their heads (example: https://elknetwork.com/wp-content/uploads/2016/09/bull_elk.jpg). To navigate through the woods I imagine they have a kinesthetic awareness and don't stray much beyond that. But to compare antler sizes requires some visual acuity -- my reasoning with this is that I wonder if confidence rather than perfect accuracy might play a role in this form of competition.

Maybe they make sense by weight.

I think you anthropomorphise in your question going by how you have worded it. It is an ongoing debate but so far only a limited number of animals have been shown to have a sense of self-awareness. Without self-awareness and a notion for length, the question of "who's got the longest" becomes irrelevant. It probably just so happens that the biggest animal (which also happens to have the biggest antlers) is a little stronger and thus asserts more dominance.

@Jamie: Without some data on the elk's visual field (and I couldn't find any in a quick search), we're both just guessing.


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The smaller the cell the greater its surface-to-volume ratio?
I read in a book that the smaller the cell the greater its surface-to-volume ratio (the surface area of a cell compared to its volume).
And larger cells have limited surface area compared to its volume.
How is this possible? I don't understand.

also consider the width of the surface and the number of atoms it contains as a lipid, it's not strictly geometry.

@comprehensible It is just geometry: http://www.brooklyn.cuny.edu/bc/ahp/LAD/C5/C5_ProbSize.html

This is more about understanding geometry than biology.

This is a very basic question that requires you to think in terms of geometry. Just think.

Did you try finding an answer yourself? Please share it and see our homework policy.

I am preparing for a entrance test.  I read this in a book for that test.  ...its not a home work

Homework policy should explain what questions are considered Homework, elementary topics which may appear trivial to biology professionals fall in it.

This is a basic property of geometry: for any given shape, area will be generally proportional to the square of the length, and volume will be proportional to its cube. (this isn't true for all shapes by any means; the "generally" refers to the principle that length, area and volume are 1, 2 and 3-dimensional properties respectively, not that all or even most shapes behave this way... although a lot of the shapes that happen to be common in the Universe do. See end of the answer).
For example, if a sphere has a radius of R, its surface will have an area of 4*Pi*R², and its interior will have a volume of 4/3*Pi*R³. This means its surface-to-volume ratio will be 3/R, which is inversely proportional to R, meaning when R increases it will decrease and vice-versa.
Like so:
\begin{array} {|l|l|}
\hline
R~(\sim length) & R^2~(\sim surface~area) & R^3~(\sim volume) &  1/R~(\sim surface~area / volume) \\
\hline
1 &   1 &   1 & 1~(= 1/1) \\
\hline
2 &   4 &   8 & 1/2~(= 4/8)\\
\hline
3 &   9 &  27 & 1/3~(=9/27)\\
\hline
4 &  16 &  64 & 1/4~(=16/64)\\
\hline
5 &  25 & 125 & 1/5~(=25/125) \\
\hline
\end{array}
Put another way, if your shape is growing in 3D then whenever you add a bit of length you'll tend to add much more area (because area is increasing along two directions of length) but you'll be adding even more volume (because volume is increasing along three directions of length), and more volume than area means the area-to-volume ratio becomes smaller.
It helps that cells are convex and can often be approximated as spheres, so the rule absolutely applies to them. It's different with squiggly shapes, or cases where you aren't growing along every axis (for example this principle is true if you increase a cylinder's radius and length, but not if you just increase its length; at that point length, surface area and volume are all increasing along a single dimension and thus all at the same rate; check the equations to see this). You often do find such squiggly, long or thin shapes in nature, and this is often an adaptation to get around the surface-to-volume decrease issue. Examples include your intestines, or the interface between the placenta and the uterus.

Its still not clear but thank you a lot for the answer

If the above answer is not clear to you, you might want to review your basics in geometry and algebra. You can as well comment specifically on what you don't understand from the current answer to let @Rozenn (and other users) what specific point needs to be clarified.

Got it now,.............

The answer of Rozenn Keribin and Gerardo Furtado already explains the basic principle very well. I'd like to add another aspect, though. The effect of the increased surface to volume ratio also comes into play in the case off nanotechnology where small particles are compared to bulk material.
Consider the following example, where a cube with edge length 1 m is devided into smaller cubes with edge length s:
\begin{array} {c c c}
\hline
edge length ~s & number~of~particles & surface~area ~A (m²) & total~volume\\
\hline
1~m & 10^0 & 6*10^0 & 1~m^3 \\
1~cm & 10^6 & 6*10^3 & 1~m^3 \\
1~mm & 10^9 & 6*10^5 & 1~m^3 \\
1~µm & 10^{18} & 6*10^{11} & 1~m^3 \\
1~nm & 10^{27} & 6*10^{17} & 1~m^3 \\
\hline
\end{array}
As you can see, the total volume of all particles is always 1 m³ since you only cut the original cube of 1x1x1 m into smaller pieces. However, this example highlights that you have a much larger total surface area for all particles if they are smaller when compared to larger particles.
This means that the effective surface area of the obtained particles increases with the inverse of the square of the size while the total mass (and volume) stays constant. The surface of the particles is proportional to their (bio-)activity.

The other answer is not mine, I just edited it to add a Mathjax table (as you did here) :-).

Anyway, you contributed ;-)

Still not clear but thank you a lot

@roxaite I modified my answer - please check, if it is more clear to you now.

Got it chris..thank you for simplifying your answer...

Let's approximate a cell by the simplest possible shape, a cube. Let's say the sides of the cube are 1mm (that'd be a large cell...). It's volume is obviously 1 mm3, and since it has 6 sides, a surface area of 6 mm2. That gives us a surface to volume ratio of 6. Now let's cut this cube in half. Now every part has a volume of 0.5 mm3. But what happens to the surface area? Four of the six sides are cut in half, and we keep one of the original side. But we also get a new side from where the cut took place. So our new area is 1+1+4*0.5 = 4 mm2. This gives us a surface to volume ratio of 4/0.5 = 8, which is greater than the original 6.

Tthnx bro.. your answer was also helpful

Others have mentioned cubes, and the principle is the same, but I prefer to think in terms of spheres.
The volume of a sphere is $\frac43 \pi r^3$
The surface area of a sphere is $4 \pi r^2$
The surface-volume ratio is thus $\frac3{r}$.
You can plot the function $\frac3{r}$ (see here), or just know that this is an inverse relationship -- as $r$ goes up, the ratio goes down; as $r$ goes down, the ratio goes up.
This is a different way of saying -- a smaller object (which has smaller $r$) has a greater surface-volume ratio.


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If our eye lens and cornea were flat would we still receive the world upside down?
Usually the effect of a pinhole (or camera obscura) and the lens of our eyes are creating the world upside down on our retina.
Now imagine the lens and cornea would be flat is the pinhole effect still capable of creating a reversed image or would our vision be total blurred because (parts of) objects  shining straight in the middle into our eye would not be reversed while parts above or beneath the middle would be reversed?

Is this question about visual-cognitive orientation or the physics of a lens focusing light? If it's the former, see this CogSci answer about how visual orientation is perceived relatively- https://cogsci.stackexchange.com/a/339

Cross-posted at Physics: https://physics.stackexchange.com/q/337807/44126

The question is definitely more on-topic on Physics.SE


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What DNA does a self-fertile plant's seedling have?
Some plants are said to be self-fertile. An example is Prunus tomentosa.
Assuming that no cross-pollination happened with other plants, if a self-fertile plant such as prunus tomentosa produces a seedling, what DNA will the seedling have? Is the seedling's DNA an exact copy of the parent plant's DNA, or do the genes get rearranged?

