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If life began at sea, why organisms are less salty than the sea?
We may take it for granted that a fish, a seaweed, or clams are not too salty to eat, although the sea around them is salty. I know about the existence of a mechanism which prevents their body from becoming as salty as the sea itself, but this raises an important evolutionary question.
As life evolved from single-celled organisms, those organisms started as very simple cells with the bare essential metabolic functions. Possibly their DNA had no nucleus, and obviously they could not (yet) balance the salts within their body. In theory, this would say that their metabolism should have evolved to function is a salty environment. Yet, we see that this is not the case of modern organisms.
Which of the following scenarios describe the evolution of marine creatures with no excess salts in their body?
1- Metabolism may have started in a salty environment, cells have later "discovered" that less salt makes metabolism more efficient, and therefore the energy expended to clear-out the salts is worth the effort.
2- The time it took for salts to accumulate in the seas allowed marine creatures to adjust to a gradual increase in salinity.
3- Fresh water bodies (Rivers and lakes) are better suited for life to evolve. Eventually, some of the rivers will pour into the sea with all their content, including any living thing facing the challenges of salty sea water. This article mentions "ponds", but larger bodies of water are a better means of transporting those organisms to the sea.
What do we know about the timeline of changes in oceans salinity vs. timeline of evolution? Do we have fossil records that show the salinity content of the organisms?

Many biological processes require regulation of the salts (or more precisely ions) in fluid compartments of an organism. These processes include muscle contraction, filtration of the blood by the kidneys, and so on. Without these processes, a fish would certainly be dead. So it's not necessarily that regulating ions aids evolution or metabolism, nor that the sea changed salinity - the reason is that many biological processes required for an organism's survival wouldn't work without proper regulation of ions.
One such important process is active transport. In essence, by creating gradients of ions across a cell membrane, you can let the flow of ions into the cell drive other processes. This is a bit like how the flow of water through a water wheel can drive other machines.
I've never come across any reference to a cell with an ion concentration of its intracellular fluid greater than that of the ocean, though I'd slightly doubt that to exist since it would disrupt active transport. I'd also doubt that you could discern the ion concentrations of any fossilized cell since ions need to be dissolved, but how would you see this in a fossil?
I'm not sure whether I've completely answered your question, so let me know if something's still unclear.

I'm not sure that we take it for granted that marine organisms  are substantially less salty than seawater.
As to my knowledge, elasmobranchii, e.g., sharks, and echinoderms, e.g., sea urchins, have osmolarities that are quite near seawater (~1000 mOsm). I expect a careful investigation would show many other kinds of marine organisms are similar.

yes, you both understood my question well. The starting point was the need to regulate ions concentration by active transport. The assumption was that even for a single-celled, not all metabolic features have evolved in just one step. Before active transport ever evolved, organisms may have been restricted to a narrower range of habitats. So would they be restricted to bodies of fresher water? This may be a key issue in the debate whether life may evolve under the ice cover of Europa, one of Jupiter's moons.


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Is it possible to extract tissue-culture material from a seed?
Here is the problem: Tissue culture is cloning, and all plants from the same mother plant are identical. On the other hand, plants grown from seed are all different. If parent plants are genetically diverse (not inbred), growing from seed is the best thing in the long run.
The problem starts when some plants have a low germination rate, or are difficult to grow from seed. We want to grow a large number of plants as fast as tissue culture does, but we want diversity. Suppose the plant can produce a large number of seeds or at-least can produce them easily.
Can we extract cells from the seed and grow them via tissue culture? Which part of the seed should be used, and how different it is from using vegetative parts such as the apical meristem?

Yes. It's quite common, to the degree that it's done by some hobbyist plant breeders. See en.wikipedia.org/wiki/Embryo_rescue  However, AFAIK (I'm not an expert), it wouldn't be done for raising multitudes of plants, like tissue culture.
Rather, it's used in hybridization, where you hope to produce hybrids from plants that don't readily hybridize.  You would typically rescue a number of embryos, grow them on until mature, then perhaps use tissue culture to mass-propagate the ones that have interesting characteristics.

Can you add some more references to this (i.e. not just a Wikipedia page)?

source: Stack Exchange

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Is the inhalation of ammonia a possible health problem for bats in an artificial small volume winter roost?
About 70 bats (Nyctalus noctula) spend their winter in an artificial small volume (0,050 cubic meters) winter roost located in the attic of a building. There is a single small exit to the outside directly from the roost. The roost has been cleaned before winter from bat droppings.
Is inhalated ammonia from bat droppings a potential health risk for them?

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What kind of beetle has fuzzy orange antennae and can flip its head down for digging?
Some years ago I found this beetle while hoeing potatoes in Iowa in the United States. It had something like branches on its legs and could bury itself out of sight in five seconds! If I recall the beetle itself was mostly black.  It had the ability to flip the front part of his body up to reveal the face which was normally down facing the ground. I suppose because it usually lives underground. But when it flipped its head up, it's antennae came out and were bright orange, fuzzy ,and had round ends similar to an old-fashion side mirror on a car. When it's head was down it had a horn almost like a rhinoceros beetle.  But when it flipped its head up it had buggy eyes - the cutest little face.  I have never been able to find out what this little critter was. I just ran across my description of it in my journal today and tried to look it up online, finding your website.  Sorry, I didn't own a camera back in 2000 to take a picture of him.

I'd guess that the beetle you found was of the genus Nicrophorus ,family Silphidae . They are commonly known as Burying beetles and are true to their name
was this the beetle you saw?


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What problem does the Dobzhansky-Muller Model resolve?
This page describes the Dobzhansky-Muller model and I can follow the illustration of the split leading to incompatible hybrids.
But at the start of the page the author states "[Dobzhansky and Muller] both realized that hybrid inviability or sterility was unlikely to arise from a single change at one locus." I don't really understand the explanation that follows i.e. what exactly is the issue with having a single change at one locus?
I wonder if someone here could explain the issue more clearly.

If reproductive isolation was to be caused by a single mutation, then the first individual to carry this mutation would likely have a very low fitness. At the extreme, in a purely sexually reproducing species without hermaprohiditism, this individual carrying the first mutation causing reproductive isolation would have no-one to reproduce with and would have a fitness of zero.
Hence, reproductive isolation is unlikely to arise from a single mutation as these mutations are unlikely to raise into appreciable frequency. Hence, Dobzhansky and Muller (and Bateson) created this minimalist model involving only two loci with negative epistatic interactions.

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V(D)J recombination on homologous chromosome
V(D)J recombination is known to recombine IG locus of a B cell. Is anything known about how the recombinations on two homologous chromosomes are connected? For example, are the selected V(D)J couples(triples) the same on both homologues?

I did not understand the selected V(D)J couples(triples) the same on both homologues part, but if you are asking about it's mechanism, then Wikipedia, this paper and this article are places to start.

There are two alleles (variants of the same genetic region) for the Ig and TCR loci, one on each chromosome. The cell will try first with one allele to obtain a productive arrangement, and then with the other. If the cell fails on both alleles, the cell undergoes apoptosis. If at least one allele has a productive arrangement, the cells move on to selection.
Groups are still uncertain, however, how the cell chooses which allele to initiate recombination on, and ruled out parental imprinting as a culprit last year (1).
To be certain, the regions are the same, though not the same sequence. However, mechanisms during recombination ensure that recombination events among individual cells result in robust junctional diversity and a suitably diverse repertoire of immature antibody or TCR sequences (example).
In activated B cells, however, class switching and somatic hypermutation can result in gross changes to the Ig locus not seen in immature or pro-B cells.

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Is this a shell operculum? If yes, can I get more info on operculum
I came across this strange shell some years ago and my research concluded that it was an Operculum (gastropod)(https://en.wikipedia.org/wiki/Operculum_(gastropod)) and I am interested in knowing more about the operculum.
What is its uses, how is it formed, will I fine something inside if I break it, how does the animal feed itself inside this, and so on.
Bottom View

Top View


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Could alternatives to Photosynthesis be possible?
I'm working on a world for stories and games, and I'm trying to figure out some more diverse plantlife. There are areas of the world that won't get enough sunlight for Photosynthesis, so I'm thinking about alternatives.
We can use Piezoelectric components to charge batteries, so could Piezosynthesis be possible in plants, if there was enough air movement to, say, move a sail-like fin back and forth enough to generate a similar "power" to photosynthesis?

I think this is actually a cool question. I don’t have time to give a shot at the answer, but take a look at some thermophilic archaea or some nitrogen fixing fungus and you may be able to get some ideas from that realm. As far as wind-power, that may not be practical—the sail fin idea may seem cool, but my bet is that it wouldn’t generate nearly enough energy for a whole organism even if everything else worked.

There are whole communities - e.g. undersea vents - based on chemosynthesis: http://noaacontent.nroc.org/lesson05/l5text.htm

Unfortunately, however interesting the question may be, any answer, by definition, is speculative and hence puts the question off topic on SE Biology. As a reading of the Help will remind users, this is a question and answer site, not a discussion site.

Then treat the question as "are piezosynthetic plants feasible from a biological standpoint" - speculative or not, it's still a question about biology. The issue I have is that there are very few places where discussion about fiction can occur, where the people are going to be as educated on the subject as they are here.


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Chunks of cells after trypsinization
Recently I've came across a problem after trypsinization of my stably transfected CHO-cells. When I add medium to rinse off the cells from the bottom of the flask, there are usually big chunks of cells, which I almost cannot resuspend properly... I also tried to increase the incubation time with trypsin, but it did not help much.
Does anyone have a solution for this? The trypsin I use is the same batch as usual and in the meantime I also thawed 2 different freezing stocks, but I still have the same problem.
I also tried different pipettes, from 25 to 5mL. But I can pipette like a maniac up and down and up and down... still there are big chunks of cells floating around...

