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Why dogs move their noses when smelling?
I read on Wikipedia that:

The wet nose, or rhinarium, is essential for determining the direction of the air current containing the smell. Cold receptors in the skin are sensitive to the cooling of the skin by evaporation of the moisture by air currents.

That explains why their noses are wet. Why they're slightly moving them when smelling, like on this video (see the close-up in the second part)? Could this very little movement create enough air currents around the nose to determine what smells are coming from what directions? Or is there another reason?

Might just be mechanical, note that your nose also moves if you inhale strongly enough.

The dog's ability to smell the world around him and to interpret these odors depends on a complicated chemical sensory system. First of all, it possesses mobile nostrils, that help to determine the direction of the smell. Then comes sniffing, the ability to disrupt the air with a regular pattern of breathing that, through laboratory testing, is structured in a series of 3 to 7 snorts. Most of the sensory organs of the dog's nose, the septal organ, are probably responsible for the outbreak of sniffing behavior.
The air is scented, it passes over a bony structure called "projection sub-ethmoid", that man does not possess, and nasal membranes that cover it. The area above the protrusion is not sweep, when the dog exhales air and it allows olfactory molecules to settle and accumulate.
When a dog breathes normally, air is introduced into the nasal passages, it continues its way to the lungs. The action of smell allows air to remain "at rest" in the nasal passages. The intricate complex surrounds the maxillo-turbinate bones of the skeleton provides that the nasal membranes are capable of creating models of air flows odors that lead content in the air to hit the regions of the olfactory receptors.
The odor molecules disintegrate and are concentrated in the nasal mucus that adheres to the receptor cells. Once the mucus, load odor, adheres to the microscopic hairs of receptor cells, the chemical signal odor turns into an electric signal and is sent to the cerebral cortex and the limbic system, ie, the part of the brain that regulate behaviors feeding, drinking and sex. Small molecules stimulate the olfactory nerve of smell. Big odor molecules stimulate the trigeminal nerve, one of the largest nerves of the skull, and the volatiles of sex hormones probably stimulate the vomeronasal organ, the other part of the anatomy of the dog that does not exist in primates.

http://www.ucsuggiatevedano.it/l-olfatto

EDIT @ kmm
Their nostrils can move, like the eyes to focus and channel the light energy. Or the highly mobile ears of many predatory animals, including cats and owls, which can rotate, also independently one from the other, not only to improve the perception, but also to identify the direction of the sound.
The principle is the same as the frontal binocular vision, which allows us to calculate the distance.

EDIT II @ terdon
When the dog sniffs, "taste" a smell with a series of inhalations shorter and faster than normal, as we do when we feel a bad smell, breathes quickly several times to understand what smell is that.
Of course we are well-educated people and we do not do this in public. But the gesture is the same. =-]

EDIT III @Petr
"Smell is the ability to detect and discern the odorous emanations from the air. The snuff is the ability to intercept and discern the odorous emanations from the ground. They act with a pattern of regular breathing and is structured in a series of one / three smells accompanied by a series of three / seven snuffs.
The behavior is controlled by the organs of sense of smell nasal septum."
(Section 3.3.3.4.1 and the following)

http://www.fongaros.it/ana2.pdf
http://www.cacciapassione.com/cani-e-cacciatori/1956-olfatto-del-cane-tutta-questione-di-naso.html

The dog is able to absorb the chemicals present in the air, thanks to the characteristics enjoyed by its olfactory cells. To further stimulate their sense of smell to the dog no choice but to expand with some emphasis their nostrils sneaking in a strong "suction" of odors. The air will be retained more or less long and the dog will recognize odors also very weak.

http://www.ucsuggiatevedano.it/l-olfatto
http://en.wikipedia.org/wiki/Olfaction

The nose of the dog is also called truffle, at its end there are the nostrils or the cavity, through which sucks air, and the vibrissae, equipped with sensory hairs. The dog's nose is particularly sensitive, is equipped on the inside of an organ said "of Jacobson", which allows to perceive any kind of substance, able to distinguish between a million of specific molecules, over that of perceiving pheromones, i.e. substances that indicate important information about the physical and mental state of others like it.

http://www.comeaddestrareuncane.com/blog/tag/cani-molecolari/

In the dog, the surface of the olfactory mucosa varies between 70 and 150 cm2 - in this tissue the number of olfactory receptors varies from 250 to 280 million - In 1962, Becker et al. showed that dogs are able to recognize substances in dilutions from 1/100 to 1/10.000.000.
- http://milano.corriere.it/milano/notizie/cronaca/12_febbraio_19/cani-olfatto-parere-esperto-1903358352720.shtml
Have you noticed how a dog sniffs the urine of a female "tasting it"? It is the same action that makes the viper when it follows the track of the mouse: it evertes the tongue and carries on it the odorous particles in the buccal cavity, and this organ has a function in the middle between the olfactory and gustatory ones. "Pointing dogs" is as pointing "the wild" taste the smell.
"Eat the scent", in the jargon, because savored, not only in terms of smell, the smell of the wild. The Jacobson's organ is then a second organ capable of perceiving odors, the first we've said is represented ciliated epithelium of the mucous membrane of the nose.
But there is a third organ called the "Rodolfo-Masera" which also serves to sense the emanations chemical (not yet known which), that way you could explain a specialization of these organs to perceive certain groups of biochemicals than others.
- http://www.laciotola.net/Cani/la-funzione-olfattiva-del-cane.html

Could you explain what you mean by "nostril furniture" and how this helps them determine the direction of the smell (which seems to be the crux of the question)?

What do you mean by "3:00 to 7:00 snorted"?

A thorough answer, thanks. Could you please elaborate how the movement of nostrils helps to improve the perception of smells? In particular, my question is focused on the barely noticeable, shivering-like movement of dogs' nostrils. This can be observed when a dog tries to analyze a faint smell in the air coming from some distance - it stays completely still and only smells and moves its nostrils (as in the second part of the video).

"The odor molecules disintegrate". Huh? Not sure what that was supposed to mean. The molecules are dispersed in the air, are breathed in, and bind to receptors.

Animals smell in stereo. Just the way you need 2 ears to know the direction of sound, you need 2 nostrils to know the direction of odor source. Sniffing around helps in doing exactly that as you sample from different locations; there is inter-nostril concentration difference and inter-nostril timing difference of when the molecules hit the olfactory membrane.
Here are links to well known studies in this area:
Rats smell in stereo
Humans smell in stereo
Dogs smell in stereo


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Identifyication of small delicate shell found on the beach
I found this item on the beach today in north west England. It’s very light weight and delicate, about 3cm long and some interesting patterns on it. Any ideas on what it is would be greatly appreciated

This is almost certainly the shell of a Sea Urchin. These are spiny echinoderms that are found almost world-wide in many different species in the littoral down to ~5000 m (16,404 feet) depth. They have five-fold symmetry, meaning the shell is divided into 5 parts that are more or less symmetrical, like a five-pointed star.
The reasons I say this is so, is that the shell (called a "test") is hollow, it is covered in small protrusions that are the remains of the spines. You can also see some of the smaller spines in the top picture at the edges of the bottom two seams in the shell, and you can see the symmetry in the top picture. You can see a sea-urchin shell with the spines removed, in a bit better state than your one, at the bottom of this page from Arizona State University

I knew it was an echinoderm, but didn't think of a sea urchin, as I've seen a bunch of different ones, but never this. Is it a heart urchin/sea potato (here and here)?  I've never seen those.

@anongoodnurse No idea on the species at all. Chances are it's one of the common ones. Having had a quick look for "heart urchin test" it could well be a heart urchin - it's definitely an asymmetric test, so something along those lines is probably right.

This is a Sea Potato (Echinocardium cordatum).

Welcome to the Biology Stack Niels. Please take a [tour] and visit the [help] for more information on how this particular Stack works. Your answer looks like a good start for an answer as we value answers that provide a bit more than the basics - reasons why you think it is E. cordatum and some references/links to back it up would help.

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How to reduce the viscosity of an extract from a plant seed
I extracted a sample from a plant seed using PBS buffer. The extracted sample is very viscous, even after centrifugation at 15000 rpm for 30 min. The sample is like a thick mucus so that it becomes difficult to do a hemagglutination  assay, and it keeps falling off the pipette tip because of its slimy nature. I can't even estimate the protein content accurately. What can I do to reduce its viscosity?

I cannot speak for plant extracts, but a major cause of viscosity with bacterial cell extracts and some animal tissue extracts is the presence of DNA.  The problem may be alleviated by adding DNAase.  A good example may be found here

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DNA slippage as the cause of insertion mutations in cancer cells?
I'm a computer science student who has started working with DNA. I know the basics but not everything.
While working on the ICGC data, I found a weird pattern in the insertions:
In around 60% of the samples in the following setup, I have the INSertion (the "mutation_allele") already in the "ref_context".
Setup:

I have the "ref_context" which contains the reference of where the mutation occured (around 10 nucleotides to the left and 10 to the right)
I have the "mutation_allele" which is the mutation that occured (the inserted sequence in the case of insertions).