Selfing (aka self-fertilizing) differs from cloning. When selfing occurs, the offspring is not an exact copy of the parent. When cloning occurs, the offspring is an exact copy (except for a few mutations) of the parent.
Selfing implies that an individual will produce two gametes (typically a spermatozoid and an ovule but that might be a bit more complicated) and these two gametes are fusing to give the zygote (egg or offspring if you prefer).
As a consequence, when selfing, meiosis is occurring (and therefore segregation and recombination) so that the offspring is not an exact clone of the parent but rather some kind of a rearrangement of the parent genome (with a few mutations of course).

This question might be of interest: Peach pits with multiple seeds: Do the seeds have the same DNA?

This question might be of interest: Peach pits with two seeds: Are the seeds identical twins?


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Why do 60S & 40S ribosomal subunits make an 80S ribosome (not 100S)?
Why do 60S & 40S subunits make an 80S (not 100S) ribosome and, similarly, 50S & 30S make 70S? 60+40 is not equal to 80, nor is 50+30 equal to 70, so why are the subunits of the 80S and 70S ribosomes named so weirdly? I couldn't come up with any other mathematical explanation.

That's not a simple mathematical addition!
If those units were mass, for instance, you could (and should) add them: a 60g Lego piece combined with a 40g Lego piece will, of course, form a combo that has 100g.
However, those numbers are Svedberg units, which is...

a non-metric unit for sedimentation rate [...] The Svedberg coefficient is a nonlinear function. A particle's mass, density, and shape will determine its S value. (emphasis mine)

Funnily enough, most of my students thought that that S stands for Sedimentation. However, it's a tribute to Theodor Svedberg, winner of the Nobel Prize for Chemistry in 1926.
Thus, in a oversimplified explanation, the prokaryotic ribosome has two sub-units. The large sub-unit sediments at 50s, the small sub-unit sediments at 30s, but the two together (that is, the whole ribosome) sediments at 70s, not 80s.
The same way an eukaryotic ribosome has a large sub-unit that sediments at 60s, a small one that sediments at 40s, but the whole structure sediments at 80s, not 100s.
Also, the rRNAs that constitute the sub-units have their own sedimentation rates (in svedberg units) as well:

For a detailed explanation with all math you need, the other answers here and here explain it beautifully.

When a complex mixture of particles undergoes ultracentrifugation, they separate based on their shape and mass due to the force applied by the centrifuge and the counteracting frictional force of the solvent. You can read more about this procedure here. S stands for Svedberg, which is a measurement of the sedimentation rate of a particle. This is given by the formula $s=\frac{v}{a}$ where $s$ is the sedimentation coefficient and $v$ is the velocity a particle moves when an acceleration, $a$, is applied.

One svedberg is defined as exactly 10−13 s. Essentially the sedimentation coefficient serves to normalize the sedimentation rate of a particle by the acceleration applied to it. The resulting value is no longer dependent on the acceleration, but depends only on the properties of the particle and the medium in which it is suspended. Sedimentation coefficients quoted in literature usually pertain to sedimentation in water at 20°C.

A 1S particle, for example, would move at 10-13 m/s when an acceleration of 1 g is applied (ignoring diffusion).
What's important to realize is that the sedimentation rate of a particle depends not only on its mass but also on its shape (among other things) since its cross-sectional area determines the effective frictional force it experiences.
When this was done with E. coli extracts, peaks were seen at 32S, 51S, 70S and 100S, depending on Mg2+ concentration. The researchers concluded that the 32S and 51S peaks were components of the 70S peak and that the 100S peak was a dimer of two 70S particles. They also determined that the mass of the 50S particle was about double the mass of the 30S particle which, together, added up to the mass of the 70S particle.

Svedberg unit means 10^-13 sec.... So that means 70s will take 70×10-13 seconds to settle down?

@roxaite I've edited my post to answer your comment.

The other two answers give nice detail, so I want to give a bit more mathematical answer here.
First, the S you are talking about is Svedberg units (of sedimentation coefficient, named after Swedish chemist Theodor Svedberg), used to characterize the behavior of a particle in sedimentation process, especially centrifugation. One svedberg corresponds to exactly 10-13 seconds (see other answers for more details).
Now, lets begin with equations. Sedimentation coefficient is written in equation as:
$s = \frac{v_t}{a}$
where $v_t$ is the terminal velocity. Terminal velocity of a particle in a given medium is constant because the force of gravitation (or centrifugation) is cancelled by the viscous force of the medium. In such case, terminal velocity is calculated as ratio of centrifugal force to the viscous resistance (from Stoke's law) and its equation becomes:
$v_t = \frac{mr\omega^2}{6\pi\eta r_0}$
Also, centrifugal acceleration:
$a = r\omega^2$
Putting the value of $v_t$ and $a$ in first equation:
$s = \frac{v_t}{r\omega^2} = \frac{m}{6\pi\eta r_0}$
As you see, although sedimentation coefficient is the ratio of terminal velocity to centrifugal acceleration, it does not depend on either of them! Now, all other things are constant, and mass would add linearly. So why does the value of $s$ decrease? It is because of non-linear addition of $r_0$ (radius). See the diagram below:

It is clearly visible now that the subunits don't just mix into each other (like two oil droplets joining to form one bigger droplet), the small subunit fits on the large subunit (real shape does vary, but roughly the shape is like this). This makes the average value of $r_0$ of ribosome larger than the sum of average value of $r_0$ of subunits i.e. $r_0 (small) + r_0 (large) < r_0 (ribosome)$. This makes the overall sedimentation rate a bit lesser than expected (remember that $s \propto \frac{1}{r_0}$). I hope this makes the concept more clear.
References:

Sedimentation coefficient - Wikipedia
Difference between 70S and 80S ribosome

You are too polite, mate: the other answer does, but my answer don't provide any detail! It's a very general, oversimplified explanation!

@GerardoFurtado I think all 3 answers complement each other quite nicely; it's always good to have different explanations.

@canadianer bringing back the traditional way of answering, something SE missed a lot ;)

@gerardofurtado you mean I need to incorporate more details in my answer? If I do, who would want to scroll down and see other answers? :P

@another'Homosapien' If you do add more details, people will say "wow, that's more than my average reading for a week... here, have my upvote"!

@canadianer I was about to add technical details to my answer when you posted yours, that explains the issue perfectly. So, I just left mine as it was.

@gerardofurtado I've added all the details I could. What if people say "wow, these 3 answers explain everything so beautifully...here, have my upvote, all of you"! ;)


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Self-fertile PRUNUS: Approximately how much of the genome gets rearranged by meiosis?
I'll admit that I don't have a background in science, so this might be a stupid question. Suggestions and edits are welcome. The question is related to a similar question I had here: What DNA does a self-fertile plant's seedling have?

Some prunus plants are said to be partially self-fertile. An example is prunus tomentosa. I've been informed that through self-fertilization (a.k.a. selfing), meiosis occurs, which rearranges the genome.

...when selfing, meiosis is occurring (and therefore segregation and
  recombination) so that the offspring is not an exact clone of the
  parent but rather some kind of a rearrangement of the parent genome
  (with a few mutations of course). Source

Approximately how much of the genome of a self-fertilized seed is impacted by meiosis? Is a large amount of the genome rearranged, such as 25%? Or less than 1%?