Gibco has an anti-clumping agent verified for CHO cells, as does Lonza, but I like Gibco reagents more. Cells tend to clump for a number of reasons, including extracellular DNA from lysed cells and the presence of Ca and Mg ions (important ions for cell adhesion and aggregation).
You could try these:
1) Wash and resuspend in balanced salt solution without magnesium or calcium. Like Hank's balanced salt solution.
or
2) Treat with DNase I. I think you could go as low as 1 IU/mL for 30min-1hr to bust up a fair amount of DNA clumping. You can do this in a basal medium (like RPMI, DMEM, etc.), or the balanced salt solution. Your medium can contain serum only if the serum has been heat-inactivated as proteases in the serum with inactivate your DNase. Incubate with DNase under gentle agitation at 37°C (I always had a tube rotator in an incubator for this purpose, just put your cells in a 50mL conical and set them to agitate for 1hr. You could also use a heated shaker unit). If you don't have this setup, you can agitate at room temp, but for a little longer perhaps.
and maybe
3) Once of the other obvious choices is to avoid passaging your clumping cells and collect the rest. You can do this by putting all your cells into a flask incl. the clumps, agitate for a moment, and let it sit so that the chunks quickly fall to the bottom, and collect everything but the stuff that fell to the bottom.


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Are all of our hormones synthesized in the same gland that they are secreted from?
For example, growth hormone is secreted from the anterior pituitary; is it also synthesized there?

For many, yes. But for some, like oxytocin and ADH, which are secreted from posterior pituitary, are synthesised in hypothalamus, the sites are different

Ah, I remember learning about that for those two, for sure. Thank you.

Vitamin D is synthesized in multiple sites though classically it is said that final hydroxylation occurs in the kidneys.

Vitamin D is a hormone the kidneys produce that controls blood calcium concentration and impacts the immune system. It is also known as calcitriol, ergocalciferol, calcidiol and cholecalciferol. Of those, calcidiol is the form doctors most commonly focus on when measuring vitamin D levels in the blood.
The body makes vitamin D in a chemical reaction that occurs when sunlight hits the skin. This reaction produces cholecalciferol, and the liver converts it to calcidiol. The kidneys then convert the substance to calcitriol, which is the active form of the hormone in the body.

https://www.hormone.org/hormones-and-health/hormones/vitamin-d


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How are cell death like apoptosis and entropy related?
In Perspectives on Statistical Thermodynamics, Yoshitsugu Oono, it is written that

Do not conclude, however, that since the second law is invincible,
  information thermodynamics is unimportant. It is possible for a system
  we are interested in to perform something that ordinary thermodynamics
  does not allow, and to pay the price somewhere else. For example, it
  may be possible to go beyond the limit of thermodynamics for the time
  being by shifting the average value of fluctuations, although the
  price must be paid (dearly) later. There must be such cases in
  molecular machines. It is argued that cell senescence is due to the
  accumulation of defects and wastes, but cell death could have a more
  active implication of carrying away the debt caused by utilizing
  information. Thus, entropic apoptosis and entropic altruism are
  conceivable.

but I don't understand the following two points.

Why is cell death associated with "debt caused by utilizing information"? Do cells die for increasing entropy to compensate the entropy decrease which caused by their using information (but what kind of information)?
Why can we conclude "Thus, entropic apoptosis and entropic altruism are conceivable."? Does this mean, to let other cells decrease the entropy by consuming information, some cells kill themselves to increase entropy?

Unless you have a closed system, don't bother with the second law. These sound like some poetic descriptions but they won't tell you much about biology.

It is argued that cell senescence is due to the accumulation of defects and wastes, but cell death could have a more active implication of carrying away the debt caused by utilizing information.

The first part of sentence which I italicized here is sufficient to understand the biology: cells age and die off because they accumulate defects. Organisms, whether single-celled or multi-celled, ultimately get around this by making lots of copies of themselves and expecting some to fail.
The second part of that sentence says "could" and is poetry to describe the first half, as well as the sentence that follows. It doesn't add any more science, unless you care about the existence of "entropic altruism" in the universe, which sounds to me like a religious rather than scientific approach. It's just stating that cell death (and perhaps, to an extension, death of multicellular organisms) can be useful to organisms/species rather than merely destructive. There is nothing wrong with finding beauty in physics and mathematics, but beauty in itself says nothing about how things work or how things should be.
In the context of a multicellular organism, cells kill themselves to not kill/harm the whole organism (e.g., to not develop into cancer, or as a planned event during development). The biological reason they do this is because multicellular organisms that have evolved genetic mechanisms to identify potentially harmful cells and have those cells die are more likely to reproduce and produce more multicellular organisms like themselves. If you want to interpret this as "entropic altruism" because cell death increases entropy, that's fine, but no thermodynamic argument is needed or even all that helpful in explaining the biology.
Note also that the book you cite doesn't seem to be in common use; it has no reviews on Amazon or Google books, and a previous book by the same author only has 1 review. I don't have anything against the author and they could be an excellent statistical physicist, but language like this makes me think they are not a biologist.

As far as I know, apoptosis has nothing to do with entropy, except in the degenerate and trivial case where a cell is utterly voided of energy for enough time that it stops working.
Entropy is informally defined as a low-energy state. Cells that are low on energy are typically designed to pick up more energy from the environment. A simple example: Consider a cell that metabolizes glucose into an organic acid for energy. Assume that the cell lives in an environment where glucose is readily available, organic acids are regularly cleared away, and it has transport protein channels that readily allow glucose and organic acid waste-products to cross the membrane.
As the cell uses its own glucose for energy, it gets converted into an organic acid (waste product) which builds up in the cell. Now the cell has a lower concentration of glucose than its surrounding environment - and due to the transport protein channels, glucose from the outside will tend to move into the cell down the concentration gradient. Likewise, as organic acid waste-products accumulate, they tend to exit the cell over their own protein channels because the concentration of acids in the cell is higher than its environment.
Higher-order life forms (extremely complex with billions of highly differentiated cells) implement apoptosis as a form of quality control over cells. Over time, cells accumulate damage and mutations. Exact mechanisms vary significantly by species. In humans, there are specific proteins that scan for nonrepairable damage to protein structures in cells or dangerous DNA mutations. In some cases, a cell may be programmed to stop replicating itself; extremely dangerous (oncogenic) mutations may trigger apoptosis where the cell "takes one for the team".


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How do plants take in only carbon dioxide?
There are only 400 molecules of CO2 in 1 million molecules of air.
How do plants only take in CO2 but not the other gases?
My teacher told me that's because there is less concentration of CO2 in the leaves than the air and the CO2 rushes in the leaves.But, then how does the leaf maintain the concentration of CO2 and other gases?

Plants don't take in only CO2, they take in whatever the atmospheric concentration of gases is: gases travel freely across membranes, so it is difficult to select for certain gases.
What your teacher is explaining is based simply on the laws of diffusion in that diffusion results in a net flow from areas of high concentration to areas of low concentration. If CO2 is being used up in chemical reactions in the leaves of a plant through photosynthesis, that means that concentration of CO2 is low there, so the net diffusion of CO2 will be from outside the plant to inside.
Calling it a rush might be a bit misleading, but in general gases mix fairly rapidly (compared to, say, liquids). The plant doesn't really have to do anything to facilitate this except to have surface area available for gas exchange.

where do the other gases go?

@Dhruva They don't really go anywhere, you will find gases of all types in the atmosphere dissolved in plant tissue, they freely come and go.

@ Bryan Krause         If other gases are also found in the plant tissue why don't they combine with hydrogen or oxygen?

@Dhruva Why some reactions happen and others don't is what chemistry is all about. Hydrogen is not present as a gas in any appreciable quantity, it's in other compounds like water, so you are really asking "Why doesn't water react with nitrogen gas?" for example.


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why finger of hands and feet become wrinkled due to to water?
Mostly due to bathing or washing clothes our finger become wrinkled what was the reason behind it??

There are a few hypothesis around it, but it is known that its associated with the function of distal nerves of the hands and feet. I suggest reading this short case for a glimpse at this - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2464382/
Also another tip I can give is that professional swimming athletes for example, eventually experiment an adaptation process in which this wrinkling reaction diminishes due to being exposed to the same stimuli repeatedly and for long periods of time.

I am not talking about swimming, it it different thing I am simply asked about how to prevent this?

Mmm I thought you wanted to understand the biological  behind it :(

@Anum In your question you do not mention about this. And therefore it will be closed as a duplicate.


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Are there any diseases that can harm and kill flies and mosquitoes?
For decades I have heard about how flies and mosquitoes carry diseases around and infect humans and indirectly kill them in mass numbers. Somehow these diseases do not appear to harm these insects, I am not sure why. This brings me to my question, are there no diseases that infect and harm flies and mosquitoes at any stage of their life? Are there really no microbes that are out to kill them? How is this even possible? I have not found anything related to this yet through my google search.
If the flies and mosquitoes are immune to harm from every disease on earth, then why is this so? Certainly we should be able to find out the secret behind this.

The top result of my search for "pathogen mosquitoes" was this abstract, which shows that there are (as expected) many disease that affect this group of flies. Adding "bacterial" as a search term yielded this article. Similar results are undoubtedly available for other groups of flies ...

My answer to a narrower question on insect diseases contains an example of a disease of the silkworm Bombyx mori.

There are plenty of diseases that affect insects, Dicistroviridae is one.
There are also plenty of fungal & bacterial ones, it's just that they aren't generally of concern to us so study of & information on them is somewhat light.
If you Google 'insect disease' you'll likely just get links for human diseases they're vectors for.
If you want to find links on diseases OF insects (rather than human ones they're vectors for) try refining your search to something that's important or useful to us like bees.
Diseases of the honey bee is the sort of thing you'll get hits for then.