To analyze this problem in an easier manner, I kept only the insertions of at least length 4.
Result:

There are 8325 samples where the reference context contains the INSERTION: 60%
There are 5383 samples where the reference context DOES NOT contain the INSERTION

A snippet:

I understand that there is a concept of DNA slippage, which can occur during enzymic repair of a repetitive sequence without checking how many repeats should be inserted (and perhaps other reasons).
This could be a possible explanation of this.
But in 60% of all samples?
I double-checked if I have an error in the ref_context and that somehow the mutation has been already added to it, but no, the ref_context is correct. I queried the position in UCSC and it is indeed a reference.
Another problem is that I have many very long insertions. Is that normal?
Out of the 5383 , we have 1511 samples where the len(mutation) > len(ref_context): i.e. 10% of the time. Here is a snippet:

Welcome to SE Biology.  Your question is reasonable, so I have gone to the trouble of editing it, but please make a little more effort with English sentence structure, and capitalization of DNA. And it is good if you read to the end of the [Tour] so you get the badge that shows us you have made the effort to find out how our site works.

Thank you David, my vocabulary in Biology is quite limited, making it hard for me to express what I mean. I will go through the tour. Thank you for your edit!

Microsatellite instability (which is present in some cancers) is a process mediated by slippage of the kind that you describe.
I am not sure that I exactly understand what is shown in your table (VCF?) or what ref_context is, but mutations from microsatellites are indeed probably a very large contribution to mutational profiles overall, they are merely less famous and often undersampled due to technical constraints, even in healthy people.
I am not seeing a lot of low complexity sequence just eyeballing your variants and contexts, so it is a little funny. Since you only give images I can't do the normal text stuff I would do to check.
A quick way to check this might be to overlay your mutation table with an annotation track of repetitive regions and see whether the mutations are overrepresented there.
Note that many people use repeat-masked genomes when doing mutation calling because it is notoriously difficult to call mutations in repeats, where it can be difficult to distinguish a mutation from a merely mismapped read. Knowing more about your mapping/variant calling process might enlighten us a bit.

I saved those insertions in a csv excel file, here is a link to it:
https://drive.google.com/file/d/1w3CvcMZ_kR2uXtbdiCiMkLrH6L6dY2bi/view?usp=drive_link

ref_context is just a column in the ICGC data that shows you the neighbors of where the mutation has occured, in the reference genome. The mutation happens in the middle of the ref_context.
I didn't undertand the "quick way to check" you said. Where should I get the annotation track of the repetitive regions from ?

@WassimJaoui thanks for the link, though it looks like I can't access it. a quick way to check would be to just search short snippets of the context/mutation to see whether they are repeated since it's sometimes hard to see that with eyeballs alone. For the annotation track, UCSC has annotations for basically anything that you could imagine. I don't know which genome build you're working against (GRCh38? T2T?) but they have explicit microsatellite and repeatmasker tracks that you can get at. You can then just run some overlaps with bedtools.

Thank you! I will look at that, I'm actually working with an older version: GRCh37 (also known as hg19)
I made the link public now: https://drive.google.com/file/d/1w3CvcMZ_kR2uXtbdiCiMkLrH6L6dY2bi/view?usp=sharing
Sorry for that error! and thank you very much for the help!


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Does hematoxylin interact with histones or with nucleic acids?
As far as I understand, at physiological pH, the phosphate groups in the structure of nucleic acids are deprotonated, therefore, are conjugate bases. The histones they interact with are positively charged. Hematoxylin is a basic dye that stains acidic/basophilic structures, so I would not expect it to interact with the conjugate bases.
My question is: at normal pH, would hematoxylin interact with the protonated histones or the nucleic acids?
I tried looking this up but found contradictory information:

"Hematoxylin, not a dye itself, produces the blue Hematin via an oxidation reaction with nuclear histones causing nuclei to show blue."

"Previous investigators have disagreed about whether hemalum stains DNA or its associated nucleoproteins. [...] Staining experiments with DNA, histone and DNA + histone mixtures support the theory that DNA, not histone, is progressively colored by hemalum."

"Haematoxylin is used to dye cell nuclei. It binds to histones via the mordant."

"Hematoxylin has a deep blue-purple color and stains nucleic acids by a complex, incompletely understood reaction."

I would really appreciate if someone could clarify this for me, I'm a bit confused.

What is the chemical structure of hematoxylin? You are focusing on a single aspect of its chemistry, but that may not be what’s important.


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What mechanisms do animals living in groups (herds, packs, swarms) have against spreading contagious diseases?
While for example a wolf pack provides protection to a sick wolf, increasing its chance of survival, there is a risk of infecting other members of the pack, decreasing their total chance of survival.
Do animals have mechanisms for preventing that? For example the sick member leaving its group temporarily?

Diversity in immune genes within the population could be something.

Three proposed mechanisms:

altruistic self-removal (i.e., diseased individuals leave the group to prevent transmission to kin) has been documented in eusocial insects (ants and bees); Rueppell et al 2010 J. Evol. Biol. say:

altruistic self‐removal by sick social insect workers to prevent disease transmission is expected under most biologically plausible conditions. The combined theoretical and empirical support for altruistic self‐removal suggests that it may be another important kin‐selected behaviour and a potentially widespread mechanism of social immunity.

social distancing/avoidance: This is a commonly used term in human infectious disease epidemiology for the practice of avoiding contact with infected people. I don't know of any great references, but Loehle 1995 Ecology "Social Barriers to Pathogen Transmission in Wild Animal Populations" says:

Data on animal behavior in this regard [social avoidance] are sketchy. Sick individuals in cattle herds do seem to be isolated somewhat from the group (L. R. Rittenhouse, Department of Range Science, Colorado State University, and Ray Strickland, University of Maryland, personal communication 1988), though whether by chance (failing to keep up with the group due to listlessness), by voluntary isolation, or by avoidance on the part of others is not clear. Edwards (1988) found a higher degree of investigatory behaviors but a lower degree of touching between other group members and mice infected with Trichinella spiralis, though this disease is not transmissible by contact. This example would fit the proposed behaviors perfectly. More study is needed.

seasonal migration has been proposed as a way for group-living organisms to temporarily leave their habitat, allowing the built-up parasite burden in the environment to diminish before they return; it may also have a group-level effect of filtering out diseased individuals.

Folstad et al. 1991 Can. J. Zool. Parasite avoidance: the cause of post-calving migrations in Rangifer?

Intensities of warble fly larvae, Hypoderma tarandi (L.), were examined in slaughtered reindeer (Rangifer tarandus tarandus L.) from different summer grazing areas of Finnmark County, northern Norway. To test the hypothesis that larval abundance decreases with increase in post-calving migration distance (i.e., distance from calving grounds), herds with differing migration distances were sampled. The prevalence of infection in the total sample of 1168 animals was 99.9%. The study revealed significant differences in larval abundance among herds from different summer grazing areas. Herds with post-calving migrations have significantly lower larval abundances than herds remaining on or near the calving grounds for the whole summer. Between-herds variation in abundance of H. tarandi larvae is assumed to reflect differing densities of the infective stage (adult flies) on the herds' summer ranges. Larval abundance in a herd is in turn negatively correlated with the distance between the main larval shedding areas (i.e., calving grounds) and the areas of greatest transmission (i.e., summer pastures). These results are discussed in relation to transmission of other parasites common to Rangifer and suggest that this host's post-calving migration may be a behavioural adaptation that reduces levels of parasitic infections.

Loehle 1995 also discusses this (qualitatively/speculatively):

A more subtle effect results from migration. Consider a species that migrates seasonally some large distance. An area that becomes fouled and unsanitary during one season will become largely clean again by the following year. In between, nest and skin parasites such as ticks and fleas will have nothing to eat and will be greatly reduced in number. For example, wide spacing in rabbits results in reduced flea numbers (Mohr 1963) for these same reasons. Excrement piles will decompose between seasons and wash away. Significant benefits could thus accrue to migratory species, even though long distance migratory behavior is not likely to have arisen from this cause alone. (It may result from predator avoidance [Fryxell et al. 1988], or more commonly be due to weather and food supply factors.) Abandonment of rookeries during the non-mating season might, however, be the result of disease avoidance. Another consequence of migratory behavior is the effect on internal parasites ...  Consideration of epidemiology thus leads to some unexpected benefits of migratory behavior.

Hall et al. 2014 J. Anim. Ecol. "Greater migratory propensity in hosts lowers pathogen transmission and impacts" explore a theoretical model of migration effects.

Almberg ES, Mech LD, Smith DW, Sheldon JW, Crabtree RL (2009) A Serological Survey of Infectious Disease in Yellowstone National Park’s Canid Community. PLoS ONE 4(9): e7042. doi:10.1371/journal.pone.0007042

The authors found that the majority of Yellowstone wolves had been exposed to a number of different viruses (evidence from antibodies in blood samples).
They also found evidence for historical outbreaks of canine distemper virus in wolves, coyotes and red foxes in 1999 and 2005. These outbreaks correlated with peaks in wolf pup mortality.
This evidence suggests that wolves have no mechanisms for avoiding the spread of these viral diseases. Perhaps periodic episodes of increased mortality are the price that has to be paid for a longer-term 'herd immunity'?
Edit - in response to OP comment below:
The data indicate very high levels of seropositivity to the viruses. I would say that 'not 100% successful' is an understatement. But I must admit that I am way out of my area of expertise here!
From the abstract:

We found high, constant exposure to canine parvovirus (wolf seroprevalence: 100%; coyote: 94%), canine adenovirus-1 (wolf pups [0.5-0.9 yr]: 91%, adults [>or=1 yr]: 96%; coyote juveniles [0.5-1.5 yrs]: 18%, adults [>or=1.6 yrs]: 83%), and canine herpesvirus (wolf: 87%; coyote juveniles: 23%, young adults [1.6-4.9 yrs]: 51%, old adults [>or=5 yrs]: 87%) suggesting that these pathogens were enzootic within YNP wolves and coyotes.