It makes little sense to give a percentage of the genome impacted by recombination and segregation. I think you should read about segregation and recombination and that would be clear to you why giving a percentage makes little sense.
Segregation
Segregation causes that the two haplogroups of the parent can be rearrange at the among chromosome level. So, for example if, in this lineage, each individual has 3 pairs of chromosomes. Let's denote each haplogroup by a capitalize vs non-capitalize letter, we can represent the genome as
a|A b|B c|C

Without segregation (and recombination), a parent could only transmit either
a b c

or
A B C

in a given gamete. This results in the three possible zygotes
a|A b|B c|C
a|a b|b c|c
A|A B|B C|C

segregation allows the creation of gametes like for example
A b C

resulting in possible zygotes such as for example
A|a B|B c|C

Recombination
Recombination typically occurs at a rate of one recombination event per chromosome (that is 100 centiMorgan per chromosome as a rule of thumb; see here to understand what a centiMorgan is). Further rearrange creating new haplogroup from the two existing haplogroups. So for example, from the pair of chromosome
A|a

an individual could create a new haplogroup from recombining the end of A with the beginning of a (or vice-versa).
Related posts
There are probably a lot of related posts. Here are a few of them:

Do only one or both pairs of homologous chromatids exchange genetic material during the process of crossing over?
Gene distance and Recombination Frequency: Mechanism
Is the discovery of dominant and recessive genes the only reason Mendel matters?
What is Mendelian Segregation and how is it related to the Hardy-Weinberg equilibrium?
Genetic linkage greater than 50 centimorgans
What are the exceptions of Mendel's laws?

As has been pointed out, it isn't so much a question of how much gets rearranged (because everything is potentially shuffled) but is really a question of how much is lost or changed, since any genes/alleles present are going to be subject to expression.  This is a simple Mendelian genetics problem, but to really answer it you need to know whether your alleles are in a heterozygous or homozygous state.  If you take locus A, for example and cross Aa x Aa, you will find the next 25% of the progeny will be AA, 50% will be Aa and 25% will be aa.  In essence, you lose 50% of your heterozygosity with each generation of selfing.  Why is this important?  If you are highly heterozygous to begin with, you will have difficulty recovering selfed progeny that resemble the parent.  The more homozygous the parent is, the more likely you are to recover selfed progeny that closely resemble it.  For crops like peaches, which are self-compatible and descended from a narrow genetic base, that means that lots of important alleles are more likely to be homozygous to begin with and less will be lost from each generation of selfing, whereas some other type of crop which might have higher levels of heterozygosity (an F1 hybrid strain or species that evolved as an outcrosser and/or has a wider genetic base) will be quite different.
For something like Prunus tomentosa my guess is that "domesticated" clones in circulation are probably all descended from one or a few individuals.  If they tolerate selfing it is quite possible that seedling strains have come about over the last Century (either intentionally or just because people found it easier to grow out seedlings than to propagate clonally on a large scale) since it was introduced.  Since each generation of selfing leads to loss of half of heterozygosity, you can very quickly reach a situation where alleles for major characteristics have become fixed in a small population.  Thinking about it this way if you start with a scenario where EVERY gene is heterozygous, in one generation only half will be, in two generations only 25% will be and with three generations of self pollination only 12.5% of your genes are in a heterozygous state.  At this point you can see that just 3-5 generations of selfing can lead to fixation of most of the alleles and that if only one plant is saved and moved forward from each selfing event as "the best" you will have something that will give progeny that are phenotypically very similar to the selfed parent.  This doesn't always work from the standpoint that many plants don't tolerate selfing and suffer from inbreeding depression, but this is usually related to the breeding systems that they have evolved with and species that evolved as self-compatible in the wild tend to be more tolerant than those which largely evolved as self-incompatible.

Can you please add sources?


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What is the name of a gene whose effect comes from the dominant and recessive alleles
The p53 gene has a mutation which results in the cell having a cancerous phenotype.  This effect is dominant as one allele being mutated is enough to result in this effect.  However when both alleles are mutated then the phenotype changes / become more pronounced so it's not a simple dominant mutation.  What is this kind of mutation called?  Is it hemi-dominant or something?

Allelic effects

What is the name of a gene whose effect [..]

The concept of dominance make sense for alleles. The gene has no name to refer to the allelic interaction.
Patterns of dominance
Patterns of dominance and recessivity are typically used for quantitative traits. Can you somehow put a a number into the phenotypes of all three genotypes? Making some kind of association table would help even if the phenotypes are not quantitative. See below.
Attempt to answer the question
It looks like you are considering a case where the phenotypes
aa -> healthy
Aa -> sick
AA -> very sick

Under this model, it is hard to tell whether you would consider sick half way through healthy and very sick or not. It feels like you want to consider sick as being closer to very sick than to healthy so if we put numbers we could get something like
aa -> 1 (healthy)
Aa -> 2 (sick)
AA -> 2.5 (very sick)

As such, A shows partial dominance (aka incomplete dominance or semi-dominance).


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Analogous organs: coevolution or opportunism?
The question reads as: "The lens of many vertebrate eyes is a crystallized form of a protein that also functions in digestion as a metabolic enzyme. This shows that
A. Vision and digestion co-evolved
B. Digestion necessarily evolved prior to vision since it is a more basic function
C. Evolution is opportunistic
D. Vision and digestion evolved around the same time"
My approach: Based on the given information it appears the protein might have given rise to analogous organs. I don't feel B has to be true in all cases. C is a good candidate but its meaning isn't clear. I'm not sure about D. To me the answer appears to be A but I would be happy to be have this confirmed.

If you think your question has been answered, you can click on the check sign next to your favourite answer.

I think the question you have to answer is a bit badly phrased. Overall, I mainly agree with you, except for point A. Here are my comments for each points:
A
co-evolution is defined for the evolutionary dynamic between two lineages. It is typically not used to talk about two body parts. Consider for example the definition from Understanding evolution:

The term coevolution is used to describe cases where two (or more) species reciprocally affect each other's evolution.

, wikipedia

In biology, coevolution occurs when two or more species reciprocally ("co-") affect each other's evolution.

or dictionnary.com

evolution involving a series of reciprocal changes in two or more noninterbreeding populations that have a close ecological relationship and act as agents of natural selection for each other, as the succession of adaptations of a predator for pursuing and of its prey for fleeing or evading.

I would note that the term coevolution can sometimes be used in its border line case as in this paper for example. It is particularly confusing as the term co-adaptation is sometimes used to talk about the interaction of two phenotypic traits. But stil, I would NOT check A
B
I agree with you! The conclusion is not valid from the premise (which means that it is not necessarily true, so even if the conclusion may be true, it cannot be concluded from the premise)
C
I agree with you! The statement is a bit unclear.
Typically, evolution is opportunistic would mean that throughout evolution history, a lineage may well evolve to reuse an existing gene for another purpose (neofunctionalization for example) which is very likely what happened here.
D
I agree with you! The conclusion is not valid from the premise.
In short
I would check C.

I would say C is the right answer. Here, "Evolution is opportunistic" means something like "Evolution is a process that re-uses structures and mechanisms".
The question is about what you can conclude from the information given. The other three answers (A, B, D) are about the relative timing of when these functions appeared. Only C talks in more general terms about re-use of an existing protein for another purpose.
Of course, it seems reasonable to suppose that digestion evolved before vision - however, we can't really conclude that from this one example.

As a side note, I did a project a while ago about eta-crystallin, which is thought to have been an aldehyde dehydrogenase that is 'moonlighting' as a structural protein in the eye lens.
See : Crystal structure of eta-crystallin: adaptation of a class 1 aldehyde dehydrogenase for a new role in the eye lens


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What is the difference between phylogenetic tree "construction" and "reconstruction"?
When I look through papers, there are two terms

Phylogenetic tree construction
Phylogenetic tree "Re"construction

What is the difference between phylogenetic tree "construction" and "reconstruction" ?

There is no difference! In both cases, they refer to the building of a phylogenetic tree from data.
The expression 'phylogenetic tree construction' is less common.


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If mantis shrimp have 16 photoreceptors then how many other colors on the spectrum are there?
Mantis shrimp have 12 to 16 photoreceptors and humans have 2, and in rare occasions even 3. But if mantis shrimp can see 16, how many other colors are out there? How many photoreceptors is possible? How much of the spectrum is not ever going to be seen by any creature ever?