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UV-lamp, DNA and RNA extraction lab
I'm equipping a lab room (~3x5 meters) that's supposed to be used for DNA and RNA extractions. I know  about the basic safety precautions when working with RNA and DNA extraction (fresh gloves, labcoat, separate workstations/pipettes, RNase-free workspace etc), but it is my first time seting up this sort of things
so I'm a bit unsure how strict I have to be about some of these things, so my question might seem a bit silly/stupid to some but here it goes anyways.
The question; I want to buy UV-lamps to clean out old DNA in the environment so I don't contaminate my fresh samples. I don't work in any hoods. I have a downdraft ventilation table and a bench that both stands along one wall on which I'll be Working on. I wonder if it is enough to just have one UV-lamp that covers my working area, or should I buy enough UV-lamps that cover the entire room (since I'm not working in any hood -> risk for airborne contamination)? Or is it over-kill to cover the entire room? I don't want to spend to much money.


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Regarding Passive Aritficial Immunity: Why does the concentration of the foreign antibodies decrease over time?
So, like suggested in question, I am extremely confused about this one concept. That whether or not the injection of foreign antibodies ( passive artificial immunity ) triggers an immune response.
From what I have learnt, the general idea is that the antibodies injected into humans, which may have been extracted from another animal or synthesized artificially using hybridoma cells, act as foreign antigens to the body and trigger the cells of the immune system such as neutrophils to engulf and destroy these antibodies and anything they are binded to it ( bacteria or viruses ).
But I was doing some CAIE past papers and got confused by a question and the answers provided in marking scheme;
Question:
"Two people took part in a study to find out the effectiveness of two types of immunization. Person A received an injection of antibodies against tetanus and person B received a tetanus vaccination.
Over the new few weeks the blood from these two people were analysed for the presence of antibodies to tetanus. The results are shown in figure 5.1A and 5.1B
(b) Explain why the antibody concentration in person A,
(I) decreased during the study period,
(II) did not increase. "
The graph provided is similar to that shown in https://i.sstatic.net/obZ8V.png except that the rise is not seen (instantaneous) and that the x axis is in days, and most IMPORTANTLY the graph depicts concentration of antibodies to tetanus (as injected earlier).
Now the marking scheme for this question has the following guidelines for marking:
" mark (I) and (II) togeather...
(I) antibody destroyed/broken down;
    antibody excreted;
(II) no antigen entered body;
     no immune response;
     no (active) B Cells/plasma cells/memory cells;
     no antibody made; "
Now, the reason I don't understand this is because it doesn't quite align with what I have learnt. Wouldn't a foreign antibody trigger an immune response causing the neutrophils to engulf and break the antibody down.
And wouldn't the reasoning for it not increasing be that it is simply an antibody that cannot produce copies of itself as it lacks the machinery and only injection was provided, followed by its removal by the immune system?
Even lets suppose if there was an immune response, why would the concentration of TETANUS antibodies, which were injected, increase?
This is on an AS (Advanced Subsidiary Level) for CAIE.
Please, if someone can explain this concept and the answer suggested by the marking scheme, I will be extremely grateful.

This is a very long question relating to an examination for which there is presumably a syllabus, nobody here is likely to be familiar with. We really prefer real questions people have encountered that have definite answers.


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Neanderthal and Sapiens DNA
From WIKI:

Modern humans and Neanderthals share 99.7% of their DNA

and

1–4% of the DNA of living non-African humans are found by the Max
Planck Institute to likely come from Neanderthals, a result confirmed
in 2012, and refined to 1.5–2.1% in 2014

What do they mean? If it is similar for 99.7, how it could be that 1.5%-2% is unique genes from Neanderthals?
The Africans do not have them, so African different from European in 1.5-2% ? But that's not true.

Q. “What do they mean?”
A. Two different things

“…share 99.7% of their DNA” is fairly straightforward.

This means that if you compare, base for base, the total DNA sequences of a group of Neanderthals with a group of humans — doing appropriate statistics — you will find, on average, 99.7% identity.

“1–4% of the DNA of living non-African humans…likely come from Neanderthals” is more nuanced.

This is because that 1–4% (generally thought nearer 2%) that is thought to come from Neanderthals could still be 99.7% identical to the human DNA it is thought to have replaced.
How can that be?
First let us assume that there are no genes unique to either humans or Neanderthals. (This may not be true, but the assumption emphasizes that we are considering the same genes.) Now suppose that after the divergence of Neanderthals and humans from their common ancestor the Neanderthals acquired a mutation that produced a new haplotype for a particular gene that spread to all Neanderthals. The percentage difference in DNA would be small, but the haplotype and hence the gene counts as Neanderthal. If it enters the European human population by interbreeding after emergence from Africa, then that gene is regarded to have come from Neanderthals. So the idea is that this is true for approx. 2% of non-African genes, even though the originating Neanderthal DNA may be 99%+ similar in sequence. Likewise, differences are observed between Africans and non-Africans in these gene haplotypes, even though the DNA sequence otherwise is very similar.
I have not discussed the evidence for this 2% gene haplotype difference here as I recently covered it in an answer to another question, specifically on that topic. (Hence my somewhat late interest in this question when it re-emerged.)

This answer is not essentially different from that posted by @John, but I have tried to explain it in biolgical/genetic terms rather than by analogy, in an endeavour to make my answer clearer.

start by checking to see if they are comparing the same thing, are they comparing base pair sequence, functional genes, non-functional genes, whole sequence or only the variable portions, one could even be comparing nuclear or mitochondrial DNA or both. I could not determine whether mitochondrial DNA latter was used in the listed estimate for last study.
the first is comparing exact nucleotide sequence while the second is comparing functional gene differences (for the listed numbers, they compare them several ways) so of course the numbers do not match. Note both are also comparing different reconstructed genomes, and with different methods no less.
imagine comparing two dictionaries, one person checks to see if definitions  match letter for letter exactly and ignores missing definitions, the other checks to see if they cover all the same words and give the same definitions considering them the same even if the exact wording and punctuation are different, of course the two people will get different percent differences.

Yes, the genes are the same, even between humans and chimps. They are talking about pairwise differences. Lining up 1000 nucleotides of DNA between the two species, 997 would be identical.

except they are comparing portions of a reconstructed genomes and saying the genes are the same can have two meanings they may match in base pair comparison or they may have the same functional gene, humans and chimps do not have all the same genes, there are unique genes in humans.

Almost no genes are unique to humans.

The 99.7 is a percent pairwise similarity. If it were percent genes shared, it would be much higher.


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How is the reflectance spectrum of solids measured?
I was reading this question about autumn leaf colors. One of the answers refers to an article by Archetti et al. In the article, box 4 (page 5) shows the reflectance spectra of leaves of different color. How is the reflectance spectrum of such solid materials measured? There was a recent question about spectrophotometers but it appears to assume the sample is in a liquid form.

As the name implies, reflectance spectra are measured from light reflected off an object. Any object with reflects light, such as any opaque object) will work for this technique; to me this seems like solids are ideally suited for reflectance spectrphotometry. You might be used to transmission or absorbance spectrophotometry, which measures the amount of light transmitted or lost after passing through a sample. These methods are typically used for liquids which allow passage of light to some extent.
The paper (1) cited by the review you mention says that they used a "RAMSES-ARC hyperspectral radiance sensor," which is probably just as awesome as it sounds. In principle reflection spectrophotometry works very similarly to transmission-based spectrophotometry: generate monochromatic light, shine it at the sample, and measure the intensity of light that comes back at that wavelength (or over a range of wavelengths)$^†$. If you do this for many different wavelengths of light, you have a reflectance spectrum. This link might have some useful information.
$^†$ Edit: Modern-day spectrophotometers use a more efficient method in which broad-band light is passed onto the sample and the response at a single wavelength can later be mathematically reconstructed. If you're interested in these types of details, refer to Fourier Transform spectroscopy.

(1): Doring TF, Anchetti M, Hardie J. (2009). Autumn leaves seen through herbivore eyes. Proc. R. Soc. B 282(1801): 121-127.

is it really a matter of serially sampling different wavelengths? Or can you perform some kind of FFT-like procedure and analyze it all at once? (+1 nonetheless :-)

@ChrisStronks fair point. I wasn't really aware how spectrophotometers are actually built/implemented, more just the conceptual idea behind them. I can edit the answer to reflect this.

I would have given you another +1 but alas I can't. Very interesting addition (I am interested in computer vision applications but pretty newbie on the topic :-)


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How does the stomach differentiate between liquids and solids to initiate churning?
Or maybe it doesn't at all. Can the stomach tell the difference between liquids and solids and change its churning process accordingly despite that it has no nerves? Because liquids don't need to be churned, so I figure there's a chance animals, or at least humans, evolved in such a way that the stomach wouldn't waste the energy trying to do it.

"...despite that it has no nerves" Why do you think that?

Because there are very very very very very very few cases where people generally "feel" anything they have eaten in their stomach in any way, shape or form. Of course, it still has neurons that transmit signals for motility and secretion.

So, simply because you believe that, you state it as a fact? To use your words, there are very very very very very very many cases where people generally "feel"stuffed they have eaten a Thanksgiving meal. Your stomach isn't 'wired' to feel like your fingers. But it has plenty of a variety of afferent neurons.

I don't need to believe anything, it's a commonly held fact that there are no "nerves" in the stomach. The "feeling" from turkey has nothing to do with any nerves in the stomach, it's commonly known that not only does meat take a lot of energy to digest, but tryptophan also contributes to sleepiness.

It's also a commonly known fact among scientists that most people don't know much of anything about human anatomy and physiology. You are living proof. I didn't say anything about sleepiness, and if you want real "facts", look up orexin/hypocretin. Also see this for afferent nerves of the stomach.  You should quit while you're only behind to an acceptable degree. Keep showing off your "commonly held facts" and you'll only come out more behind.