That's very interesting. But I think the conclusion is not completely correct. I'd rather conclude that "based on the evidence, if wolves have mechanisms for avoiding the spread of those diseases, they're not 100% successful." It could be that they have such mechanisms, and without them, the mortality would be even higher. The last sentence is an intriguing point. Perhaps from evolutionary perspective it's better to let the whole pack/herd become infected and if it survives, all the survivors will be immune.

(This answer is still a work in progress, but I'll work more on it eventually...)
It's not terribly controversial to say that infected hosts may be more likely to be eaten by predators. However, at least one author (Smith Trail et al 1980; full reference below) has suggested that this could be adaptive; in some sitautions there could be a net gain to inclusive fitness if, by 'submitting to' predation, infected hosts are able to reduce the force of infection acting upon close relatives.
(Full reference: Smith Trail DR. 1980 Behavioral interactions between parasites and hosts: host suicide and the evolution of complex life cycles. American Naturalist 116, 77-91)

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What was the first animal having fur?
Did all early mammals have fur? Is it possible to trace the origins, how early animals with fur looked like and how it evolved?

https://en.wikipedia.org/wiki/Evolution_of_mammals#Hair_and_fur

@Thaina That's what I was looking for, thank you.

Czech version: http://www.memento.junweb.cz/clanky/spzo20.htm

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Can a bumblebee hive be positioned high above the ground?
We'd like to set up a hive for bumblebees and I wonder if it can be positioned high above the ground, for example on a balcony.
As bumblebees usually nest in holes in the ground, I'm somewhat concerned if they'd find the hive comfortable and be able to navigate back to it.

Depends on the species. Some bumblebee species makes nests in bird boxes high above ground.


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How did butterflies evolve to have eyes on their wings?
Some butterflies, such as the UK native Peacock butterfly (Google Image Search) have markings on their wings that look just like eyes, complete with a white fleck to imitate a convex, transparency effect, as though the "eye" is reflecting sunlight.
Presumably, this pattern is designed to deter prospective predators, because the predator will see a creature with massive eyes looking at them and think twice before attacking.
But how did the pattern evolve?  Was the first one a fluke / a genetic mutation that happened to work, or is there another explanation?
For possible bonus points, is there any way of telling when this occurred, and therefore making a guess as to which creature's eye is being imitated?

All evolution is due to random changes which are selected for. Change is random, selection is not.

Kahn Academy does an amazing job at this one: Introduction to Evolution and Natural Selection

@Armatus love Kahn Academy

There has been quite a bit of study on the development of eyespots. How did they evolve is still unclear, but several experiments have elucidated the molecular mechanisms underlying their formation.
The Wikipedia page about eyespots gives a good basic introduction and some interesting references.
So, first of all, how does an eyespot form?
During the development of wings, eyespots arise at specific locations called foci (singular focus).
If you take cells from a focus in a developing wing, and transplant them into another region of the wing, an eyespot will develop at the transplanted site.

Adapted from: Pattern Formation on Lepidopteran Wings: Determination of an Eyespot - Nijhout, Dev. Biol, 1980
The photo on the left is a normal wing from an adult Buckeye butterfly, Precis coenia. In the middle and right photos, some cells of the big eyespots have been transplanted in a new position during development. As you can see, a third eyespot develops. Note that the middle photo is from an autograph, that is, the cells were transplanted on the same wing. This results in a shrinkage of the normal eyespot. In the right picture, instead, cells were transplanted in another individual, and this does not result in shrinkage of the eyespot.
The authors conclude that:

It is evident from these experiments that the development of the large eyespot on the forewing of Precis coenia depends on the presence of a small group of cells that lie at or near its center. This group of cells corresponds to a "focus": a small region, occurring in each wing cell, that is postulated
  to be responsible for the induction of most color pattern elements in butterflies and moths (Nijhout, 1978). Cautery experiments establish an upper limit for the size of this focus in the neighborhood of 300 epidermal cells, though it is probable that the actual size of the focus is much smaller.

They further speculate that a specific morphogen may be involved:

The response of the eyespot pattern to cautery or transplantation of the focus is most readily interpreted if we assume that the focus is the source of a morphogen that is somehow able to induce synthesis of specific pigments.

The idea that a morphogen was involved has been confirmed in later years.
From: Development, plasticity and evolution of butterfly eyespot patterns - Brakefield et al., Nature, 1996

The focus is proposed to be a signalling source for a morphogen, the levels of which determine the pigmentation of surrounding cells. Recent investigations have indicated that regulatory genes, such as the Distalless homeobox gene, are specifically espressed in the eyespot focus.

During the development of the wing the expression of the Distalless (Dll) protein (shown in green in the picture) corresponds to the location of the future eyespots.
Several mutations exist that will provoke changes in the eyespots patterns. Some of this with the evoking names of Cyclops, Spotty and Bigeye were analysed in the paper.
Now, without going much into insects genetics (which is far from being my domain of interest), you can clearly see that, although the number, position and size of the foci are affected by the mutations, their position always correspond with an increased expression of Dll during development.

Left column: ventral hindwing patterns of a wild type (top), Cyclops (middle) and Bigeye mutants. Right column: forewing pattern in a wild type (top) and Cyclops mutant (bottom).
From the conclusion of the paper (bold mine):

The selection experiments on B. anynana rapidly produced dramatic differences in eyespot size which were due to genes of small phenotypic effect. The mutants described here show that genes also exist with large phenotypic effect on eyespot development (including size) that have no perceptible effect on other wing or body patterns. It is likely that the evolution of eyespot patterns in nature involves both genes with large and small effects on eyespots development. [...]
  These observations suggest that the regulation of the eyespot developmental pathway is such that eyespot patterns can evolve rapidly and independently of other wing-pattern elements and body structures.

Finally, another interesting read is:
Wings, Horns, and Butterfly Eyespots: How Do Complex Traits Evolve? - Monteiro and Podlaha - PLoS Biol., 2009
where the authors propose that:

Complex traits require co-ordinated expression of many transcription factors and signaling pathways to guide their development. Creating a developmental program de novo would involve linking many genes one-by-one, requiring each mutation to drift into fixation, or to confer some selective advantage at every intermediate step in order to spread in the population. While this lengthy process is not completely unlikely, it could be circumvented with fewer steps by recruiting a top regulator of an already existing gene network, i.e., by means of gene network co-option. Subsequent modifications of the co-opted network could further optimize its role in the new developmental context.

Please note: I am not an insect development expert, so I may have missed some important paper/evidence etc. If you know some more that are worth citing please do!

You're correct with the genetic mutation bit. A basic explanation would be:
Some gene or genes became mutated that lead to the coloration you see, and the end result was that the butterfly or butterflies with the mutated gene were able to produce more offspring or offspring which survived better than the eyeless versions.
There are ways of dating genetic mutations by comparing one organism's genes to another, but accuracy can be an issue without some significant genomic study to confirm mutation rates and other aspects.
However, the butterfly wouldn't be purposefully imitating another creature's eye. It may be by chance and/or predator behaviors that the eyespots look like the eyes of another creature, but the adaptation wasn't a willful act. It was a random genetic mutation or mutations that lead to beneficial coloring, and the eyespots may have improved over time as more mutations occurred.

Is it possible that the butterfly could have been wilfully imitating another creature's eye, but that the conscious part was genetically mutated out later on?

Possible? I suppose it's possible.
However, the likelihood is zero. The chain of mutations and lack of evidence of similar behavior by other butterflies is a Sysiphisian mountain to overcome to prove it happened.
The easiest explanation, and the one observed in nature, is that a mutation causes unique coloration. Over time, the butterflies which have the coloration closely resembling eyes are left alone, while those that aren't get eaten - instantly taking them out of the gene pool and leaving only the ones with eyespots.
Much, much, much easier.

Good old Occam and his Razor.

I read above ;
''Some gene or genes became mutated that lead to the coloration you see, and the end result was that the butterfly or butterflies with the mutated gene were able to produce more offspring or offspring which survived better than the eyeless versions.''
But, for the genes to mutate randomly, an eye would not form, but a mess.
Further,  how strange it is, that neither the butteryfly nor the genes are able to see this manifestation. Yet any preditors, from above sees it clearly.
To apply that this random mutation and natural selection, makes up everything that we know, is in itself blind and calls for an eye.
I will state, it is positive variation and nothing more nothing less.
No lifeform goes downhill in terms of evolution. Random anything would render any 'random' lifeform , lifeless.

An eye doesn't need to form with the first mutation. If any marking gives an advantage over non-marked butterflies, that would be sufficient. Then natural selection would refine the mutations to an eye-shape. Evolution acts over multiple generations, always. The butterflies don't have to see what gives them the advantage - as long as an advantage is given, that's enough. I have no idea what you mean by "positive variation," and there's no such thing as "downhill" in terms of evolutionary biology - only better able to survive or less able to survive. Your last sentence is also meaningless.

But, for the genes to mutate randomly, an eye would not form, but a mess: do you have proof of that? An eyespot is a fairly simple round pattern, is not such a complex thing to encode.

You just delivered some pretty opinionated statements. What knowledge/science/evidence are you basing them on? Could you please provide references?

@MCM - you said 'If any marking gives an advantage over non-marked butterflies, that would be sufficient. Then natural selection would refine the mutations to an eye-shape'. I am sorry, but here you are inferring 'direction' via natural selection. Please, explain how nature performs this selection. The mechanics behind it please?