Some sources - http://phenomena.nationalgeographic.com/2014/07/03/natures-most-amazing-eyes-just-got-a-bit-weirder/        https://en.wikipedia.org/wiki/Mantis_shrimp     https://phys.org/news/2013-09-mantis-shrimp-world-eyesbut.html

Not really answerable, since color is a subjective term.  I suppose an upper limit would be in the Xray or gamma part of the spectrum, where photons become energetic enough to destroy receptor molecules.  Some aquatic creatures sense electric & magnetic fields, so it would be theoretically possible to detect radio wavelengths: https://en.wikipedia.org/wiki/Electroreception

Related for your final sub-question: https://biology.stackexchange.com/questions/57708/what-is-the-biological-potential-for-vision-of-wavelengths-outside-the-human-vis

The first source you posted pretty much answers your question. Here are some others, probably referring to the same study but talking about it differently:
The Mantis Shrimp Sees Like A Satellite (National Geographic; this article is referred to in your first source)
Study Offers Insights into Unique Color Vision of Mantis Shrimp
Mantis shrimp's super colour vision debunked (Nature)
Here is the paper that those three articles are based on:
A Different Form of Color Vision in Mantis Shrimp
And what seems to be the author's (slightly more recent) thesis on the subject:
Colour vision in mantis shrimps: understanding one of the most complex visual systems in the world
The big thing to understand is that there is no such thing as "the color spectrum". There is the electromagnetic spectrum, which is one-dimensional: you can describe an electromagnetic wave's position on the spectrum with one number, its wavelength. But if you look at a picture of the electromagnetic spectrum with the colors associated you can notice something immediately:

You don't see a uniform increasing of a single quantity from one number to the next, you see several distinct colors following each other.
That's because the point of color vision isn't to detect variations along the electromagnetic spectrum per se; the aim is to allow our brains to get more information about the world around, based on the fact that light comes in many different wavelengths. Different objects will reflect different combinations of those wavelengths, meaning being able to tell some of those wavelengths apart improves our ability to tell objects apart based on those differences.
The key here is that there isn't a perfect way of doing this; nobody has a system where you detect the exact wavelength of each photon and tell exactly how many of each wavelength you receive. What human eyes do is have some specific receptors be more receptive to some wavelengths than others, and then the brain compares how excited each receptor is and puts all that information together to generate a sense of "color", which is basically a way of telling some things apart when they reflect certain different wavelengths. It's related to wavelength, but isn't the same thing; for example our brains recognize wavelengths that excite the red and green receptors equally as "yellow". This includes wavelengths that fall between the red and green wavelengths, but also combinations of red and green wavelengths. That's how you get the color wheel, the ability to make some colors out of others, and the fact you can generate all colors that we see from three primary colors. An organism with an extra receptor between the red and green would be able to tell those different combinations of wavelengths apart so that "yellow" to us would look like several different possible colors to them. Conversely, trichromatic humans are able to tell colors apart, like red and green, that are one single color to dichromatic mammals.
So the answer to "how many colors on the spectrum are there" is "there is no universal color spectrum". Every organism with its own system of light receptors can theoretically have its own color spectrum; how many colors they see is a question of how many different combinations of wavelengths they can tell apart, and that's a function of how many receptors they have but there can also be other factors (like the sensitivity of given receptors, how much processing power they're dedicating to color vision, exploiting different aspects of physics that affect wavelength... In humans even language and culture can influence color discrimination to some extent).
And where does the mantis shrimp come in? Well this is interesting, because it's been generally thought as you put it that the mantis shrimp would be able to see many more colors than we do, due to its much more numerous receptors, but the recent studies mentioned in the first source you linked to suggest that the mantis shrimp is worse at discriminating colors than we are, i.e. it sees fewer colors. However it appears its color vision functions very differently, and that's where the 16 different receptors come in. It's possible that the different receptors allow the mantis shrimp not to detect more colors, but to process the colors it does detect much faster. To quote the Nature article:

If the shrimp eye compared adjacent spectra, like the human eye does, it would have allowed the animals to discriminate between wavelengths as close as 1–5 nanometres, the authors say. Instead, each type of photoreceptor seems to pick up a specific colour, identifying it in a way that is less sensitive than the human eye but does not require brain-power-heavy comparisons. That probably gives the predatory shrimp a speed advantage in distinguishing between different-coloured prey, says Roy Caldwell, a behavioural ecologist at the University of California, Berkeley.

And the National Geographic one:

Their working hypothesis is that the mantis shrimps analyse the outputs from all of their 12 receptors at once. Rather than making comparisons between those receptors, they pass the entire pattern of outputs onto the brain, without any processing. “One could imagine that they have a look-up table in their brain,” says Marshall. So rather than discriminating between colours like we do, their eyes are adapted for recognising colours.
“Oddly enough, the closest device to stomatopods would be a satellite,” says Marshall. “Remote sensing algorithms have look-up tables of colour to fill in the image that the satellite forms.”

For your other questions:

How many photoreceptors is possible?

Theoretically the limit would only be how many you can pack in an eye and how many chemical pigments exist, but in practice there is a trade-off between color and spatial discrimination (after all any color receptor is a light receptor that's limiting itself to certain wavelengths only, so you lose in overall light perception). Another article in the Science journal the article on Mantis shrimp color vision appeared in suggests the optimal number is isn't over 4 (in organisms that use our system of color vision of course, not the mantis shrimp's):

In fact, theory predicts that two to four receptor types are optimal for discriminating the spectra of natural materials and maximizing the number of objects that could be distinguished by color.

And:

How much of the spectrum is not ever going to be seen by any creature ever?

Again, considering every set of photoreceptors leads to its own color spectrum (and every brain probably cooks it to its own sauce beyond that), that question applied to the set of all colors isn't really meaningful. The answer would probably be along the lines of "almost all of it" because the set of actual color vision systems in the natural world is an infinitesimal percentage of the set of theoretically possible color vision systems... but it's not like those colors are "out there to be seen" in anything but the most abstract sense; they exist in the same sense that a child that's the combination of a sperm and egg that haven't met exists.
If by "spectrum" we mean "electromagnetic spectrum", then there is likely an upper and lower bound to the wavelengths that can be detected, where wavelengths on the upper bound are too deadly for a cell to survive let alone detect (though bodies can and do sacrifice cells to exploit inhospitable environments, see the cells lining our stomachs, so even that might not be an absolute obstacle), and on the lower bound aren't energetic enough to cause pigment molecules to react to them. I don't know what those bounds are though; it's likely that more important constraints are how useful it is to detect those higher and lower wavelengths, that any organism would bother evolving the ability. (also, for the lower wavelengths, whether their detection is associated with forming an image. For example we can detect infrared radiation as heat but we don't think of that as "seeing". On the other hand "eyespots" that detect visible light without forming an image are often thought of as a primitive form of sight; there is a level of arbitrariness there but it's also true that lower wavelengths have different optical properties).

"You don't see a uniform increasing of a single quantity from one number to the next, you see several distinct colors following each other." That is simply an artifact of the computer process used to make that image, likely in sRGB, which has far less of a color range than Adobe RGB or ProPhoto. Using a larger color space and having a monitor capable of displaying it would would produce a gradient with no human discernible steps to it.

@AMR it's not a question of discernible steps (in fact the previous image I had for this didn't have such visible ones but it was https), it's a question of yellow not being perceived as a shade of red or blue. Compare with one-dimensional entities that are perceived as one-dimensional (if not linear), like temperatures from warm to hot, sound from quiet to loud, luminosity from dark to light...