Also, just ask yourself: if your stomach has no (afferent) nerves, why  do ulcers hurt? Why do antacids (like Mylanta) help?

Subjective opinions aren't commonly known among scientists because opinions such as yours aren't science. Humans don't have somatic receptors like nociceptors in the stomach. You have the legal right to pretend whatever you want, but your article doesn't disprove that, viscera only encompass the area around organs, they are not the organs themselves, and viscera are sensitive to things like stretching and inflammation, that's why ulcers hurt.

How about you ask yourself why you're so desperate to feel superior to other people? What shortcomings have you made of your own life that lead to be that desperate? At this point it's obvious you're just a troll.

@VaneVoe Please watch your tone. As I already said in your other question, writing answer is voluntary. With this kind of behaviour you will not attract anybody to spend time writing an answer.

@Chris Actual experts have expertise for the benefit of society. If these self-proclaimed stackexchange "experts" are so childish as to impede the assistance of potentially hundreds of viewers over their own childish, arbitrary whims, then they were never experts in the first place and their words were never worth regarding. Remember that it is your site that brags about experts answering questions Chris, so I expect to see questions answered if no one is lying about the presence of experts. Otherwise, the site should reevaluate its false-advertising campaign.

@VaneVoe Nope, you are wrong. We don't have to - we can.

@Chris Other than the fact that it literally says "expert communities" on the stack home site, you only don't have to if and only if the site is fraudulent, if there aren't actual experts here. Otherwise, if there are, then the question will be answered. You can say there are experts all you want, but the more the question goes unanswered, the more and more evidence there is that you too are a fraud.

@VaneVoe One last time: Your attitude is one of the problems. EOD

It's clear that I am teaching you some science (you read an abstract and learned some things) but not enough, e.g. you state, "...viscera only encompass the area around organs, they are not the organs themselves..." however, the actual definition follows: vis·cer·aˈ, visərə/ noun: the internal organs in the main cavities of the body, especially those in the abdomen, e.g., the intestines. (emphasis mine) I'm done here too.

You're not trying to teach anything because you're too busy trying to pat yourself on the back. Neither somatic nor visceral pain are perceived within the organs, only in the areas around. When people have heart attacks, does their heart hurt? Nope, that's why people report "chest" pain and not "heart" pain. Your arrogance defeated you before you even arrived, you were already done.

Confirmed: there are no experts here, or such a simple question would have been answered, which means stackexchange is false-advertising when it claims experts reside here.

Tbh I'd like this question to be answered but I can see now no one would even bother.Man,why fight over stuff? I daresay youre the one in wrong when you said it had no nerves but anyways this is a really good question. How does the stomach differentiate between liquid and solid food?And what bout semi solid food?

No one is fighting over anything, if you choose to argue instead of answering, then you can only inevitably be the problem you complain about. Clearly stackexchange only cares about having self-absorbed excuses to pat itself on the back rather than contributing to humanity which is not the mark of an expert. Stackexchange has had every opportunity to prove me wrong and yet has failed to do so. The fact that such a simple question is still unanswered despite that an actual credible graduate has already answered it proves me right.


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Do animals with their eyes ~180 degrees apart have depth perception?
Lots of animals have their eyes more on the side of their head, like an octopus or a parrot. Are animals with eyes more on the side able to tell the depth of objects at different distances? It seems like the line of sight in each eye wouldn't be able to cross to a singular point to triangulate distance.

Good examples of animals with eyes 180 degrees apart are the hammerhead sharks. Here is a good read with very clear illustrations, explanations and quantification across sister taxa. And to address your question, the fields of view of each eye must overlap to produce stereoscopic, binocular vision that allows for (instantaneous) depth-perception. This is called stereopsis. However, many animals perceive depth through head turning - parallax and holding images for comparison - but this is obviously not instantaneous, nor as accurate..!

Yes. Animals can also calculate the distance to object based on the senses of smell, color, and hearing.

Nope, depth perception specifically refers to sight. https://en.wikipedia.org/wiki/Depth_perception but depth sensation would qualify that.

hammerhead vision actually overlaps on the front and back, so in theory they have two different depth perceptions.

Worth noting, even you can perceive depth with one eye closed if you slide your head left and right. It's the same reason we can have 3d gifs that just rely on sliding the camera. Look up stereoscopic 3d lke these:

Welcome. tanks for your nicely illustrated answer. Can you add some references to your answer, and can you add web links to the images you shared? It allows people to background read on your material. +1

Many such creatures do overlap in part of their field of view. Some don't.   Presumably, the former still have some range sense. It's generally accepted that range judgment it's far more valuable to predators while herbivores focus on movement over a wide range. (at least in the sources I've read on this.)
That said:
Focal length can provide some amount of depth information, but not like comparing two angles. ("accommodation " in the wiki article on depth perception)
Parallax can provide some useful depth information. This is a function of basoc geometry. (In the same article, see "motion parallax", "occultation", and "perspective")
Theoretically, if a creature is precisely enough aware of its movement, it could pick up depth by rotating its head. This is because of the previously mentioned geometry. (https://en.wikipedia.org/wiki/Depth_perception#cite_note-5)
Not sure if any animals actually do this, but some birds seem to.

This answer is, fundamentally, just a summary of elementary information. The wiki entry on depth perception chops up the list of factors a lot more fine than I did off the top of my head.
https://en.wikipedia.org/wiki/Depth_perception
https://en.wikipedia.org/wiki/Equine_vision#Visual_field

The rotating of the head in order to improve depth perception is pretty common amongst prey animals.  I have seen this countless times in lab rats of nervous disposition.  When you have them in a box with an open top and are moving around above them, it is very common for the rat to crane its neck so that one eye is looking up at you and then start rolling its head back and forth, presumably to improve its ability to see when you are moving toward and away from it.  As you mentioned, birds do the same thing, and do so even when not under stress, whereas I've only seen stressed out rats do it.

True. My uncertainty is whether that's figuring distance. I'm not sure how you'd test that, but it sure seems likely. I'd sure be interested in any clever studies that demonstrated or disproved this, since I'm not aware of any.

Hmm.  That's an interesting question.  I suppose I just never thought too much about it.  Depth perception improvement just always seemed like the obvious reason for that behavior whenever I've observed it.  I just looked more into it.  There doesn't appear to be any rigorous study of this behavior.  Rats have often been observed doing this same thing before jumping long distances and albino rats with poorer vision roll their heads more often than dark-eyed rats so this seems to lend some credence to the depth perception hypothesis in their case.

Birds seem to be more complicated and have a number of reasons for head rolling, including the inability to move their eyes and the existence of two fovea, which allow switching between binocular and monocular vision.  Interesting stuff.

I didn't know that any birds had multiple fovea. That's interesting. I'll have to look deeper into this. Yeah, that rat note really is pretty compelling, albeit not proof.

In the paper "Rats Maintain an Overhead Binocular Field at the Expense of Constant Fusion", the authors monitor rats eyes while they are doing a task that definitely required visual depth perception: jumping across a gap. A more accessible write up is here. As @the-nate stated, you don't need overlapping visual fields for depth perception. Another depth cue, which he didn't mention, is size. If i know that an object is 1 meter tall, then the visual angle tells me how far away it is.

The size cue is fooled by the Ames room optical illusion.

@Barmar Every system can be fooled. The only question is whether it's sufficiently useful to pay for itself.


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How many species can have the same scientific name?
For my science homework, a question came up asking how many species can have the same scientific name. I'm pretty sure that each species has a different scientific name, but just to be sure...

It is actually possible for two species to have the same genus and species names. The two-part name (binomial) is unique only within a kingdom, so organisms in different kingdoms can have the same genus and species names. For instance, Orestias elegans is the scientific name of both a plant and a fish.

The scientific name (better known as latin name or binomial name) of a species is unique to this species. No two species can have the same latin name. Also, a single species cannot have two different latin names. But of course, mistakes happen and we don't seem to bother too much about them (esp. when the two species are very unrelated; see What instances are there in which two species share the same binomial name? (thanks @fileunderwater and @HRA).
Of course, the above is true as long as there is agreement in the limits of the definition of a species. In absence of such general agreement, there can be some issues. Consider for example, Homo neanderthalis who is often called Homo sapiens neanderthalis. See the post How could humans have interbred with Neanderthals if we're a different species? for more information about the definition and delimitations of species.
Have a look at wikipedia > Binomial nomenclature for more information.

I thought so too. However, the link provided by @fileunderwater proves that there are examples of a species name not being unique. #looking dazed and confused#

This is not to try and replace Remi.b's great answer, but just to supplement it for any later visitors: biological nomenclature is controlled by international codes which regulate how and what species can be named.
For example, the ICN (International Code of Nomenclature for algae, fungi, and plants) governs the naming of species and groups within those taxonomic groups, while the ICZN (International Code of Zoological Nomenclature) governs naming of animal species.
One piece of trivia about the two: tautonyms, or tautonymous names, are species names where the genus and species epithet are the same, for example Rattus rattus (black rat) or Vulpes vulpes (red fox). These are allowed under the ICZN, but are explicitly prohibited in the current edition of the ICN (the Melbourne Code published in 2011).


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Hummingbird cross Bering Strait
Hummingbirds travel to Alaska during summer. If global warming continue, allow birds stay longer in Alaska, can hummingbirds cross Bering Strait to Russia, then spread in Asia?

The ruby-throated hummingbird flies 500 miles nonstop across the Gulf of Mexico during both its spring and fall migrations
The Bering Strait is about 82 kilometres (51 mi) wide at its narrowest point, between Cape Dezhnev, Chukchi Peninsula, Russia
Based on the two facts above, it appears possible for a humming bird species to cross the Bering Straits if the weather becomes suitable to survival. Who would have thought?
That said, I am not sure how a humming bird who know which direction to fly in to make a successful crossing.