@Nico . An eyespot is geometric, geometric is nothing to do with random. That it should resemble an eye, is enough to suggest it is intended to be a 'fake' eye. Please afford me some evindence, of your mathematical formula, which acts on random operations, to form geometric patterns?

@Lubo I am basing them on mathematics. No mathematical formula exists which can operate on random numbers, to form complex organic geometric patterning. Please, can you prove i am wrong?

@user1310: I never mentioned any mathematical formula... you are the one who should provide references for your assertion that a pattern cannot arise from a random mutation. Anyway I will be writing a bit more detailed answer (should probably have time tonight), but essentially eyespots form because of gradients of homeogenes, there is quite a bit of literature at this regard.

@user1310: Directionality can occur in evolution, it's just not willfull direction. Say the first mutation creates an amorphous dark blob which survives better than the previous phenotype. Then another mutation occurs where the dark blob gets more circular, and that phenotype survives better than the amorphous. Continue in that vein until you have the current eyespot phenotype. As soon as the eyespot is no longer advantagous, another mutation could enter the population and produce another phenotype.

@user1310, again you make a statement without proof, and you happen to be spectacularly wrong. Fractals generate the exact type of patterns that you are referring to, and I refer you to the Wikipedia entry: Fractals. BTW, this is Q/A site, not a debate site, so if you have some knowledge to share, please provide the source of your assertions - a publication, well-known theorem, whatever.


text:
How many human cells are there in our body, on average?
How many human cells are there in our body, on average?
Wikipedia says 1013:

Bacterial cells are much smaller than human cells, and there are at least ten times as many bacteria as human cells in the body (approximately 1014 versus 1013).

The Nobel site says 1014:

An adult human being has approximately 100 000 billion cells, all originating from a single cell, the fertilized egg cell.

The Physics fact book insists it's 1013:

(length of 1 bp)(number of bp per cell)(number of cells in the body)
  (0.34 × 10-9 m)(6 × 109)(1013)

Finally, Wolfram Alpha gives 1.0 × 1014 as fact:

Estimated number of eukaryotic (human) cells in the human body: 1.0×1014

I am quite confused: who is right here?

Well, the Nobel quote is wrong whichever way you turn it (for the reason outlined in the Wikipedia quote). But I wouldn’t be surprised that, even taking the average, there’s an uncertainty of a factor 10 about the correct number. Because all the factors used to determine the number are crude estimates indeed.

@Skivvz  Another interesting number is that of neurons in the human cerebral cortex: 16 billion, 8 billion pairs.  Fascinating isn't it.    Also, it is worth noting that one commonly cited number for cells in the human body, around 37 trillion is approximately 2^45; which means that if one cell divided to its Hayflick limit of 45, for argument's sake, then in order to maintain adult equilibrium, an equivalent number would need to die in a comparable period, of 6 or 7 weeks on average (for a cell type mitosing daily for instance).  ''Numbers'',  Isn't that an old Book or something?

Bianconi et al. 2013 give an estimated lower bound of 3.72 × 10^13 (which, by the way, is approximately the geometric mean of 10^13 and 10^14).
However, from the table in their Supplemental Information (where estimates for about fifty different types of cells are added up), it is clear that the vast majority of these are the erythrocytes, also known as red blood cells: estimated at 2.63 × 10^13. While the second largest class are the glial cells (from the nervous system), estimated at 0.30 × 10^13. Three other classes (endothelial cells {vessels}, dermal fibroblasts {skin}, and platelets {blood}) add up to another 0.58 × 10^13. These, in total, is about 3.5 × 10^13, and we can stop there, because the uncertainty in all these estimates swamps all the other cell type populations, which are much smaller.
This means that if we only consider the 5 most abundant cell types in the body, we already get a very good estimate. Is it likely that we have missed a cell type of which there are a trillion cells in the body? It's not impossible, but unlikely, because it would be hard to miss all these cells.
Maybe there is a long tail (i.e. a large number of minor cell types, each with a small, but significant population) that wasn't considered? Together, these could add up to a significant adjustment to the above figure. I don't know.
This estimate is for a typical human person: 30 year old young adult, 70 kg, 1.72 m tall and with a surface area of 1.85 m^2. For this person, the figure is given with roughly a +-20% uncertainty.
Given all the above, it's probably safe to say "30 to 50 trillion".
(This obviously doesn't take into account any of the bacteria mentioned above.)

That paper is behind a pay wall. Can you reproduce the contents of that table here? The data itself isn't copyright-able.

I was able to find a copy of the paper at http://nanoimmondizia.ge.ibf.cnr.it/UserFiles/documenti/Bianconi_AHB_2013.pdf

In Mike Lynch's "The Origins of Genome Architecture", he claims 10^13.  I forget the primary source he cited, and since the book is in my office I can't check it now.
** Found the snippet that contained the reference.  I think it's really worth including in its entirety.

A crude estimate of the amount of DNA within currently living
  organisms can be made by noting that the length spanned by one base of
  DNA is ~0.3x10^-12 km (Cook 2001).
The number of viral particles in the open oceans is ~10^30 (Suttle
  2005).  Assuming that there are twice as many viruses on land and in
  fresh water does not change the global estimate very much at the
  order-of-magnitude level.  Thus, assuming an average viral genome size
  of 10^4 bp, the total length of viral DNA if all chromosomes were
  linearized and placed end to end is ~10^22 km.
The estimated global number of prokaryotic cells is ~10^30 (Whitman et
  al. 1998), and assuming an average prokaryotic genome size of 3x10^6
  bp yields an estimated total DNA length of 10^24 km.
With a total population size of 6x10^9 individuals, 10^13 cells per
  individual (Baserga 1985), and a diploid genome size of 6x10^9 bp, the
  amount of DNA occupied by the human population is ~10^20 km.  Assuming
  there are ~10^7 species of eukaryotes on Earth (~6 times the number
  that have actually been identified), that the average eukaryotic
  genome size is ~1% of humans, and that all species occupy
  approximately the same amount of total biomass, total eukaryotic DNA
  is ~10^5 times that for humans, or ~10^25 km.
Given the very approximate nature of these calculations, any one of
  these estimates could be off by one or two orders of magnitude, but it
  is difficult to escape the conclusion that the total amount of DNA in
  living organisms is on the order of 10^25 km, which is equivalent to a
  distance of 10^12 light years, or 10 times the diameter of the known
  universe.


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Is there any study to find the plant with the absolute minimum light need?
Is there any study to find plants with absolute minimum light need?
Consider a bathroom without windows that you have occasional artificial light (e.g. white LED light).
Another question is there any numeric system assigning a number to each plant representing its minimum and maximum light tolerance?

That's not so difficult, if you look on the north side of densely forested mountains. ferns come to mind.

Some deep sea plants get very little light.

Not all plants even do photosynthesis.  Consider saprophytes, which live on dead plant or animal tissue.  Or an even stranger example, the mycotrophic plants like the snow plant (Sarcodes sanguinea) that is a parasite on a fungus (which in turn seems to be a parasite of conifers): https://botany.org/Parasitic_Plants https://www.fs.fed.us/wildflowers/beauty/mycotrophic/whatarethey.shtml/Sarcodes_sanguinea.php

@jamesqf thanks for your note. can any of them be kept as an in-door plant?

@PHPst: I don't know, though I doubt it, since they need the fungus that parasitizes/commensalizes with conifers.  In the case of the snow plant (the one I'm most familiar with, since it's fairly common hereabouts), the flowering stalks only appear for a couple of months in the spring, right after the snow melts.  The rest of the year there's nothing obvious above the surface.

@com.prehensible I doubt any mountain can be as dark as a room without any windows.

there are parasitic plants that need zero light, so you may need to clarify.

ZZ plants are the most dark tolerant that you can get, if you get 2 you can always swap them out every 6 months if you want. Other than that, a grow light of some kind is advised.

Gardening forum knows more about low light plants, the question exists there as a duplicate. check this bathroom: https://youtu.be/hC3wNrDYzzE?t=385

@John I reckon the host of parasitic plants needs light, so they indirectly need light

@PHPst well yes but by a definition that loose nearly all life on earth requires light. the term you are looking for botanically then is "shade tolerance".this study may help you search. https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/shade-tolerance


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How are new staining protocols designed for microscopy?
How are new staining protocols designed for microscopy? Is it manual work or does it rely on computer simulations?
Say for example I thought the H&E staining does not bring enough contrast. How would I go about producing The Superb H&E Staining Protocol (not necessarily using just hemalum and eosin Y)?
Looking this from a mathematical point of view, the staining is some operator O applied on image I to produce enhanced image E. While clearly the operator O depends on the particular type of specimen, what I want to see, etc., there are surely some general principles guiding the search for finding an appropriate operator O? What are they?
Since the question is on hold, maybe I can try to put it even more clearly. How was the H&E staining invented? What was the process for its invention? I don't see why it would be unclear what I am asking. Dear biologists please take a more interdisciplinary approach.. If the question really is not answerable as such, please explain why. There's probably an answer in that.

About what new staining protocols are you thinking? And what kind of simulations do you think of?

Added example to the question.

Put on hold now after I added the requested example? Duh.

At least I still don't understand where you want to go.

The reason why could be an answer. Clearly I have little knowledge on the topic.

I mean, H&E staining was developed for a reason. That reason I believe is contrast (indirectly resolution). Surely there are means to make things even better? If you need to stain your specimen, and there is no known way how to do it well, what will you try to do then?

The question is what you want to stain and how. A newer method would be fluorescence micropscopy with specific antibodies coupled to fluorescence dyes. You can also couple the dyes to proteins which bind to cell surfaces.