Then your answer is not explaining that point correctly. Electromagnetic waves are not one-dimensional. They have amplitude and frequency as well as wavelength. All of these contribute to the energy of that photon, which in turn excite electrons in opsins that can then create an action potential that causes the neuron to fire. The number of conjugated bonds determines what range of wavelengths the opsin will respond to. You are also making assumptions that I am not sure you can back up, and you should avoid doing that. You could add as a comment or clearly label that it is your opinion.

@Rozenn Keribin: But I do percieve the yellow grdually transitioning to orangish-yellow, then orange at one end, and greenish-yellow then green at the other.  And I dare say any interior decorator worth his/her salt could put at least a couple of dozen names to various shades in the transition: peach, tangerine, chartreuse, &c.

@jamesqf, AMR: these points should be discussed in chat I think. https://chat.stackexchange.com/rooms/60137/discussion-of-question-if-mantis-shrimp-have-16-photoreceptors-then-how-many-oth

@AMR I created a chat room to discuss this if you wish https://chat.stackexchange.com/rooms/60137/discussion-of-question-if-mantis-shrimp-have-16-photoreceptors-then-how-many-oth

@Rozenn Keribin: But alas, you can not create a functional chat.

@AMR There is no meaningful distinction between frequency and wavelength for EM waves, they are merely inverses of each other describing the same property. Photoreceptors are excited by single photons, so there is no meaningful distinction with energy, either. The only meaning of amplitude in terms of EM radiation is number of photons.

@jamesqf: it doesn't work? Can you create one?

@jamesqf : well ok then... I never said the colors don't gradually shade into each other, the point is that there are several different basic colors involved. Blue shades into green shades into yellow shades into orange shades into red, and in that spectrum we might call "peach" a shade of orange, but we won't call green a shade of orange. Compare with a white to black spectrum, where all shades in between are considered shades of gray, belonging to one overall transition.

@AMH: "Then your answer is not explaining that point correctly." -- Clearly so, and thank you for pointing it out; if I think of a better way of explaining I will change the answer. -- "Electromagnetic waves are not one-dimensional." They aren't, but the electromagnetic spectrum which is what I was talking about, is a representation of the variation of electromagnetic waves along one dimension - wavelength/frequency (as Bryan Krause points out those are two measures of the same quantity).

@Rozenn Keribin: You misunderstood me.  I didn't mean that chat doesn't work, in the sense that it appears to function in the manner its designers intended, I meant that it's basically useless to try to use it to hold any sort of discussion.

@jamesqf and comments are better for that? Or you didn't intend your comment to be part of a back-and-forth in the first place? I don't understand what you are saying at all.


text:
Definition of a Katal (unit of enzyme activity)
I am very confused about what one 'Katal' actually is. From Wikipedia,

"The katal is not used to express the rate of a reaction; that is expressed in units of concentration per second (or moles per liter per second). Rather, it is used to express catalytic activity which is a property of the catalyst. The katal is invariant of the measurement procedure, but the numerical quantity value is not and depends on the experimental conditions. Therefore, in order to define the quantity of a catalyst, the rate of conversion of a defined chemical reaction is specified as mols reacted per second. One katal of trypsin, for example, is that amount of trypsin which breaks a mole of peptide bonds per second under specified conditions."

So if a Katal is a specific AMOUNT of trypsin, then why is it expressed in units of moles per second. This is not dimensionally consistent! An 'amount' could be expressed as moles or mass, but certainly not as moles per second which is like a rate of reaction multiplied by volume...? The units and definition just seem to be all wrong.
If I were to take it that the Katal is the amount of enzyme catalysing one mole of a reaction per second, then this would mean that an enzyme with a smaller number of Katals of activity would actually be more active because less of it is required to catalyse one mole of the reaction per second?

A katal is indeed a specific amount of enzyme (rather than a reaction rate), but one which is measured with respect to the catalytic activity of the enzyme, rather than with respect to the number of molecules, their weight, or their size.
Roughly speaking, one katal is the amount of of enzyme which can convert 1 mole in 1 second. (Just like one pascal is the amount of pressure which applies one newton of force to an area of one square meter.) Or to rephrase things slightly, just like you can take an object of a particular length and express that length as "X meters" (being the number of meter sticks you can line up next to that length), you can take a given amount of enzyme and express the catalytic activity of that quantity of enzyme as "X katals", being the number of moles the enzyme can convert in one second.
This is not an intrinsic property of the enzyme itself. (It's an "extensive", not an "intensive" property.) The number of katals varies based on how much enzyme you have - if you have twice the amount of enzyme, you have twice the number of katals. (Just like you have twice the number of grams or twice the number of moles.)
As such, you can't talk about "an enzyme with a smaller number of katals of activity". I can understand the confusion, though, given the use of "activity" in the name. A paper the Wikipedia article references talks about the fact that there was some argument for calling the quantity being measured ‘catalytic amount’ rather than ‘catalytic activity’
As to why measuring enzyme amounts in katals versus moles or grams, the argument is similar to why there are separate units for mass (gram) and number (mole). It expresses a feature of the "size" of the enzyme not captured by the other units.

Although this is old news, as @R.M. has been good enough to provide an answer, I feel I should add my own. The reason is not that I think his answer is incorrect in any way — it is technically quite correct and I am not going to repeat or rephrase his technical arguments — but I do not think it addresses what I regard as the misunderstanding in the poster’s argument — a misunderstanding that others might make, even if the OP has progressed to other things.

The problem is one of semantics — What do you understand by the word ‘amount’?

The OP is clear. She writes:

“An 'amount' could be expressed as moles or mass, but certainly not as moles per second…”

So her understanding of the word amount is tied to the (extrinsic) mass property of an enzyme, which she clearly feels is intimately related to the number of molecules.
It seems to me that the way to deal with this argument is to point out that it is a misconception — there are properties of molecules other than mass that can be, and are, used to quantify them, and for enzymes catalytic activity is one such property, and the one that must be used in practice.
In practice, quantitation of molecules (the process that produces an amount) has to be performed in terms of their measurable properties when we are unable to ‘count their number’ (as it were). Mass is actually indirect — to be of use we need to know the purity of the compound and its molecular weight. Likewise we may quantify molecules by e.g. their light absorbance at a particuar wavelength, but to do this we need a molar reference value which will differ, e.g. between NADH and the amino acid tryptophan. Quantification using enzyme activity may be thought of in this light.


text:
What is the name of this South India plant?
Location: South India.
Month: June.
Branches of the tree:

Lower part of the Plant:

Plant's leaf:

Whole plant:

Hi Welcome to Bio.SE! Please upload all of your images using the url option of the image uploader. Simply adding links is dangerous because they might become nonworking and your question becomes unusable /unamswerable. Thanks!


text:
Evolutionary term for multiple, related adaptations
Is there a term in biology for when adaptations are compounded on (or by) other adaptations?
One example in whales: the tail flukes, reduction of rear limbs and development of the blowhole were all part of a number of shifts that aided the transition from land to water. Is there a term, like chain shift, for that?
Also with humans, encephalization led to pelvic adaptation for larger infants.

Co-adaptation
The term you are looking for might be co-adaptation. Co-adaptation is kind of a generalist term that fits many scneario, its definition (source: wikipedia > co-adaptation)

In biology, co-adaptation, or coadaptation is the process by which two or more species, traits, organs, or genes undergo adaptation as a pair or group. This occurs when two or more characteristics undergo natural selection together in response to the same selective pressure. While the parts may be functionally independent they are only beneficial when together, sometimes leading to increased interdependence. Coadaptation and its specific examples are often seen as evidence for the broader process of coevolution.