Good answer, I read Berng Strait have two Diomede Islands in center of strait, 40 km from both coasts. Probably need strong wind blow hummingbirds across, probably can't see islands from coasts.


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Osmotic Pressure in Capillaries
In this diagram, D is apparently the point at which "the osmotic pressure into the capillaries is the greatest", but I cannot figure out why. Any help would be much appreciated!

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

Fluid movements across capillary wall is determined by 2 main factors.

Hydrostatic Pressure (Blood Pressure) - tends to push fluid out of the blood vessel
Osmotic Pressure - Tends to pull fluid back into the blood vessels mainly due to the presence of plasma proteins. (especially albumin)

Important points you should know

Hydrostatic pressure or blood pressure is the pressure exerted by blood on the capillary walls.
Osmotic pressure depends on the number of osmotically active, non diffusible particles in the solutions separated by the membrane.
The main substance responsible for the osmotic pressure between blood and tissue fluid are the plasma proteins. Especially albumin.
Plasma proteins are absent in tissue fluid.

Filtration of fluids across capillaries is described by Starling Forces. (Forces were introduced by an English physiologist Ernest Starling.)
There are four main forces

Capillary Hydrostatic Pressure (Pc) - This forces fluid out through the capillary membrane.
Interstitial Fluid Pressure (Pif) - Tends to force fluid from interstitial spaces across capillary membrane
Capillary Plasma Colloid Osmotic Pressure (∏p) - Tends to cause osmosis of fluid inward through capillary membrane.
Interstitial Fluid Colloid Osmotic Pressure (∏if) - Tends to cause osmosis of fluid outward through capillary membrane. -Negligible

According to Starling forces,
Filtration = k (Pc - Pif) - (∏p - ∏if)
Filtration = k x Net Filtration pressure
Here k is the capillary filtration coefficient which is depend on permeability of capillary wall and surface area for filtration.
Look at the following diagram

In your diagram A is the Arteriole end and D is the Venous end.
Now we can calculate Net Filtration Pressure at A and D.
At Arteriole end (A);

Outward forces are;

Capillary hydrostatic pressure (Pc) = 37 mm Hg
and
Interstitial Fluid Colloid Osmotic Pressure (∏if) = 0 mm Hg
So outwards force is 37 mm Hg.
Inward forces are;
Capillary Plasma Colloid Osmotic Pressure (∏p) = 25 mm Hg
and
Interstitial Fluid Pressure (Pif) = 1 mm Hg.
So inward force is 26 mm Hg.
Therefore net force is 37 - 26 = 11 mm Hg and it is outwards.

At Venous end (D);
 Outwards forces;
 Capillary hydrostatic pressure (Pc) = 17 mm Hg
and
Interstitial Fluid Colloid Osmotic Pressure (∏if) = 0 mm Hg
So outwards force is 17 mm Hg.
Inward forces are;
Capillary Plasma Colloid Osmotic Pressure (∏p) = 25 mm Hg
and
Interstitial Fluid Pressure (Pif) = 1 mm Hg.
So inward force is 26 mm Hg.
Therefore net force is 26 - 17 = 9 mm Hg and it is inwards.
So that's why

In this diagram, D is apparently the point at which "the osmotic pressure into the capillaries is the greatest"


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Can boiling water without high temperatures kill bacteria?
If you use a vacuum chamber to reduce the pressure of water such that it can boil at around room temperature will it still have the same effect on reducing harmful bacteria as boiling at the usual 100C?

No, it's the temperature that kills, not the fact that some water is being evaporated quickly.

@mgkrebbs Well the water inside the bacteria would also be evaporating rapidly

Pasteurization is usually at less than 100 centigrade

of course if you evaporate then collect the water and recondence it separately it will contain far less bacteria.

No, you do need to reach high temperates to kill the bacteria.
It's not about the evaporation, or the pressure that kills bacteria, rather it is the temperature that does. Higher temperatures have drastic effects on the molecular structures that occur within the bacteria, such as the denaturing of various proteins present inside the cell. As a result, if you wish to boil water to kill it, it must be done at an elevated temperature.
Wikipedia mentions that the optimum temperature for killing microbes is around 70°C,

Boiling water is used as a method of making it potable by killing microbes that may be present. The sensitivity of different micro-organisms to heat varies, but if water is held at 70°C (158°F) for ten minutes, many organisms are killed, but some are more resistant to heat and require one minute at the boiling point of water.

Hi! Do you have a source that temperature causes destruction of the cell wall? I've never heard that and given that the phospholipid bilayer forms spontaneously, that sounds kinda strange?

TLDR: No, as its not the "boiling" itself that kills the bacteria, its the effect of temperature on proteins. But maybe?, in that you can kill bacteria by changing pressure without changing temperature.
Effect of Boiling at a Constant Temperature (No)
As other answers have suggested, the aim of boiling water to kill bacteria is to denature (i.e. change the shape) of proteins in the bacteria such that the proteins required for life stop working. The other facets of the boiling (e.g. water evaporation, turbulent bubbling, etc.) are unlikely to kill the bacteria. So if we had some bacteria in water and mimicked all the qualities of boiling except for temperature change, I doubt we'd see the bacteria die. This sounds like quite an interesting experiment to try though!
Effect of Changing Pressure (Maybe?)
There are many ways to denature a protein other than high temperatures! You suggest that we could change the pressure of the environment, which might also denature the proteins and kill the bacteria. In fact killing bacteria with high pressures (~340 MPa) is called Pascalization. As per your suggestion of lowering the pressure, there are some bacteria that can survive in a vacuum (BBC, 2010) so you might only be able to kill the bacteria by raising the pressure. On the other hand, it is known that you can denature a protein with low pressure (Wiedersich, 2008) but whether this protein denaturing would actually be fatal to the bacteria is another question. The effect of low pressures may be species dependent.
Something to Consider
Lastly, consider the phase diagram of water below (from Wikipedia). Where on the diagram can bacteria survive? Most (non-extremophile) bacteria seem to be bounded from above by around 340 MPa, and bounded on the right by around 72°C, but where else are they bounded? Furthermore what is the maximum pressure at which bacteria can survive in boiling water?


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Is a spore 'alive'?
Referencing this article: What are spores?
'A spore is typically a single cell surrounded by a thick cell wall for protection.'
So a spore is a 'cell'? This implies that a spore is a living thing; and not just a means to a living thing.
If this is the case, where does the spore get its energy? Oxygen, water, etc.?  Is there a name for the mechanism with which a spore extracts/obtains energy?
So many questions!

Welcome to Biology.SE. I'm voting to close this question as off-topic because the answer is based upon the definition of life and there is no such definition in biology. Ultimately, the definition of life is a matter of philosophy, not biology. Also, the post contains several question which make it too broad.

Welcome to BiologySE! Feel free to take a [tour] of this site. I appreciate your curiosity and eagerness to learn, but please limit yourself to one question per post. This is enforced to make sure answers are not too long. You may however ask multiple questions for different aspects though :)

Somewhat related: Why isn't a virus “alive”?

Spores generally do not need energy; the cell's metabolic activity is suspended indefinitely a technical source.

Thanks all. Wasn't looking to start trouble. 'Alive' was the wrong word to use I imagine. Basically does it require energy since it is classified in some circles as a 'cell'? mgkrebbs touched on what I was trying to get at.


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Pigmentation in dermatophytes
Dermatophytes are cutaneous keratophilic fungi. They cause concentric skin lesions. As a sample, usually skin scrapings are collected.
When viewed under the KOH mount, they appear transparent but when cultured, they show varied pigmentation. In fact, there is different pigmentation both on the obverse and reverse of the culture media (SDA), which makes pigmentation a differentiating and identification feature. These colors vary from species to species from red to violet.
So here are my questions

Is the pigment secreted out in the medium or retained in the hyphae?
How are the fungi transparent on a KOH mount.
Why is there a different pigmentation on the obverse and reverse?
Why is there no colour in the skin lesions? There is just erythema
if I'm not mistaken.


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What is the reason for 'microcytic' anaemia?
I know the causes for microcytic anaemia are Fe deficiency, prolonged inflammation, Thalessemia, Sideroblastic etc. All these logically point to a decrease in Haemoglobin synthesis - either Haeme or globin.
But my doubt is, what exactly causes the microcytosis? Lesser Hb can explain the hypochromicity, but how does it explain the decreased MCV?

The reduced iron availability affects the red cell size during differentiation.

The presence of red cells with reduced mean corpuscular volume (MCV) reflects reduced hemoglobin synthesis, which can have several causes. It can result from defects either in iron acquisition or availability, or in heme or globin synthesis. Experimental data in mouse demonstrated that early mitotic divisions are accompanied with no reduction of MCV, whereas during differentiation mitotic events are associated with a substantial reduction of MCV[1]

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2649346/

Coopersmith A, Ingram M. Red cell volumes and erythropoiesis. II. Age: density: volume relationships of macrocytes. Am J Physiol. 1969;216:473–82.


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What is the rationale behind tapering of immunosuppressant dose a while after transplant?
MMF, Cyclosporine, Prednisolone, Tacrolimus the dose of whatever immunosuppressant used is reduced in around 6 months - 1 year after the transplant.
What is the rationale behind this?
Wouldn't any allograft, howsoever old, still remain foreign? Does the body learn to consider the graft self? Or is the response still there but the destruction is reduced?
Why should a new graft elicit more response than an old one?