Ok. I was trying to view this from a generic point of view. For example, if I google "a new staining *" I may find multiple scientific papers, mostly behind paywalls unfortunately. I understand that the protocol varies case-by-case (depending on what I want to do), but probably there are some general principles? For example, if you want to solve an optimization problem in mathematics, you need to model the problem, but need not to reinvent how to minimize a function. Similarly, I am trying to understand the general background for particular staining protocols.

As far as i understand staining, you have to primarily know what it is that you want to observe since most of the time, the sample of interest can not be seen unaided. Once you determined, what the nature of the sample is i.e. protein, or lipid or a specific structure, then you think of molecules/dyes that are known to interact/bind to it, preferably in a specific manner, providing a good contrast against the background. For example for staining DNA, you use DAPI. So its highly dependent on the nature of the molecule/structure you want to observe!

Are you particularly interested in HE stain?

This answer addresses the question of how stains were developed historically, which may bring into perspective your overly modern assumptions.
Most of these older (but stil very usefull!) staining techniques, such as haematoxylin (or rather haematein), cochenial/carmine etc. were inspired by the work of textile dyers of that era, starting somewhere in the middle of the 19th century.
It was more a question of trial and error, coïncidence and luck, rather than it being a case of systematic, structured research, starting from the well known molecular structure of the dye and the sample to be stained... Most of the time those were still -at least partial- mysteries.
You should keep in mind, that many of the protocols still in use, were developed in an era when the dye industry as well was still in its infancy, so to speak. Standardization of dyes, Biological Stain Commission and all that, came later. Biologists, histologists etc. used what worked for them. At that time, at that place, with that lot of dry dye powder. Much inspiration, the right idea at the right time and a fair amount of luck. Up to well into the 20th century.
As an illustration: in 1917-1918 there was a shortage on haematoxylin in the German histopathological labs, due to the allied blockade. A lab worker, Fraulein Wilhelmina Schmidt, inspired by the impossibillity to remove elderberry stains from her hands, wondered if it would be possible to use elderbery juice as a substitute for haematoxylin. As there wasn't really an alternative, it was tried. Elderbery juice was concentrated by boiling, diluted with an alum solution and tried. It turned out to work very well.
The story went unnoticed until 1949, when an article on it was published in the German “Zeitschrift für die Wissenshaftliche Mikroskopie”. In the article, the author, Grüber, pointed out that, even after more than 20 years of storage, the slides were still vividly stained, not showing any trace of fading.

I think this is a useful answer, but I have edited the first sentence as it seems to me that site policy does not allow answers that explicitly claim not to be answers.

I have noticed that indigo dye doesn't seem to dissolve in anything. Wonder if that would make a usable stain, or if it would totally stain everything blue. But the natural precursor to indigo is a glycoslyated molecule, similar to X-gal, maybe the precursor could be used in a manner similar to beta-galactosidase staining.

Do you mean indigo carmine, CI 73015 (synthetic)/ CI 75781 (natural)?


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What makes certain obligate anaerobes viable in fermentation starter cultures?
If Propionibacterium are obligate anaerobes (to wit, poisoned by oxygen), what makes 'Dairy' or classical propionibacteria (e.g. P. shermanii, P. jensenii, P. acidicpropionici, et al) viable in Fermentation starter cultures?

Do you have a reference for the fact that they are obligate anaerobes?

they are not obligate anaerobes..

@AlanBoyd Obligate anaerobe on wikipedia

@WYSIWYG What are they?

@WYSIWYG Here's a quote from this source: "Their [Propionibacteria] exact atmospheric requirements remain a matter of controversy, and they are often described as obligate anaerobes."

http://mic.sgmjournals.org/content/127/1/121.full.pdf

link to a paper in which P. shermanii is grown in flask culture. Although the conditions are clearly designed to achieve low oxygen concentrations in the culture, they also indicate that oxygen is not toxic for this organism. This is from the WP page you linked to: "Obligate anaerobes are microorganisms that are killed by normal atmospheric concentrations of oxygen (21% O2). Oxygen tolerance varies between species, some capable of surviving in up to 8% oxygen, others losing viability unless the oxygen concentration is less than 0.5%."

Here (mic.sgmjournals.org/content/127/1/121.full.pdf) is a link to a paper in which P. shermanii is grown in flask culture. Although the conditions are clearly designed to achieve low oxygen concentrations in the culture (the flask is almost full and is only shaken occasionally), they also indicate that oxygen is not toxic for this organism.
Also, this is from the WP page you linked to:

Obligate anaerobes are microorganisms that are killed by normal atmospheric concentrations of oxygen (21% O2). Oxygen tolerance varies between species, some capable of surviving in up to 8% oxygen, others losing viability unless the oxygen concentration is less than 0.5%.


text:
Which Lactobacillales (Lactic acid bacteria — LAB) strains are capable of degrading starch?
I've been researching bacteria strains but am having trouble finding amylolytic LAB strains with amylolytic and lactic acid producing character. The only species I've found, that are capable of amylolysis (correct me if I'm wrong) are Lactobacillus amylovorus, Lactobacillus manihotivorans, Lactobacillus plantarum.
If any, what other LAB strains provide amylolysis? Also, can anyone verify if the above strains also meet the criteria?
Edit
The keyword here is strains. Many species can degrade starch but most strains cannot.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3458588/ L. acidophilus can be another species on the list.

http://www.genome.jp/kegg-bin/show_pathway?lrl00500 Lactobacillus rhamnosus

http://www.tandfonline.com/doi/abs/10.5504/BBEQ.2011.0124 it is not that hard to find articles in the topic. there are many species with this ability

@inf3rno That's only partly true. e.g. Propionibacterium freudenreichii subsp. shermanii CIRM-BIAlT is able to metabolize lactose, although this trait is strain-dependent, since the Lac genes may have been acquired through a horizontal transfer event mediated by phage infection. Many strains can degrade starch but few species cannot.


text:
Why does wood become darker when it ages?
I have lots of pieces of pine furniture which have different colours depending on how old they are. So, I just wondered why that is. I guess it has something to do with structures and chemical compounds that were already in the wood when it was still alive, so I hope this is not off-topic here.
What processes take place in dead wood when it ages?
What determines the colour it will have? For example, pine and spruce wood looks very similar when freshly cut, but will develop very distinct colours afterwards.
Is there also wood that does not become darker?
Is it something to do with the processing of wood, or will that happen to any stick you leave lying around in your room (so it doesn't rot)?

Not sure- but maybe because of accumulation of resins and other secondary metabolites.

While most wood we see comes from stain or oils, wood left on its own will darken.  As far as this article suggests, this is caused by the polymerization of polyphenols from lignin into tannins which are dark red or brown in color when they are highly polymerized.
The specific content of the lignin in different woods will affect the density, strength and color of the wood.
This woodworking reference shows that intense UV exposure to wood will darken it to give it an aged look.


text:
How frequent are selective sweeps?
Introduction
Selective sweep is the most famous genetic signature of selection. We know of a number of classical examples of selective sweeps, some of them in humans. See the classical example of the sweep on a sequence relgulating the lactase gene in the post Are humans the only species who drink milk as adults?.
Question
I do not have a good intuition about how common such sweeps are. Are there constantly 5 to 10 sweeps happening in a species genome or is there a sweep every 1000 generations only?
How frequent are selective sweeps?
Clarification
Of course, the answer will vary (and will probably vary greatly) among species. I would welcome empirical estimates and/or theoretical expectations coming from any species (I would prefer an estimate coming from a eukaryote species though).

Check out these papers: one / two / three

I know this question is a bit old, but I read a paper recently which (claimed) to answer this question.
I think the answer to this question is suprisingly controversial. I don't really have a formed opinion yet of which answer is correct, but I will try to discuss the different viewpoints here.
Argument 1: Sweeps are rare
On one hand, we have the people who are sceptical of how common sweeps are. This, in my understanding is most researchers. Many people believe that polygenic is the predominant form of selection in humans.
There is the paper by Hernandez et al (2011), who find scant evidence of selective sweeps in recent human history. Essentially, they looked at the reduction in diversity (something which is associated with sweeps) around amino acid substitutions and synonymous substitutions and found that the two were statistically the same. They say it's probably more likely that this is caused by strong purifying selection at linked sites rather than sweeps.
Szpak et al (2019) suggested that most of the time, the criteria for designating something a sweep in human populations was probably too lax, and many of the previouly claimed sweeps were probably artefacts of some kind. In fact, they only find compelling evidence for 2 sweeps in recent human history.
Argument 2: Sweeps are more common
Alternatively, there are some studies which have apparently discovered a relative abundance of sweeps in human history. Some might make the argument that sweeps are likely to be common, since humans have a relatively small effective population size (~20,000) and low mutation rate.
Souilmi et al (2020) claimed to have discovered 57 (fpr<10%) sweeps using genomes from ancient Eurasian individuals. 35 of these 57 were inferred to have occured before 35kya. The reason they claim to have found many more sweeps than previous studies is because they used ancient DNA. It is well established (Hellenthal et al 2014) that admixture is virtually ubiquitous within modern and ancient human populations. Admixture likely obscures the signal of sweeps by introducing non-selected haplotypes from the admixing population, making hard sweeps look like soft sweeps, or perhaps not even sweeps at all. They confirm this using simulations and show the power to detect sweeps is massively reduced when you are looking at admixed populations.
However, their method uses ancient DNA, which is highly prone to various artefacts, which they didn't appropriately test with simulations. It also hasn't been peer reviewed, so there may well be other potential issues.
References
Hernandez et al 2011
Szpak et al 2019
Hellenthal et al 2015
Souilmi et al 2020

Good job! You might want to add Booker et al. (2019) who make back-of-the-enveloppe calculations and estimate that over its whole genome and at any time "D. melanogaster has approximately [..] 80 incomplete sweeps of alleles that will ultimately reach near fixation."


text:
Why do flies fly in circles?
Lying on my bed, doing nothing I recently noticed flies usually fly in small circles, right under my ceiling lamp. Worth noting - the lamp was off as it was middle of a day. And those flies kept flying like this for hours, not moving anywhere else! Later I noticed it repeated every day, pretty much the same pattern. Why is that?