You seem to be thinking about a chain of adaptations, where the first adaptation changes the selection pressure on another trait causing another adaptation. For this purpose co-adaptation is not the perfect term but I am afraid there is no perfect terms. You might want to consider the following ones though that help you express your ideas.
Structural interdependence
Ziegler et al. 2009 talk about structural interdependence and interdependence of internal organ.
Phenotypic space
Of course, you can use the frameworks of the phenotypic space (as in Pigliucci 2007) and of fitness landscape to talk about how a change in a given phenotypic trait affect selection pressures at other traits.
Phenotypic constraint
A phenotypic constraint (as in Pigliucci 2007) is a case of fitness valley in fitness landscape in the correlation between two of more phenotypic trait, hence causing a trade-off. Absence of such constraint are cases of interest to you
Phenotypic plasticity
It is common to talk about the ability of a specific phenotypic trait to vary to fit into the broader context of the whole body as phenotypic flexibility or phenotypic plasticity. There is a difference plasticity and flexibility for many but I don't think all authors use the exact same definition.
Phenotypic plasticity

Phenotypic plasticity refers to the changes in an organism's behavior, morphology and physiology due to its adaption to a unique environment.2 Fundamental to the way in which organisms cope with environmental variation, phenotypic plasticity encompasses all types of environmentally induced changes (e.g. morphological, physiological, behavioural, phenological) that may or may not be permanent throughout an individual's lifespan. The term was originally used to describe developmental effects on morphological characters, but is now more broadly used to describe all phenotypic responses to environmental change, such as acclimation or acclimatization, as well as learning.5 The special case when differences in environment induce discrete phenotypes is termed polyphenism.

Exaptation
This is a poorly related term but it may eventually be of interest to you. The definition from wiki > Exaptation

Exaptation [..] and the related term co-option describe a shift in the function of a trait during evolution. For example, a trait can evolve because it served one particular function, but subsequently it may come to serve another. Exaptations are common in both anatomy and behaviour. Bird feathers are a classic example: initially they may have evolved for temperature regulation, but later were adapted for flight. Interest in exaptation relates to both the process and products of evolution: the process that creates complex traits and the products (functions, anatomical structures, biochemicals, etc.) that may be imperfectly developed.

Phylogenetic signal
Phylogenetic signal is used way more often than the term exaptation. It is however also quite unrelated to what you are looking for but I added it because... well we never know what you'll find helpful!

Phylogenetic signal is a measure of the statistical dependence among species' trait values due to their phylogenetic relationships.

For example, the existence of 4 limbs in vertebrates is a phylogenetic signal (see Why don't mammals have more than 4 limbs?)

@Tom let me know if it helped!


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What kind of crow is this?
Years ago, when I lived in Greece, I saw crows from a close distance, but never with this peculiar colouration. Today I saw two individuals, both with these gray parts.
Location: Austria, Vienna. Pretty much in the city centre. Specifically Altes AKH Hof 2 near the rear yard of the department for East Asian studies.
Time: I am not sure. Probably before my lecture (around 10am) or after it (12am). I'll see, whether I find the timestamp of the picture anywhere.
Size: Now, at this I am really bad. I would say roughly the length of my boot, which is a 47-48 European continental size.
Behaviour: nothing interesting. Two of them came, stalked around the benches, did not make sounds and as far as I remember were gone quickly. They were not afraid of people.

My guess is Corvus cornix , but I have always been bad at identifying birds.
EDIT:
Unfortunately, I didn't see the linked answer. But had I seen it, I would probably have assumed my bird wasn't Corvus cornix. The plumage  in the linked answer looks significantly more colourful. Whether you want to mark it as duplicate or not, I am fine with your decision, since I have little practice in identification. However, I find the answer here more detailed when it comes to differentiating C. cornix from other corvids. The linked answer only states the results. The answer here teaches us what to look for!

Its a hooded crow or grey crow. Their common in the uk and they are a plague in Ireland.

Can you add some more details to the question - habitat and location where you saw it (more specifically than 'Austria'), what time of day you saw it, and its rough size?

Similar coloration is found in the most common type of crow at my locality, which I know as Corvus splendens

@AlwaysConfused interesting! To me it looks like C. Cornix but I can't pinpoint the difference!

I'd say you guessed correctly. This does appear to be the hooded crow (Corvus cornix).

In German, it's called Nebelkrähe (meaning "mist crow").

 A Hooded Crow Corvus cornix in the garden of Belvedere (Vienna). [Source].
Description: ashy grey bird with black head, throat, wings, tail, and thigh feathers, as well as a black bill, eyes, and feet.
C cornix is a Eurasian species that would be present in Austria:

Similar but incorrect species:
The only other similarly grey crow species I know are the grey crow (Corvus tristis), which is only present in New Guinea, and the western jackdaw Corvus monedula. The jackdaw is present in europe, but it can be ruled out because of its grey eyes and because of the grey feathers that creep superiorly from the birds nape onto its head (unlike your specimen).

Note: I exhaustively checked all commonly recognized species of the Corvus genus


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Have we succeeded in building a living organism from inanimate material?
Following the Miller-Urey experiment where we were able to produce organic compounds with basic primitive atmospheric gases, high potential and water in a closed system. Have we been able to create a living organism fully functional with only inanimate material (dead material, or atoms, or anything that is not coming from a living organism such as a clone, or already existing DNA)?
I mean building a living organism from scratch. Are we able to do this?

We have not been able to do this, though whether or not we can in a reasonable time scale is unknown.

We've made organisms with 6 different nucleotides (instead of 4) though.

Do you have a source to support this? I'm guessing it's more prion or virus looking than plant or sheep looking...

https://www.sciencealert.com/new-organisms-have-been-formed-using-the-first-ever-6-letter-genetic-code and https://phys.org/news/2017-01-scientists-stable-semisynthetic.html

The most recent paper on the subject is Feldman et al. 2017. They worked on E. coli. This video by Sciencium (same author of Veritasium) report their findings for the general public.

You will have serious problems defining the "non-animated material" aspect of the question. Does this designed genome of a bacteria made from yeast cells count? Hutchison et al. 2016

I edited your question and replaced non-animated with inanimate. In between, I find an issue in the last part of your post - 'dead material' and  'not coming from a living organism' are contradictory. Also what you meant by 'or already existing DNA' is unclear to me. Did you try to imply, forming an organism only with inorganic substances?

It could be with organic and inorganic compounds as defined in chemistry. I just wanted to know if we are able to take chemicals like H2O, N2, CO2, CH3, etc. and form a life/a living organism.

In short, no https://biology.stackexchange.com/questions/60331/synthetic-life-creation-status-of-attempts

It depends on your definitions.
we have built organisms with an entirely synthetic genome. basically the genome was "printed" from a computer file and inserted in a cell which had its DNA removed, it continued to function and replicate just fine.
We have not built a modern cell from scratch, mostly because even the simplest living cells today need to compete with other more complex cells so they are still extremely complex in their own right. The simplest possible cells would never survive in the current world due to competition and "predations" so we don't know exactly how it has to be arranged to function.
You may want to look at the much more modern experiments like the Urey-miller one, Jack Szostak has been trying to work up to what you are looking for, his lab has created RNA from abiotic (non-life) sources.
This is probably the closest since we know a slightly longer sequences of RNA can be self-replicating. And Harvard scientists have put manufactured self replicating RNA in an artificial lipid capsule and gotten it to function.
 Getting the right sequence of RNA to form by itself is possible but would probably need several billion repetitions of the first experiment.


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Why summation takes place at Initial segment?
I know that many EPSPs summate at initial segment to produce action potential.
But I don't understand why if EPSP can travel from dendrite to initial segment, then why it doesn't travel further?
What halts it there and make it to wait for other EPSPs to come and add to make Action Potential?
Why does it can't propagate as such and cause release of small amounts of neurotransmitters?