This is a very interesting question. One of the most important considerations in patients on long-term immunosuppression is the risk of complications, whether infections or (more dangerously) cancer development; because of this if we can taper the dose then we would like to. This paper specifically discusses a lot of those risks. You mention prednisolone which is a glucocorticoid, and the side-effects (see also here) of chronic steroids (due to very wide-ranging immunosuppression) are well-known and always borne in mind when they have to be prescribed. The tapering of corticosteroids in long-term immunosuppression is often early to replace them with other drugs (mentioned here). With regards to the other immunosuppressives you mention, I'll mention mycophenolate mofetil and tacrolimus later with regards to how this is feasible biologically; with regards to cyclosporine, this study (admittedly old) has data illustrating the rates of rejection of renal transplants when patients withdrew from or tapered cyclosporine (here for financial reasons, but this drug also has significant adverse effects) and you can see from Figure 1 in the paper that although the patients who withdrew completely had many allograft rejections, those who tapered did not.
I'll start with answering your question about what clinical evidence we have for being able to do this; there have been quite a few studies which might help to throw some light on this. This study specifically considered kidney transplants, testing patients who were on standard immunosuppression for the 2 years after a transplant, and specifically measuring the quantity of CTLs (cytotoxic T-lymphocytes) reactive against donor cells, and they found that these cells were significantly downregulated in most patients 2 years after the transplant (while activity against third-party cells was mostly preserved). Since they found other T-cell responses to be unimpaired, they concluded that there was specific downregulation of the donor-specific cells occurring.
This paper also has some data which you can have a look at. This study specifically looked at moving patients from cyclosporine to azathioprine and mycophenolate mofetil and then tapering those. I've reproduced one of their graphs below which shows the activity of donor-specific CTLs before transplantation (the no dose group), 1 year after (still on high dose immunosuppression) and 2 years after (on low dose immunosuppression). The units are the ratio of activity of donor T-cells to activity against third-party T-blasts from spleen tissue (i.e. a control). Although you can see that some patients have ended up with increased activity after tapering, most patients appear to have low activities similar to (or even lower than) their pre-immunosuppression values, and these would be the patients considered for this tapering. This means that they now respond less vigorously to allograft cells than to control cells, and the ratio has decreased during treatment (presumably the reason why almost all of them have ratios under 1.0 before treatment is that the donor is not a random individual but matched for a lower immunological response):

And for another comparison with the body's response to non-donor substrates, the same study looked at response to tetanus toxoid. As you can see in the graph below, although the high dose caused the response to drop, it appears to have bounced back up again in most following the taper, similarly to the 3rd-party T-cell response but unlike the allograft response (the y-axis is proliferation of patient spleen cells in response to the toxoid divided by control rate):

As to the immunological reasons that we can taper the immunosuppressant dose, this is not particularly clear but there are known processes which might help to elucidate it. This paper (also on kidney transplants) suggests that there is a specific downregulation of the activity of CTLs directed against antigens presented by the direct pathway, and that this could be caused by anergy, deletion or regulation. The authors suggest that the most likely cause is an effect of the chemotherapeutics (here MMF and azathioprine) on the T-reg cells, and they speculate from the tests they did (the Discussion of the paper has the details) that the cessation of suppression of T-regs that occurs during the taper is what is responsible. They also mention a role for IL-2 signalling (necessary for T-reg function, and some immunosuppressants suppress it leading to rebound on tapering) and dendritic cells (whose costimulatory function may be altered by MMF).
As to the precise mechanism, it is not yet particularly clear, but it is thought that in the interaction between a suppressing T-reg cell and a CD4 effector T-cell, the latter actually induces the T-reg cell through as yet unknown mechanisms, so that continued activity of T-cells (e.g. in chronic inflammation or the presence of an allograft) may upregulate T-regs that suppress them. It is known that T-regs are important in downregulating chronic inflammation (presumably this is responsible for the pattern in the first graph I reproduced above where the activity against donor cells seems to drop more than that against control cells, even on high immunosuppression), through mechanisms which have been hypothesized to include CD4 T-cells undergoing receptor-ligand interactions with T-regs and providing signals to them to upregulate their production of IL-35 (which is important in suppressing all types of T-cells). Given that it is known that upregulated suppressive activity of T-regs in chronic inflammation downregulates the immune responses of all non-T-reg cells, it appears that donor-reactive T-helper cells will induce T-regs which will then downregulate donor-reactive CTLs. This paper I mentioned previously postulates that on release of immunosuppression this population of T-regs would bounce back and greatly downregulate the donor-reactive CTLs and T-helper cells.
This paper also mentions the fact that an introduction of tapered mycophenolate mofetil in liver transplant patients promotes immunological tolerance to allogeneic transplants. They mention the effect of this on T-regs as well as other immune cells.
For interest, this paper presents some interesting alternative speculation on the nature of the T-regs involved in organ transplantation tolerance. In certain cases, self-tolerance may develop to 'new' tissues, and the authors postulate that the main T-regs involved in transplantation tolerance are newly formed in response to the prolonged presence of the allograft, rather than predefined. Because of this, the tolerance might develop to some extent regardless of the chemotherapeutic regimen.
Finally with regards to tacrolimus, this study has data on the immune response during weaning off the drug after an intestinal transplant. They found that patients with a low immune response prior to weaning had a better response to the weaning, and that their immune function remained low after weaning. This is a bit different to the MMF situation I mentioned above where immune function in general seems to return and only donor-reactive immunogenicity remains low (this tacrolimus study doesn't specifically mention the effect on infection rates, but their Figure 7 seems to imply that those patients with low immune function (presumably those weaned) had lower intervention rates). Specifically the authors conclude here also that self-downregulation of the immune system (probably by T-regs) is likely to be the cause.
So in summary it is not yet fully elucidated as to why we can do this, but the upregulation of T-regs that downregulate donor-specific effector cells, and (at least for certain chemotherapeutics) the release of T-reg suppression on tapering may be important.


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Why do polyneuropathies affect the extremities first?
Polyneuropathy is an anatomic pattern of nerve damage most commonly seen in Diabetes mellitus.
To quote Robbin's Pathology,

In most polyneuropathies, axons are affected in a length dependent fashions leading to deficits that start in the feet and ascend with disease progression. The hands often start to show involvement by the time deficits extend to the level of the knee, resulting in a characteristic 'stocking and glove' distribution of sensory deficits

What is the reason behind longer neurons being preferentially affected?

Polyneuropathy is actually not a very specific term, so the reasons will no doubt vary depending on which specific class you are talking about.
That said, here are two reasons that longer neurons are preferentially affected:

Some polyneuropathies involve conduction problems that include "failures" where action potentials aren't propagated down the full length. It doesn't matter where along an axon the failure occurs, and longer axons therefore have more "chances" to fail.
Axons are somewhat isolated from the soma where most proteins are created, and it is common in certain neuropathies for degradation to begin furthest from the soma, presumably because the neuron has less capability to deal with problems or repair damage in those areas far from the soma. Neurons with longer axons by definition will have some part of their axons that are further from the soma than neurons with shorter axons. This is the answer that is most relevant to your question, see for example this source that reviews the causes of diabetic neuropathy.

References:
Yagihashi, S., Mizukami, H., & Sugimoto, K. (2011). Mechanism of diabetic neuropathy: where are we now and where to go?. Journal of diabetes investigation, 2(1), 18-32.

Thanks. Id like to add some more. Further reading the same chapter I came across another line. It says neuronopathies (which attack the soma of the neuron eg zoster and platinum) unlike axonopathies (which polyneuropathies mostly are) are equally likely to affect both proximal and distal parts of the body since here it's the cell body and not the axon to be damaged. So, this helps as a differentiating point bet the two

@Polisetty I don't think it is accurate to think of neuronopathies and polyneuropathies as independent groups; there is definitely a Venn diagram-like association: it is just as possible for a neuronopathy to be a polyneuropathy as not (zoster would be a good example of a neuronopathy that is not a polyneuropathy).

Yup one is an anatomical classification while the other is a functional one...


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What is the 'fallacy' in simple segregation rules in reference to polyploidy?
I was reading a paper Why polyploidy is rarer in animals than in plants’: myths and mechanisms, Mable 2004 where I found this sentence.

Stebbins (1950) suggested that autopolyploids were probably more frequent than often considered because of the ‘fallacy’ that simple segregation rules (i.e. auto- polyploids showing multivalent associations and allopolyploids showing bivalent associations) can be used to distinguish modes of origin.

What does it mean? I know that autopolyploidy is where the chromosome sets are from the same species and it is the other way for allopolyploidy. What do segregation rules mean here and what is the fallacy?

@Richard Smith-Unna Could you please answer?


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What is the sequence similarity between humans and chimps in the noncoding genome?
I've seen some papers discuss extensively how human and chimp genomes compare in many of their features, eg Suntsova & Buzdin 2020, but I have not been able to find a paper that specifically studies and determines the sequence similarity percentage between humans and chimps specifically at noncoding regions (of course coding regions are known to have similarity around 97-99% depending on the metric).
So I am curious to ask here: what is the percentage of noncoding sequence similarity between humans and chimps?

If you include a citation it needs to have a full journal reference or a link, otherwise it is of little use.

@David The use is that if you copy/paste the reference I gave into google, the relevant paper is the first search result. In any case, I was just explaining where I was coming from, the paper itself is not relevant in answering my question.