Flies use any object they can find as a landmark.

The flies patrol well-defined airspaces underneath landmarks like lampshades. ... Male flies approach a landmark from below and, in the absence of other flies, settle to patrol an airspace close to the landmark. A second male approaching the same landmark chases, or is chased away by, the patrolling fly when it comes too close and may eventually settle to patrol 10–30 cm below the airspace occupied by the first fly. ... The position of male patrolling stations relative to the landmark suggests that females might arrive at landmarks from the side (and not from below, as males do), thus crossing the dorsal visual field of patrolling males.

Source: Jochen Zeil. The territorial flight of male houseflies (Fannia canicularis L.) Behavioral Ecology and Sociobiology. August 1986, Volume 19, Issue 3, pp 213-219


text:
Is the sense for salt depending on the electrolyte level in our body?
I often noticed, after (heavy) physical activity like cycling, running, swimming or working an isotonic drink (to recover the electrolyte level) tastes less "salty" compared to when drinking it before the activity.
Is this possible or am I just hallucinating?
The object of this (if it's real) could be:

to save us of taking too much salt
to reduce the reluctance against salt if our body is undersupplied (with sodium ions)

My guess is, that the electrolyte or particularly the sodium (chloride) level in our body influences the cells/nerves that sense the taste for salt on our tongue.
Wikipedia says this:

Salts, sweet, sour and umami tastes causes depolarization of the taste cells, although different mechanisms are applied.

So, I imagine it like this:

If there is enough salt in our body, the cells are saturated with e.g. sodium ions (higher polarization since there are more ions)
NaCl and other salts (probably KCl too) will then dissociate into Na+ and Cl- (etc.)
The Cl- will then attract more Na+ from the cells causing deplolarization
Our brain converts these signals into the proper perception

But maybe I'm just hallucinating... :)

Is this possible or am I just hallucinating?

Certainly possible, but I'd peg the mechanism closer to Sensitization or De-sensitization of the neurons involved so that when you finally ingest some salt the sensation is different. The sodium and chloride levels of the ingested material wouldn't have a direct effect on the level of De-/Sensitization, but rather how low your stores are or how long you've gone without.

So, I imagine it like this....

What you broadly described is how regular sodium receptors work. They will work that way regardless of what you've been doing, and doesn't really explain an increase or decrease in your ability to taste salt - the signals will fire either way.
Check out the action of the Capsaicin receptor and how it changes sensitivity over short periods of time. I'm betting the phenomenon you're describing will be closer to this (an increase or decrease in the number of sodium receptors in response to the abundance of salts or lack-thereof) than an immediate mechanism from the drink itself.

Who else than MCM from Salt Lake City can answer this? :D -- So it's more the fact that consuming the salty electrolytes desensitizates the receptors, so they are less sensitive when consuming the electrolytes one or two hours later? Would you also say this is not directly related to the thesis of my first two bullet points (that we want to take salt if undersupplied and to avoid it if oversupplied)? From animals I know that they're searching for soil/plants that provide salt. So there must be some urge to get it (this is another question, actually).

@try-catch-finally - ;-) The desensitization is one potential reason. Subjective occurrences are pretty difficult to pin down. It could be short term desensitization, or your brain could simply be paying more attention to other ingredients (water) after such a long workout. If it's within a few hours then it's probably an attention modification - de/sensitization can work on that short a time scale, but not usually. I would say that the phenomenon is not related to your thesis. I'll add another comment.

@try-catch-finally - Regular "taste" is depolarization. For sodium that simply involves the influx of the ions over the cell membrane of the taste buds, and that will cause a depolarization without other mechanisms. That happens when you eat something with Sodium, regardless of what you taste. Taste is left up to interpretation in the brain, and the brain is great at ignoring stuff that doesn't really matter. If the drink tastes less salty, it wouldn't be the mechanism occurring - but it would be the mechanism occurring less often, or just as often but less noticed.


text:
Confusion about read counts distribution in RNA-seq
While reading old DESeq paper (Anders and Huber 2010) I came across following line.

If reads were independently sampled from a population with given,
  fixed fractions of genes, the read counts would follow a multinomial
  distribution, which can be approximated by the Poisson distribution.

I am unable to grasp this line. Why would read counts follow multinomial distribution? My guess would have been Gaussian distribution. Can anyone explain this?

Textbook example of multinomial distribution is multiple dice toss. The fair dice has following probabilities:
side 1: 16,66666666%
side 2: 16,66666666%
side 3: 16,66666666%
side 4: 16,66666666%
side 5: 16,66666666%
side 6: 16,66666666%

Lets roll a typical fair dice n = 20 times:
6 5 1 1 3 5 4 3 1 2 4 4 6 6 2 2 5 6 5 2

So this particular outcome of above multinomial variable is:
side 1: 3 rolls
side 2: 4 rolls
side 3: 2 rolls
side 4: 3 rolls
side 5: 4 rolls
side 6: 4 rolls

Multinomial distribution is not restricted to fair dice - the probabilities can be rigged. It also is not restricted to 6 sides - there can be any number of categories. Another textbook example of multinomial distribution is puling colored balls from wery (infinitely) large bag. Probabilities correspond to proportions of colored balls in the bag:
Blue: 53.283%
Green: 19.956%
Orange: 8.336%
Purple: 5.213%
Red: 4.374%
Silver: 3.920%
White: 2.751%
Yellow: 2.167%

Lets simulate n = 200 balls pulled from such a bag in R:
sample(c("B","G","O","P","R","S","W","Y"), replace = T, size = 200, prob = c(0.53283,0.19956,0.08336,0.05213,0.04374,0.03920,0.02751,0.02167))
B S O B B G G P B O B B P G B B G G G G B P G B B P B G B G B S W B B O O G B B O G G B S B O G B B B B B O O O B O B B B B B B O O G B B Y B R G B B B G P W Y G B P W B S R B W G Y B W B G O G B R B B G B B B B B B P R G P B B B G Y G S B B B G P B B B B B G B O G P B G B G P B B G B R B P R B G W B B B B O P G B B B B B B B B G B G G R W B B G G B G O B B B B B G B B B P B B B O R G B B B O B G

So this particular outcome multinomial variable is:
Blue: 102 balls
Green: 42 balls
Orange: 18 balls
Purple: 14 balls
Red: 8 balls
Silver: 5 balls
White: 7 balls
Yellow: 4 balls

In RNA-seq we are "pulling" reads (balls) out of a large set of suitable cDNA molecules fragments in a sample (bag). Each read belongs to a gene (color). We assume fixed fractions of genes in a sample:
gene 1: 0.05217%
gene 2: 0.00319%
gene 3: 0.00073%
...

But what we get from RNA-seq (n = milions of reads) are integer counts of reads:
gene 1: 492 reads
gene 2: 44 reads
gene 3: 5 reads
...

To comment on your idea of using Gausian distribution: Gausian distribution is continuous so using it we would assume we can get fractions of reads per gene which is not the case.

Much clear explanation :) I got confused with multinomial and multimodal :P

Good answer. I would like to add that for large samples binomial distribution can be approximated as Gaussian.


text:
Does a pregnant female body treat the fetus based on gender?
I have seen on a youtube video that the female body produces antigenes and antibodies when she is pregnant with a boy. But this behaviour is not produced when she is pregnant with a girl. These means that the more antigenes she produces, the more femminin the next child will be. More antigenes are produced when she is pregnant with a boy.

Is this correct? if yes, then why does the female body produce antibodies and antigenes when the fetus is a boy and not a girl?
What other pregnancy actions or behaviours are gender based?

Can you link your source? Otherwise I would consider higly unlikely.

http://youtu.be/5Tg_3OVizrA?t=2m15s

Hmm, I always have my problems with the "scientists have found out" phrase when not linking to the actual publication, but I will have a look into it.

I haven't found any articles besides the formation of antibodies against the "Rhesus"-antigen which happens when the mother is Rh- and the baby is Rh+. This is not restricted to male babies but happens against both sexes. Besides this, it doesn't really make sense for the body to react in this way. The mechanism of immunologic tolerance prevents the mother from launching an immune reaction against the fetus.

@user2360 If you don't get an answer here you may then want to ask your question on skeptics.SE. It is a SE website that deals with questions of the kind "is this claim (source) true?" question.


text:
Which of the following demonstrates the pattern of development in Greylag Geese?