Why don't EPSPs travel passively through axons?
EPSPs decay over distance. The decay is described by the length constant, which can be calculated based on the electrical properties of some compartment (i.e., a length of dendrite or axon). By definition, the length constant is the distance at which the amplitude of the signal will decay by about 37%. If you are familiar with the concept of a "time constant," the math is exactly the same.
There are two main factors that influence the length constant: the number of open channels (i.e., how "leaky" the membrane is) and the diameter of the neurite. The "leakiness" of different parts of the cell is often modulated by inhibition. Preventing EPSPs from reaching the soma or decreasing their amplitude by increasing leak is called shunting inhibition. However, for your question, it is the diameter and overall length that is important.
Dendrites tend to be a bit bigger than axons, so they have a longer length constant: that is, EPSPs travel further. Dendrites are also not entirely passive: dendrites can actively propagate signals (see review by Yuste and Tank) using voltage-gated channels to boost EPSPs, especially in cells that have a long distal dendrite, such as the deep-layer pyramidal cells in neocortex. These voltage-gated channels give the dendrite a longer effective length constant
The most important thing is that even relatively short axons are just way too long for passive conduction: that's the reason for action potentials. Length constants depend greatly on the size of the neurite, but you can expect the distances to be on the order of millimeters to 10s of microns.
That said, it isn't ever true that a subthreshold EPSP won't flow into an axon: it just will get weaker and weaker with distance. Neurotransmitter release depends on a substantial depolarization which opens voltage-gated calcium channels; a small little EPSP that has decayed several-fold from the soma has no chance to cause calcium influx and subsequent vesicle release.
Spatial and temporal summation
EPSPs don't 'wait' anywhere, the EPSP is constantly decaying because all membranes are somewhat leaky, and current isn't restricted to any compartment. Current is constantly flowing out of the membrane and out into all the other processes of the neuron (and then out through those parts of membrane too!). In fact, if you are talking about passive conduction of EPSPs, you are really talking about a form of "leak", not through the membrane but through the cytosol! The EPSP isn't traveling to the soma in any directed way, there is current "leaking" in all directions, and some of it happens to go towards the soma. To get summation at the soma or anywhere else, EPSPs have to arrive both close enough in time and close enough in space.
EPSPs can sum with each other in the dendrites if they occur close enough in space, but of course that also only works if they occur around the same time. Similarly, at the soma, an EPSP slightly depolarizes the soma but only for a brief time. If one EPSP has an amplitude of, for example, 5 mV, and another EPSP has an amplitude of 3 mV, they will only sum to close to 8 mV if they occur simultaneously. If the 3 mV EPSP comes a few milliseconds later, the peak voltage might only be 6 mV, or if they are separated even more in time, there may be no summation at all.
Why do spikes start at the axon hillock?
The axon hillock is a special part of axon, right at the beginning of the axon. This area is more than just the first section of axon, it also typically has the lowest threshold for initiating an action potential due to a greater density of voltage-gated sodium channels. Sort of by definition, a cell's threshold is going to be the threshold for whatever part of that cell has the lowest threshold (at least near the soma, which is so big compared to axons/dendrites that it is nearly isopotential).
For example, take an example cell whose overall threshold is at -45 mV. If you were to somehow remove the axon hillock, leaving just the rest of the soma and the dendrites, the threshold wouldn't be -45 mV anymore, it would be much higher, maybe -10 mV. Even if you had some really huge EPSP (or manually injected some current) to bring the cell towards -10 mV, the axon hillock would still hit its threshold first and start the action potential well before the EPSP reaches a peak sufficient to start a spike in the soma proper.
If it helps you could think of a balloon analogy. The EPSP is air flowing into the balloon, and the action potential is the balloon popping. If one part of the balloon is thinned/weakened, that part will always be the site where the popping starts. It doesn't matter if you put in enough pressure to cause the thick part of the balloon to pop, because before you can possibly get it to that pressure the weak part has already burst.
Also note that for this analogy to fit with all the rest of this answer, it has to be a leaky balloon, so it only pops if you put enough air in fast enough before it has a chance to leak out.

References
Yuste, R., & Tank, D. W. (1996). Dendritic integration in mammalian neurons, a century after Cajal. Neuron, 16(4), 701-716.


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How are micelles formed from the byproducts of emulsification in fat digestion?
It is known that fat droplets are made into emulsion droplets via the addition of bile salts. It is then said that the emulsion droplets are made into micelles through some sort of lipase, which can be absorbed and transported to different cells through the LDL and HDL pathway.
My question is what is the biochemistry for transforming emulsion droplets into micelles? How does water, lipase, and other factors make these micelles?

I guess - emulsification increases the surface area for the lipases to act and break those bigger droplets into smaller once which can enter the cells directly. http://syromonoed.com/wp-content/uploads/2016/01/Lipid-digestion.jpg

Lipases act on lipids in micelles to break them down into monoglycerides, which can break away from the micelle and be absorbed by epithelial cells. I don't think lipases are necessary for micelle formation.

They are in accordance with the textbook the "mechanism of body function 4th addition"

Fat (triglyceride) enters the small intestine in the form of an emulsion of droplets which are stabilised by surfactants from the diet including proteins and phospholipids.
Bile salts (BS) bind to the surface of these droplets, displacing proteins. The BS-stabilised droplets are the substrate for pancreatic lipase which can adsorb to the BS-stabilised surface and convert the triglycerides to monoglycerides and free fatty acids.
The products of lipolysis then enter micelles that are formed by BS and phosphatidylcholine (PC: also in bile). The prevailing view is that these micelles take the form of discs of bilayer-like structure with BS situated both around the edges protecting the exposed acyl groups, and also embedded within the PC bilayer.
I think that the mechanism by which the products of lipolysis move from BS/PC micelles into enterocytes is not known. However, once they have entered they are re-esterified to form triglycerides which are packaged into chylomicrons (a class of lipoproteins) and exported into the lymphatic system.
Maldonado-Valderrama et al. (2011) The role of bile salts in digestion. Adv Colloid Interface Sci. 165:36-46 doi: 10.1016/j.cis.2010.12.002


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Function and Characterization of poly(T) and (AT)
I came across three terms; "poly(T)45", "poly(A)45" and "(AT)15". Can anyone explain what they are? I know the number refers to strand length, possibly poly-T is a strand of thymine monomers and that ss(AT)15 refers to a 30-base (dAdT). I assume this refers to a single that looks like this;
dAdT-dAdT-dAdT...repeated 15 times.
In that case, what is the d?

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Homework tag and explanation added

Poly(T) is an oligonucleotide with only repeating thymine residues. These are generally used as primers in Reverse Transcription PCR, as mature eukaryotic mRNAs have a Poly(A) [adenosine] tail added to them as a post transcriptional modification in order to protect against mRNA degradation. You would also sometimes see this referred to as an oligo dT. It could also be the primer for some paired end adapters used in next-generation sequencing (NGS)
The 45 generally would indicate the number of residues in the oligonucleotide.
Poly(A) could be a primer for a paired end adapter for NGS, however I would need to see the context of where you saw the terms to be sure.
d = Deoxyribonucleotide, in other words you are dealing with a DNA oligonucleotide (though Thymine is also an indication). Technically the d refers to the 2' Carbon on ribose having a hydrogen instead of a hydroxyl attached to it making it deoxyribose.
Without the d it is a Ribonucleotide, indicating that you are looking at an RNA molecule and that the 2' Carbon on ribose has a hydroxyl group.
You will sometimes also see ddN (N for any base). This indicates a chain terminating dideoxynucleotide which has a hydrogen on both the 2' and 3' Carbon instead of hydroxyl groups. The reason this molecule is chain terminating is because you need the 3' hydroxyl in order to link to a 5' phosphate group to form a phosphodiester bond, which is needed to continue the elongation of the nucleic acid molecule.
As for the ss(AT)15, I think you are correct in saying that this is a 15 pair repeat of AT so a 30 nucleotide oligonucleotide. Though it didn't say dAdT, you are likely correct that they are deoxyribonucleotides as they use thymine instead of uracil as the base.
Just in case, the ss stands for single-stranded, which is often the case for oligonucleotide primers for PCR reactions.