According to "MUMmer4: A fast and versatile genome alignment system" (Plos Computational Biology 2018):
"First we aligned the current assemblies of human and chimpanzee, using the default nucmer4 options with 32 parallel threads ... We used human as the reference and chimpanzee as the query sequence. The human GRCh38 assembly contains 3.088 Gb of sequence while chimpanzee assembly, with 3.31 Gb, contains 7% more DNA. (Note that the chimpanzee genome is far less polished than human, and much of the extra DNA might be explained by haplotype variants or incompletely merged regions; thus the two genomes might be much closer in size than these numbers indicate.)
MUMmer had 2.782 Gb of the sequence in mutual best alignments, where each location in the chimp was aligned to its best hit in human and vice versa, with an average identity of 98.07%. The 1.93% nucleotide-level divergence found here is higher than the 1.23% reported in the original chimpanzee genome paper [25]. Our higher divergence is likely due to two factors: first, the 2005 report was based on 2.4 Gb of aligned sequence from older versions of both genomes, while ours is based on 2.782 Gb (16% more sequence) aligned between the current, more-complete versions of both genomes. Second, the original report used different methods, and may have counted fewer small indels than were counted in our alignments. Approximately 306 Mb (9.91%) of the human sequence did not align to the chimpanzee sequence, while 138 Mb (4.15%) of the chimpanzee sequence did not align to human. We detected 390 Mb in alignments where multiple sequences from chimpanzee aligned to the same location in human sequence and thus only one was chosen as the best alignment based on alignment identity. The genomes are very similar across all chromosomes, with the percent identity varying only slightly, from 97.5% to 98.2% for chromosomes 1-22 and X. Chromosome Y was an outlier at 96.6% identity over 84.6% of its length; however this is likely due to the fact that the chimpanzee Y chromosome is much less complete than the human Y."
A more recent 2020 paper (https://doi.org/10.3389/fgene.2020.00292) found:
"Since centromeres and unsequenced regions correspond to biological features, calculations including N’s and centromeres are listed in parentheses. Initial alignment coverage is 95.57% (90.9%) of the Hg38 reference, and identity within the alignment of 98.65%."
So, it seems that if you include the noncoding genome, the sequence identity between human and chimp genomes is around ~90–91%.

good answer too!


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Why do high cholesterol levels result in a buildup of fat in blood vessels?
As is well known, high levels of cholesterol can lead to a buildup of fat in blood vessels, which can lead to them being constricted which makes it more difficult for blood to pass through. In fact, this can end up with the formation of fatty deposits that, if they suddenly break, could result in a clot that causes a heart attack/stroke. Therefore, the resulting buildup of fat because of these high cholesterol levels is highly important.
My question is why do higher levels of cholesterol result in a buildup of fat at all? Why do fatty acids care that there's more cholesterol around? I know cholesterol and fats are both lipids, but beyond that, I don't see the connection.

I assume this isn't a homework question, but you still should have made an attempt to answer this before and shown it here. If the inside of a blood vessel were perfectly smooth, this probably wouldn't occur. But blood slushing along in those blood vessels all day every day do cause some "wear and tear" which is when lipoproteins get involved.

@anongoodnurse I did do some research. Apparently there are cholesterol deposits, where cholesterol is the raw material for the deposits, however, there are other types of deposits and I was unable to find information there.

The point of my comment is to show your research. Anyone can say they did the research and found nothing helpful. Showing the attempt is what counts.

The phrase "high cholesterol", and the measurement itself is a marker for high levels of a particular lipoprotein, Low density lipoprotein (LDL). Because cholesterol and triglycerides are not soluble in plasma, they are packaged by the liver into soluble particles called lipoproteins. Packaged in lipoproteins, these lipids are transported throughout the body, for use by different organs and tissues. As these lipids are dropped off, the lipoprotein is converted from one form to another, with characteristic biophysical and physiologic properties. The LDL is a late stage of a lipoprotein before reuptake at the liver (and other organs, but mainly the liver) via the LDL receptor. We happen to know that people who have high levels of circulating LDL are at risk for, e.g., cardiovascular disease because of The Framingham Study, and that if you can reduce circulating LDL levels you can decrease the risk for these diseases. The molecular basis of this risk was demonstrated to be, in large part, failure of clearance of LDL particles because of ineffective receptor mediated endocytosis, as described in this wonderful 1986 paper in Science.
From this presentation:

Some LDL cholesterol circulating through the bloodstream tends to deposit in the walls of arteries. This process starts as early as childhood or adolescence.
White blood cells swallow and try to digest the LDL, possibly in to digest the LDL, possibly in an attempt to protect the blood vessels.
In the process, the white blood cells convert the LDL to a toxic (oxidized) form.
More white blood cells and other cells migrate to the area, creating steady low steady low-grade inflammation in the artery wall.
Over time, more LDL cholesterol and cells collect in the area. The ongoing process creates a bump in the artery wall called a plaque. The plaque is made of cholesterol, cells, and debris.
The process tends to continue, growing the plaque and slowly blocking the artery.

There is a good overview of the general physiology here in Robbins The Pathologic Basis of Disease. Chapter 5, Genetic Disorders, reviews the physiology, and the relevance to disease, in the section on Familial Hypercholesterolemia. The review is relevant to hypercholesterolemia in general.

So with more cholesterol, it gets packaged into LDL at a higher rate. So does LDL cause a buildup of fat? How does it do this? Is it the actual raw material of the buildup?

@Korvexius it turns out to be quite complicated. Inadequate LDL uptake by the liver causes a number of problems. There are some direct effects of high levels of LDL (because they aren't being taken up), and also some indirect effects. Atherosclerosis is in many ways a disease of inflammation as much as it is a disease of lipid accumulation. LDL probably plays a bigger role through initiating an inflammatory process in vessel walls than it does by depositing lipids directly.

@DeNovo - I think an explanation of the genesis of atherosclerosis was what the OP was really asking for.

@anongoodnurse It sounded to me like they were trying to figure out how cholesterol molecules could cause fatty acid deposits. I figured learning what a lipoprotein was (and what exactly "high cholesterol" means) would have been more helpful than reading about foam cells.

@DeNovo - I agree there needed to be a discussion of cholesterol and lipoproteins, but the question was about atherosclerosis - the entire first paragraph, in fact. Also, see the follow-up question.

@anongoodnurse I'd welcome an answer from you with an overview of atherogenesis! I'd have to look through a review myself to make sure i wasn't misremembering anything.

@DeNovo I would also like to see information on the direct cause of fatty acid deposits in your answer if you could. The question is less about atherosclerosis and more about the deposits.

@Korvexius - Atherosclerosis is about the fatty deposits. Research.

@DeNovo - Apparently you're correct. The OP doesn't want to know about the genesis of atherosclerosis; they want to know how fatty deposition in blood vessels starts. Clearly any answer I wrote would not be helpful.

@anongoodnurse DeNovo is right - I'm well aware atherosclerosis is about fatty deposits and have no idea why you assumed otherwise. But my question directly relates to how those fatty deposits build up, rather than the obvious conclusion that atherosclerosis is an after effect of this buildup.


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What's the difference between releasing hormones and tropic hormones?
I've been reading my textbook and two terms have appeared that, after a bit of looking, I still can't seem to be able to distinguish. Here's what the textbook says (McGraw Hill Bio 12, 2011):

After receiving signals from various sensors in the body, the
  hypothalamus secretes what are referred to as releasing hormones,
  which often travel to the pituitary gland. The releasing hormones
  stimulate the pituitary gland to secrete hormones that act on other
  endocrine glands. Hormones that stimulate endocrine glands to release
  other hormones are called tropic hormones. (pg. 394)

From the work I've done, it all seems to indicate that releasing hormones regulate the secretion of other hormones, and that tropic hormones target and stimulate other endocrine glands (to release hormones). And yet my textbook appears to use the terms separately later on as if they're related rather than identical (e.g.: "the pituitary gland is controlled by the hypothalamus via releasing hormones and it secretes tropic hormones" (pg. 396)). So are they identical? And if not, what distinguishes between them?

The releasing hormones could also be considered tropic hormones, and indeed they fit the definition as you noticed, but aren't usually named as such.
The special thing about the ones your textbook is specifically highlighting as releasing hormones is that they communicate from the hypothalamus to the pituitary through the hypophyseal portal system, vessels that travel directly from the hypothalamus to the anterior pituitary.
Therefore, they aren't really released into the broader circulation (they can get there, but they'd be in too low a concentration). They are easily identified in a list of hormone because they all share a naming convention where they are called "____-releasing hormone" and their primary function is to cause the pituitary to release whatever is in the "_____".
In terms of overall neuroendocrine function, the "releasing" hormones all cause release of tropic hormones, which in turn cause release of hormones that affect other tissues.
Therefore, the sequence is releasing -> tropic -> non-tropic. They could have been named something else, like "primary tropic" and "secondary tropic" but this terminology keeps them separate as "tropic hormones that cause release of other tropic hormones."


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Why does fetal distress (hypoxia) cause bradycardia?
In a non stress test performed in the labor room, fetal bradycardia is a danger sign indicating fetal distress (hypoxia).
Why does fetal hypoxia cause bradycardia while hypoxia in adults cause tachycardia? What is the mechanism for both and why is it reverse?

Are you aware that in adults with hypovolemia, bradycardia is a sign of an impending cardiac arrest? Not saying ths is the answer, but asking if you're aware that the end point is similar.


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Why don't acacia trees prefer increasing tannin levels in their leaves rather than leaving them high?
According to this article, the Acacia tree has a chemical defence system which leads to the release of ethylene in the surroundings when a herbivore grazes on it. This leads to an increase in tannin concentration in the leaves not only in the plant where the herbivore is grazing but also in the acacias surrounding 45m.
The question is, what prevents acacias to store tannins beforehand? Wouldn't the giraffes totally avoid them then?  Tannins aren't poisonous by themselves (correct me if wrong).

I was unable to find the original research article. A link would be really appreciated

The original article doesn't seem to be online. A summary of the findings was in the Scientific American in 1990. A thesis by a student of van Hoven's seems to cover it (THE INFLUENCE OF PLANT TANNIN ON THE FEEDING ECOLOGY OF GIRAFFE (GIRAFFA CAMELOPARDALIS)) but only the abstract seems to be online and the thesis is in Afrikaans.

Usually the answer to these sorts of questions is that generating the toxic substance (tannins) is metabolically costly, so it's bad for the plant to produce the toxin when it's not needed. When the plant is threatened by browsers, it's beneficial to turn on the production until the threat goes away.