Which of the following demonstrates the pattern of development in Greylag Geese? {Please give specific answers, which among the following gives the best available demonstration?, If needed, have a look at the Paragraph (Image Embedded)}
(A) Geese reared by humans cannot be taught to respond to its own species.
(B) The hatching at an advanced stage is critical for imprinting.
(C) The capacity to recognize an adult of its own species is necessarily inherited.
(D) Rearing by humans does not alter the object of the behavioral routine.
Option A: “Geese reared by humans cannot be taught to respond to its own species” is correct.
This is inferred from the 4th paragraph 2nd line: “When young geese are reared wholly by human beings it is towards humans that the young geese direct their behavioural routines”. This line clearly states that geese wholly reared by humans respond only towards humans. Also from the 2nd Paragraph 3rd line It is clear.
Option B: “The hatching at an advanced stage is critical for imprinting” is false.
Hatching at an advanced Stage is not shown by Greylag Geese, it is shown by Godwits. (3rd Paragraph, 1st & 2nd Line: The young of Godwits hatch at an advanced stage of development and soon after hatching can recognize the adult bird.) (So the fact is not conclusive from Behavioural Pattern of Greylag Geese) Imprinting can be shown by Greylag Geese, which do not have a prolonged period of hatching, and imprinting totally depends on whatever creature happens to be present at the right moment in their development.
Options C: “The capacity to recognise an adult of its own species is necessarily inherited” is false. According to the 2nd Paragraph, 2nd line: The capacities to recognise the right stimulus are not always inherited.
Option D: “Rearing by Humans does not alter the object of the behavioural routine.” is false, as shown in 4th Paragraph 2nd & 3rd line: When young geese are reared wholly by human beings it is towards humans that the young geese direct their behavioural routines.
Hence, answer should be A.
So Am I correct?

Homework questions are off-topic unless you show some effort solving them.

Mr Chris, This isn't a Home-work Question! It is an exam question, I have already answered it in the Paper, I want to know from Experts what should be correct! & Please If you are unable to answer don't comment the things you don't know!
I hope you Understand.
DWITI

Still: How about adding your answer? And I comment on everything I want.

Ok I am adding my logic, (Option wise)
Option A: “Geese reared by humans cannot be taught to respond to its own species” is correct.
This is inferred from the 4th paragraph 2nd line: “When young geese are reared wholly by human beings it is towards humans that the young geese direct their behavioural routines”. This line clearly states that geese wholly reared by humans respond only towards humans. Also from the 2nd Paragraph 3rd line It is clear.

Option B: “The hatching at an advanced stage is critical for imprinting” is false.
Hatching at an advanced Stage is not shown by Greylag Geese, it is shown by Godwits. (3rd Paragraph, 1st & 2nd Line: The young of Godwits hatch at an advanced stage of development and soon after hatching can recognize the adult bird.) [So the fact is not conclusive from Behavioural Pattern of Greylag Geese]
Imprinting can be shown by Greylag Geese, which do not have a prolonged period of hatching, and imprinting totally depends on whatever creature happens to be present at the right moment in their development.

Options C: “The capacity to recognise an adult of its own species is necessarily inherited” is false.
According to the 2nd Paragraph, 2nd line: The capacities to recognise the right stimulus are not always inherited.
Option D: “Rearing by Humans does not alter the object of the behavioural routine.” is false, as shown in 4th Paragraph 2nd & 3rd line: When young geese are reared wholly by human beings it is towards humans that the young geese direct their behavioural routines.
Hence, answer should be A. (Therefore, It is not B) {Actually the examiners say that It is B SO I need expert's help}

Your logic seems fine to me..
Option B: The hatching at an advanced stage is critical for imprinting.
This is wrong because Konrad Lorenz (who rediscovered imprinting)

demonstrated how incubator-hatched geese would imprint on the first
  suitable moving stimulus they saw within what he called a "critical
  period" between 13–16 hours shortly after hatching (reference).

So saying that the hatchling should be at an advanced stage is incorrect.
Option C: The capacity to recognize an adult of its own species is necessarily inherited.
Again this is incorrect because Lorenz has also stated that

The human-imprinted gosling will unequivocally refuse to follow a
  goose instead of a human, but it will not differentiate between a
  petite, slender young girl and a big old man with a beard (Lorenz,
  1965) (reference).

Also in this article it is implied that starlings that are imprinted to humans do not relate to its own kind.
Option D: Rearing by humans does not alter the object of the behavioral routine.
From the earlier findings, this is obviously false. Moreover a duck keeper has explained imprinting thus:

An imprinted duck--a duck that was raised from the moment of hatching
  by a human and so views the human caretaker as a parent or equal--may
  become accustomed to riding in the car. Imprinted ducks might go
  camping with you (although you must keep them beside you at all times
  or in a crate) or go on play dates to a friend's house (you will not
  want to take them to a farm or a public pond where they may contract
  diseases). If your duck is in a diaper, you will need to change the
  diaper every hour or so (reference).

This shows clear behaviour changes.
Option A:  Geese reared by humans cannot be taught to respond to its own species.
It is mostly accepted that it is not with Lorenz himself stating that

imprinting is irreversible. It is essential in learning that what has
  been learned can be either forgotten or modified (reference).

However there are claims to the contrary nowadays with it now firmly established that filial and sexual preferences are reversible (reference). Another interesting article by the American Psychological Association with a few links you might want to check out.
In conclusion, Option A could also have its problems with some response to its species possible, but overall it is the most and best plausible answer.

Dr Lorenz with his imprinted geese. Also a very interesting read (reference)

See I need to claim for this, because The answer given by the question setter is B (Which according to you & me is wrong), So I am using your answer as Reference for my claim apart from my explanation!
So Permission Needed!

Help urself to it. if ur claim works toh bata dena

Ya Ya, I will tell you (How can I contact you, any e-mail or Fb account?)

This is pretty much an open forum. My answers are not copyrighted and it is very much open to change or dispute. I personally have no problems with my answers being used for any educational purpose

Buddy, according to you, B is never possible, Isn't it?

From references, lorenz used to imprint between the time period I mentioned. There are also articles that peg the best time for imprinting between 24 and 48 hours. I wouldn't call that an advanced stage. I would be very interested in his references and proof if he decided to refute what I have pointed out in the article.

Let us continue this discussion in chat.


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How are physiological reversal potentials (or ion concentrations) of neurons measured?
Patch clamp electrophysiology experiments typically use an intracellular solution that mimics the ionic concentrations of neuronal cytosol. At the same time, the extracellular solution is meant to mimic cerebrospinal fluid. If these two sets of ion concentrations are similar to their in vivo physiological values, then one might expect a patch-clamped neuron to also have physiological ionic reversal potentials. If, on the other hand, they are dissimilar, then we might expect the behavior of the patched neuron (for example its intrinsic excitability or synaptic currents) to be different from the behavior of the same neuron in vivo. In principle, one would like to use solutions that are as close as possible to physiological for this type of experiment.
My question is: how do we know what these physiological values (concentrations or reversal potentials) really are? It is easy to find these values in a textbook, but I would like to know what original research was performed to determine these values in the first place.
In many patch clamp experiments, the solutions are designed to set the reversal potentials to non-physiological values, or are otherwise constrained by the practicalities of the experiment. Let's consider these issues to be outside the scope of this question.

There are various methods to determine the intracellular ionic concentrations. One method is to register action potentials by the fowling method: inject a Voltage Active dye VAD (something like a -2di Anepp or s similar dye) into the cell or tissue and using an Optic Mapping System register the Action potentials and then determine the intracellular ionic concentrations by Nernst equations.
We could also register Action potentials by "ion-sensitive glass electrodes method" by introducing ion-sensitive glass electrodes directly into the interior of the cells. The problem with these electrodes is that they cannot register very low ionic concentrations especially of Calcium. And so the above method is superior using  VAD.

Given that multiple ionic currents set the behavior of the cell during an action potential, it seems infeasible to determine ion concentrations from only a voltage recording. Can you point to an example of this method being used to determine ion concentrations?

Sorry for the delayed response! Busy with routine.I recommend to read the information posted on http://www.utdallas.edu/~tres/microelectrode/microelectrodes_ch11.pdf for understanding how ionic concentration is measured inside the cell.

Thanks for the review! That is an excellent seed for digging through the ion-selective electrode literature. So far I have been able to find measurements in oocytes, epithelial cells, photoreceptors, neuroblastoma cells, purkinje fibers, muscle, etc. No measurements, however, from neurons in anything resembling a physiological preparation. From your reference, it seems like it would be very difficult to make such measurements in cells as small as most neurons, as this would lead to excessive cell damage.


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Why do neurons have a negative resting potential?
Neurons expend the majority of their energy powering ion pumps to maintain the chemical gradients that power their electrical activity. To have a negative resting potential, neurons leak potassium across the membrane, which seems like a terrible waste of energy to me. I would like to know what benefit a neuron receives in exchange for this seemingly unnecessary metabolic load.
I am not asking how the resting potential is achieved. I am also not interested in the trivial answer: that the voltage-gated channels are configured to require a transition across the -40mV or so threshold in order to fire an action potential. It seems to me that this threshold is arbitrary; if there was no advantage to maintaining this gradient then neurons would have evolved to avoid it.
Any ideas? Or better yet, pointers to places where this has already been answered?
My best guess so far looks like this: The total range of available voltages is more-or-less fixed from -90 to +50mV. We want to avoid getting too close to either end, since the channels become less effective near their reversal potentials, so maybe the effective range is more like -70 to +30 (to go outside that range, we must sacrifice speed). Within that 100mV range, we leave the bottom 30mV or so for EPSP integration, and the other 60mV for action potentials.  Now, if the resting potential was 0mV, the available dynamic range for integration and spiking would be much smaller which probably translates to making the output noisier.