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Is dietary fat directly stored in adipose tissue or is it immediately metabolized?
I know that fat goes to adipose tissue and even sugar gets converted to fat and goes to adipose tissue, but what happens to fat (unsalted cow milk butter) I just ate? Will it give me energy now, or does it automatically goes to adipose tissues for future energy storage?

first come, first server mechanism: for example, if you have not eaten a single thing in 2 days, the first thing you put in your mouth will be used for energy immediately and you will feel satiated. note that since you did not die in those 2 days your body is using the energy in your adipose stores (from your physical body fat) first and only then from outside sources.

What research have you done before asking it here?


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What's the difference between constitutional samples and tumor samples?
I think the tumor samples have two copies of the chromosomes. But for constitutional samples, do they only have one copy of the chromosomes?

Every cell has two copies of each chromosomes - except for sperm and egg cells.

...and some cancerous cells.

Constitutional samples do, as you surmised, refer to germ cells (sperm or ovum). Hence they have 1 copy of DNA instead of 2.
Tumours, as they acquire more mutations, often have aneuploidy, or different numbers of chromosomes, and can also have increased incidence of Xn chromosomes where X > 2. This is polyploidy for humans and organisms with normal 2n chromosomes.


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How could this fossil's soft tissue be preserved so well?
I found this article for non biologists like myself. It describes, how astounding fossils were found in China. They belong to a crustacean like animal that lived more than 500 Ma ago. The exciting thing about them is, that the nervous system -soft tissue - is fossilised in its finest detail. The article says:

“Using fluorescence microscopy, we confirmed that the fibres were in fact individual nerves, fossilised as carbon films, offering an unprecedented level of detail. These fossils greatly improve our understanding of how the nervous system."

My question is: how can these soft tissues be so well preserved?
I managed to find the scientific publication   and attempted to identify the answer myself, but it seems to me, the question is not touched upon. Perhaps, being a layman, I overlooked it, or it is obvious to biologists?

I may be proved wrong, but I doubt anyone can say for sure, it's probably to do with the very specific conditions of the fossilisation process, my guess would be that it went from living to fossilised relatively quickly, before the nerves etc. could decay.

You're right that the authors don't comment on how they think the fossilization occurred. Since that process isn't the point of their article, my guess is that any discussion of it would have detracted from their research focus.
There are some ways that soft tissue fossilization can occur, but to specifically answer your question as it relates to this case, you'd have to know more about the geological conditions in which the fossils were found, which I don't see in the article. This article provides a nice review of soft-tissue preservation processes.
The main points to consider in soft-tissue fossilization, according to the linked article, are pressure, time, charge and chemistry.
Pressure: How much pressure was the fossil under? The higher the pressure, the less oxygen and fewer organisms can access it and degrade biological tissue.
Time: How quickly did the fossil become inaccessible to degrading organisms? The faster this occurs, the less likely that any soft tissue will rot away.
Charge: Does the sediment in which the fossil found carry a charge? Electrical charge acts both as an selective barrier to some organisms and chemical compounds that can hurry biological decay and provides a means for reaction with biochemical compounds, which brings us to the last point:
Chemistry: Can components of the biological soft tissue react with their surrounding minerals? If so, then the inorganic compounds present may be able to reduce lipids and other complex carbohydrates to molecular carbon and minerals in the form of the biological organism.
So say, for instance, that this organism was suddenly encased in a thick layer of clay. As the review states:

In clay-rich environments, the large surface area and charge of clay
  grains are thought to contribute to preservation in one of two ways.
  First, enzymes produced either through autolysis or by invading
  microbes are adsorbed to the surface of the clay grains and
  inactivated, slowing or preventing degradation (Butterfield 1990,
  Garwood et al. 1983). Second, molecules directly adsorbed to clay
  grains are resistant to degradation (Stotzky 1980), whereas
  protein-protein layers are readily degraded. This mechanism may
  explain the exquisite preservation of thin carbon films in impression
  fossils such as the feathered dinosaurs of the Jehol Biota (see
  discussion below). As tissues interact with surrounding clay grains,
  only the molecules in direct contact with clays are preserved as
  monolayers, whereas the rest are degraded normally. Thus, surface
  morphology is preserved, and original carbon might be preserved as
  well

Who knows if this process explains these particular fossils. ¯_(ツ)_/¯  As I said earlier, we'd need more information. The section quoted above, though, seems (to me) to provide a plausible hypothesis.
I hope this helps!

Three major factors.

the organism itself was small and thin enough to not be exposed as it decomposed, combined with the extremely fine grained nature of the matrix (rock) means the organism was held perfectly still even as all the moisture and active enzymes were literally leached or squeezed out of it.
Most of an organism is water, and that gets slowly removed leaving behind a stain almost as if you slowly dried out the organism while pressing it between two plates. Look at the old practice of pressing flowers under glass for ideas of how this can preserve things. Removing any space in the remains prevents the molecules from moving much.
It was buried quickly under anoxic conditions so little to no bacterial action was able to alter or disturb the remains as these processes reduced it to basically a stain of all the non-water components of the organism. What is left does not take up much space and microscopic mineral grains completely surround them, the molecules cannot move much becasue they have nowhere to go, that is why such fossils become very delicate once exposed the leftover material is then free to shift.

Sources
 Burgess shale examinationand experimentation in preservation

Can you add some sources to this?

Preservation of individual nerve-fibres look quite extreme, but students of palaeo-sciences are quite familiar with seeing rock-slides containing fossilized tissues, where the contours of every cell is clearly visible.

wikipedia - image, cropped and rotated to save space.  It represents a siliceous petrifaction mode of preservation, of a plausibly soft-bodied organism.
The most well-preservation of cells are found in petrifaction or cellular permineralization modes. (Though there are disputes about when to use these 2 terms (such as second one has a broader sense use), the 2 things are same.)
Though your mentioned page did not mentions anything about its plausible mode of preservation, it apparently looks like a compression fossil , which also contain preservation of harder structure such as plant-cuticle, but preservation of individual nerve fibers are really surprising. (However just speculating, may be it is actually a petrifaction fossil or something in-between of petrifaction and compression).
.........................
No one of us know, how exactly the fossilization processes take place, but things  unanimously accepted are, fossilization requires very very special conditions/ situations, and which is very rare and chance dependent, and slow also.
It has been hypothesized that fossilization requires anoxic environment, source of sedimentary materials (preferably including finest-grain clays), soluble minerals, quiet or no-shake conditions.
For petrifaction-fossils, it has been hypothesized that a source of minerals that would deposit, is mandatory, such as the sulphides, silicates carbonates, sulphates etc of metals like iron, magnesium, calcium, etc. coming through volcanos, hot-springs  etc. and also marine sources of salts may have played some role.
In case of silicified petrifaction, presence of soluble silicates are important. An increase in acidity (decrease of pH) can trigger the deposition of insoluble forms, thus may have generated silicified petrifaction.
.............
I've read about one example observed present day, that resembles (and may explain) permineralization-type fossilization, from Stewart- Rothwell's Palaeobotany.

"A park ranger reported  finding the remains of a coyote in the outflow of a geyser. He left carcass undisturbed and found, when he returned some four years later, that the remains of coyote bones had already become silicified in the same way as the bones of dinosaurs".

Though this does not include very soft tissue, yet a present-day example of silicification.
....................

Reference:
All informations based on Paleobotany and the evolution of plants/ 2nd Edition,  Wilson N. Stewart and Gar W. Rothwell/ Cambridge University Press.