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What happens to lipoprotein lipase after a sugar only diet?
Insulin increases the activity of lipoprotein lipase thay allows cells to take in lipids from chylomicrons in the blood.
If a person takes a sugar only meal like drinking coke, insulin is released. Will this insulin activate the lipoprotein lipase despite the lack of chylomicron synthesis due to lack of fat in the diet?
Could activation of the enzyme without adequate substrate be of any harm?

From the name "lipoprotein lipase" I guess that it acts not only on chylomicrons (which are proteins, by the way, not so much different from the  "regular" Lipoproteins) but on VHDL as well, which, like chylomicrons, transport triglycerides to the "arterial wall" to unload. Now, if there is no fat in food, just sugar from coke, the liver will take up sugar then and convert it to triglycerides, of which very few is stored in liver - any surplus is said to be packed into VLDL to be delivered to arterial wall. From there to adipose tisssue - and not to muscle? Maybe that's the basis...

Highly intersting I find this question: as it is the "starvation" situation that might be basic in nature, thus for understanding. There wouldn't be much cholesterol contained in coke (smile!), what would liver synthesize cholesterol from to go with tryglycerides surely made from sugar, to go with, in the VLDL, off liver?


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Why does botulinum toxin cause only NMJ symptoms?
Botulinum toxin acts by preventing release of ACh by cleaving SNARE proteins. But if it is acting on snare proteins shouldn't all vesicle releases be effected? Why is it limited only to the acetylcholine vesicles in the motor neuron bat the end plate? Why not some other neurotransmitter at some other place like GABA in the brain?


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Do ovaries produce estrogen before menarche?
It is traditionally taught that estrogen is produced by the granulosa cells of the follicle. But before menarche, where does the estrogen come from? Is it from the thin layer of granulosa cells lining the primordial follicles?
The adrenal zona reticularis produces androgens physiologically. Are they converted to estrogen? If yes, by whom? If not by the ovary, would the levels of estrogens be same in prepubertal boys and girls?
More importantly, are there estrogens in a girl before menarche? If yes wouldn't they cause endometrial changes?

It would be better to break this into two individual questions.

@Polisetty one possibility-pre pubertal FSH release follows a circadian rhythm and this concentration is so little that only very sensitive methods could detect this rhythm...as menarche approaches the frequency and amount of FSH release increases & hence also oestrogen...so endometrial changes would not be possible before menarche.


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How was gene knock out done in pre CRISPR era?
I am trying to understand how CRISPR has made the gene knockout or gene editing process simpler to make transgenic animals. Here is an old (pre CRISPR) flowchart from Manis, 2007 that shows how knockouts can be made.

I assume much of this process remains the same even with CRISPR. But I want to understand what part of this flowchart has become easier with CRISPR? Is it that we do not need to wait for a random recombination event to occur? Is it that the yield has increased because we directly cut at the site and ask for HDR to happen rather than just sit and wait for it to happen?

Before CRISPR, homologous recombination at the target site (first step in left chart) relied on such events happening spontaneously. With CRISPR, the ability to generate double-strand breaks (DSBs) at the target site dramatically increases the frequency of homologous recombination events, since the DSB activates the cell´s own DNA repair mechanisms (of which homologous recombination is one) and directs them to the target site.

The wiki page for gene knockout lists several non-CRISPR methods for gene knockouts including zinc-fingers.


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Does *E. coli Dh5 Alpha* strain has the ability to degrade polyethylene?
Does E. coli Dh5 Alpha strain has the ability to degrade polyethylene? What are the bacteria that can be used as a control in the research of polyethylene degradation?

I am not aware of any wild E.coli strains that have been described to have the ability to degrade polyethylene. However, work to equip E.coli DH5α with the ability to degrade polyethylene, by means of transformation, has been done in the laboratory (Mahalakshmi 2012, Danso et al 2018)
Microorganisms that can be found in the wild/nature that do have the ability to break down polyethylene include (Source: article):

Pseudomonas spp
Bacillus spp
Staphylococcus spp
Aspergillus nidulans
Aspergillus flavus
Streptomyces spp


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Why biologic systems tends to become more complex?
From elements, chemical compounds, cells, multicellular organisms, society evolves and with each step possibilities increase and things get complex. We are builing structures like ribosome builds polypeptide chains.
So my question is why humans keeps continue to live, does our brain is unconsciously tries to get our society to get bigger, why life has a tendency to get complex with time?

Why was this question received so poorly? Even if the assumption does not seem to hold, it is a question asked by many, and the (already existing) answers are quite useful.

I disagree with the assumption that biological systems have evolved to become more complex.
A clear example of the contrary is found in the Rickettsia species of bacteria which live inside the cells of its host (obligated intracellular parasites). Their genomes contain split genes, gene remnants and pseudogenes that may represent steps of a genome degradation process.
Here you can find more information about  Rickettsia evolution.
Here you can find an essay about complexity as a driving force in evolution.

This is an old and interesting question: how do we explain apparent trends in evolution without falling into the trap of teleology or goal-directed evolution, the idea that evolution is working toward a particular end point?
I don't know the answer, and I don't know if anyone knows the answer, but at least two books have tackled the question in a serious way.

John Tyler Bonner argued in a 1988 book that complexity tends to increase because of the correlations between organismal size and complexity. Cosma Shalizi's summmary of his idea is that:

... [f]illing a previously empty niche does wonders for the reproductive success of an organism; variations which increase size make new niches available, and so are favorably selected. But, owing to constraints imposed by basic physics and chemistry, larger organisms must be more specialized internally, i.e. more complex, to be as efficient as smaller ones, or even just to survive, so the selection is especially favorable for larger and more complex organisms. Because of the way developmental processes work, this complexity will probably be retained even by later, smaller organisms in other niches. Voila: the evolution of complexity, by means of natural selection.

Bonner's argument might or might not work at the level of cultural evolution.

In contrast, McShea and Brandon argued in a 2010 book that random variation by itself should tend to increase complexity. McShea's summary:

even when forces and constraints are present, a tendency for complexity to increase is always present. The rationale is simply that when selection is absent, the parts of an organism should tend spontaneously to accumulate variation, and therefore to become more different from each other ... A consequence of the [Zero-Force Evolutionary Law ] is that we do not need natural selection to explain complex tissues and organ in organisms.

Part of the problem lies in measuring - or even defining - complexity in evolutionary terms.  An example I read about (though I can't vouch for it) is the difference between amphibian and mammalian reproduction.  Amphibians simply lay their eggs outside - which means their genes must be prepared to handle a wide range of environments and still produce an adult frog or salamander.  Mammals keep their embryos inside, in a tightly-regulated environment.  And then there's metamorphosis - are the different stages of a butterfly less complex than mammalian growth?

fair enough, but from a very broad perspective there are reasonable ways to define this that will distinguish bacteria from (say) kangaroos - number of cell types, variety of biochemical pathways, genome size, ...

@BenBolker Number of cell types is probably a good indicator / proxy for organisms, but it's hard to judge, because so far we have estimates for model organisms at best. Genome size is not correlated with organism complexity unless prokaryotes vs eukaryotes is all you care about. I would also be surprised if the number of actual biochemical (i.e. metabolic) pathways an organism has correlates with complexity, since higher eukaryotes are outsourcing a lot here; number of genetical pathways/circuits might again be viable though.


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What species would this be?
A common way to define species can be found on Wikipedia:

A species is often defined as the largest group of organisms in which any two individuals of the appropriate sexes or mating types can produce fertile offspring

This got me thinking. Imagine the case where we have three "groups": A, B and C, where A and B cannot produce fertile offspring together (different species) but C can produce fertile offspring with both A and B.
Have this ever been observed? And how would you classify C?

This is a good example of why reproduction is an exceedingly poor defining characteristic of species. Evolutionary biologists, and taxonomists (the people who describe species) do not use the biological species concept (based on reproduction), but rather, the evolutionary species concept, based on fixed characters.

What you describe is called a ring species. From wikipedia:

In biology, a ring species is a connected series of neighbouring populations, each of which can interbreed with closely sited related populations, but for which there exist at least two "end" populations in the series, which are too distantly related to interbreed, though there is a potential gene flow between each "linked" population.1 Such non-breeding, though genetically connected, "end" populations may co-exist in the same region (sympatry) thus closing a "ring".

Have this ever been observed?

While ring species is a classical theoretical concept, the cases of ring species is often open to some interpretation and limit case of what we want to call a ring species.
The question has been asked at Do ring species exist?, however the post is still left unanswered.

And how would you classify C?

There is no obvious simple way to answer that question. The concept of ring species just shed light into the fact that the concept of species is an outdated concept and does not have a good formal definition. For much more discussion about the concept of species you should definitely have a look at the post How could humans have interbred with Neanderthals if we're a different species?.


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Why do lions keep young preys and don't kill them right away?
I saw some (actually several) videos on Youtube of young lions and lionesses that after hunting baby preys keep them and even seem to play with them. The lions don't seem to want to hurt them but they don't seem to want to let them go either. Most of the video titles are "lions protecting baby ....", I don't believe that. On the comments people say "the lion is saving it for later". My guess is that the lion wants to give the baby animal for the younger lions. What destiny will the baby prey most probably have?

Possibly to help the cubs learn how to hunt.  Cheetah will do this but I'm not sure about lions.  A quick google search only came up with this one newspaper article, with photos, but I didn't see a source for the article.  http://www.dailymail.co.uk/news/article-3429745/Taught-kill-mummy-Lion-cub-shown-hunt-lioness-wounds-prey-lets-youngster-finish-off.html

@Kurt I think you're probably right but the Daily Mail is probably one of the least reliable newspapers in the English language so I'd be wary about using it as a source :)

@Jam - Yeah, that's why I didn't want to use it as an answer.  I'm hoping somebody can find a scientific source to back it up.