My turn to comment, lol.  The notion of membrane potential likely long predates the neuron from an evolutionary standpoint.  "Simpler" cells, e.g., an oocyte, rely on membrane potentials to gate membrane permeability to facilitate the entry of sperm. I would say it was likely due to the differential expression of membrane receptors in response to the local milieu that drove the evolution of the neuron, but I do not have a reference on hand to back that up.

(by the way, far from saying it's not an intriguing question, and the reasons you propose are plausible, so don't take any of this personally, as I implied on CogSci, you've got a good mind for this stuff)

Essentially all animal cells maintain an ionic balance causing a resting potential of about -70 mV in order to maintain their internal environment including pH, ion concentrations, osmotic pressure and volume. (Lodish, Molecular Cell Biology)  Neurons developed from existing types of cells and it's unlikely that the cost of maintaining resting potential in the neuron could have driven evolution of an entire alternative system to provide the homeostasis supported by the existing system.
Note that the depolarization of the membrane at any particular place during an impulse is very short so the impact of the ion flows have only limited effect on the cell's overall internal environment beyond requiring adjustment by ion pumps for the losses involved.  It also is not obvious how the wave-like characteristic of a nerve impulse could be generated if the membrane did not carry a nonzero potential; there would be no stored energy (in the form of ion gradients) available to make the pulse swiftly spread across the membrane.
Another point to consider is that the perhaps 15% of a neuron's energy spent on replacing leaking ions may have some hidden usefulness.  This paper suggests that neurons may actually be set up to leak at a rate higher than they would if it were minimized.

Thanks! I think your first and last paragraphs are both excellent answers. Regarding the second paragraph, I believe the bulk of the energy that drives action potentials is in concentration gradients, not electrical gradients. So it is possible that (with the right channels) one could have action potentials with no resting membrane potential (see: http://cogsci.stackexchange.com/questions/3625/how-would-synapses-behave-if-resting-potential-was-zero/3650#3650 )


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Do ants feel pain?
I have watched video on youtube where guy pours molten aluminium into fire ant colony to make casing. In the comments below there's huge discussion on is that a right thing to do. I am on the side that one should not exterminate colony of living things to get aluminium shape of questionable artistic value.
Main argument on the opposing side is that ants do not feel pain - therefore it's ok. I have done some reading around and opinions differ greatly.
Do ants feel pain?

There have been no studies that I can find addressing this issue.

I think they feel pain. Afaik. we are talking about fire ants which are invasive species, so it is better to kill them.

Not directly related to the question: I had seen the NatGeo episode on that guy. I don't think he does it for artistic value. He does it to study the architecture of ant nests. Ethics depend on ant species and their effect on environment.

Possible duplicate: http://biology.stackexchange.com/questions/19446/can-insects-feel-pain

Whether they feel pain or not the artist is still killing living organisms for art, and on purpose. This seems to be a bit of an ethical question. Is killing things for enjoyment (of art) ok?

@TylerS.Loeper we kill living organisms for art all the time, several pigments are made from dead organisms, you kill living organisms just by being alive. In the case of fire ants the artist should be killing them whether or not they produce art from it, since the fire ants are destroying the native ant species and the only way to help the problem is killing them. Art is just a side benefit.

I believe every living organism (even single cell ones) experience pain somehow, because it is important to stay alive. The scientific answer depends on how you define pain...
Related articles:

Evidence suggests that some, if not all, invertebrates have the
  potential to suffer through current practices that do not take into
  consideration that invertebrates may experience something like pain
  and stress and have the capacity for advanced and unexpected cognitive
  abilities.

2013 - Invertebrate welfare: an overlooked issue

Genetic analysis of nociceptive behaviors in the nematode
  Caenorhabditis elegans and the fruit fly Drosophila melanogaster has
  led to the discovery of conserved sensory transduction channels and
  signaling molecules. These are embedded in neurons and circuits
  that generate responses to noxious signals. This article reviews the
  neurons and molecular mechanisms that underlie invertebrate
  nociception. We begin with the neurobiology of invertebrate
  nociception, and then focus on molecules with conserved functions in
  vertebrate nociception and sensory biology.

2004 - Invertebrate Nociception: Behaviors, Neurons and
Molecules

Just to mention fire ants you possibly meet are invasive species, so you should not protect them.

The red imported fire ant, Solenopsis invicta Buren, is an invasive
  pest that has become widespread in the southern United States and
  Caribbean after accidental introduction from South America in the
  1930's. This species, which has diverse detrimental impacts on
  recipient communities, was recently discovered in Australia and New
  Zealand and has the potential to colonize numerous other regions.

Figure 1 - fire ants worldwide - source

Hi inferno, every species at some point was invasive... lol

@MatasVaitkevicius Interesting thoughts. :-)

@MatasVaitkevicius I think it is somewhat different nowadays because most of these species would be localized to a region or would spread much slower without (un)intentional help from us.

In short, scientists usually conclude that pain is unlikely to be found in insects in the way it is defined in humans, but this is difficult or impossible to test directly.
In humans, pain is often described as a "subjective experience involving a class of sensations with which is associated a characteristic 'negative affect and aversive drive'". So to simplify, pain is defined as a sensation that causes negative emotions and reduces the behaviors that an individual was performing before or during the stimulus. Note that with this definition, it is hard to differentiate pain from fear or response to an unpleasant but non-painful stimulus.

Eisemann, C. H., Jorgensen, W. K., Merritt, D. J., Rice, M. J., Cribb,
  B. W., Webb, P. D., & Zalucki, M. P. (1984). Do insects feel pain?—A
  biological view. Experientia, 40(2), 164-167.

To put this more clearly, pain in humans is defined as resulting in a "a protective stimulus-avoidance response".

Fiorito, G. (1986). Is there “pain” in invertebrates?. Behavioural
  processes, 12(4), 383-388.

Fiorito (1986) notes "Venom used for incapacitation of prey probably does not inflict
pain, as it may be disavantageous because pain may increase struggling on the part of the prey: it is indeed when venoms are painful that they can function in defense.". This is probably the argument most commonly employed to support the idea that invertebrates don't feel pain: insects can't do much about injuries or intoxications so feeling pain is unlikely to be adaptive because it is unclear how it could elicit a response that would increase their survival.
Many invertebrates are autotomic which means they can voluntarily detach legs or antennae (like a lizard's tail) to avoid being captured by a predator, in this case it is hard to imagine an insect experiencing a pain that would be comparable to the level of pain of a human loosing a leg, because it would incapacitate the insect and reduce its chances of survival. Insects could instead have a direct stimulus to behavior response without any conscious emotions or feelings, comparable to a very simple computer program: "if pressure on this leg; drop the leg".
However, there is at least one case known in ants of wound treatment that would suggest this argument is not valid at least for this species of ants:

Frank, E. T., Wehrhahn, M., & Linsenmair, K. E. (2018). Wound
  treatment and selective help in a termite-hunting ant. Proceedings of
  the Royal Society B: Biological Sciences, 285(1872), 20172457.


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Why don't bacteria eat food leftovers?
I have thrown a dirty spoon after eating some pasta into one of my desk drawers (doesn't do me much honor). It stayed there for around a year. My house is warm and I think there is enough humidity for bacteria to multiply, however I have found it today with seemly same amount of food on it when I left it.
I assume given enough time all food should get converted into bacteria (bacteria would eat and multiply until food is there and stop when it is all consumed). Is this assumption incorrect?
Why didn't bacteria decomposed the food on my spoon?
EDIT: This question has nothing to do with fried McDonald foods and is referring to bacteria consuming 'ordinary' food, plus I am asking if food should disappear completely while the other question is about it being decomposed,  answers are completely different.

why would you assume that a bacterial colony looks "clean"?

@rumtscho I assumed given enough time all food should get converted into bacteria (bacteria would eat and multiply until food is there and stop when it is all consumed). Is this assumption incorrect?

The crucial point is water availability. The Antarctic is a big mass of water. Yet it is frozen and your spoonful would survive there too. The air may be humid in your place, but that doesn't mean organisms can deploy that moist and thrive.

The assumption is indeed wrong. But even if it were right, the spoon would be covered in gunk consisting of dead bacteria bodies + their waste product.

@AliceD So had I placed spoon in conditions perfect for bacteria I would have found it 'eaten off' clean?

@rumtscho Could you post it as answer please. Thanks.

@MatasVaitkevicius - I would suspect fungi to decompose it, yes. However, as posed above, the 'clean' I am unsure of, as certain components of organic material may, or may not be digested fully.

Possible duplicate of Why don't McDonald's fries decompose?

First, your assumption is wrong. Bacteria multiplication is not limited by food availability only, it is one of many constraints.
Oxygen availability, water availability and the absence of toxins also play a role. You can easily start a thriving bacterial colony somewhere, but once one of these conditions changes sufficiently, the colony can die off. And it can be the growth itself which changes the conditions. A classic example is found in wine fermenting. The yeast there multiplies freely until it has produced so much alcohol as a waste product that it dies off. This is why wine is always in the 12 to 18% ABV range, anything above is "fortified wine" where the concentration was increased after the yeast's death. Yeast are not bacteria, but bacterial colonies' growth is limited in similar ways.
Second, even if the assumption were true, the spoon wouldn't be clean. Bacteria converting food in waste doesn't result in nothing, nor does it result in something gaseous which would literally disappear into thin air. OK, part of their byproducts are likely to be some gas. But you certainly get lots of bacterial bodies (alive, later dead) and also lots of waste product. Together, it forms some kind of sticky organic goo (frequently a biofilm).
So, about your spoon

it is entirely possible that it never got a thriving bacterial colony, because the conditions weren't right despite food availability
it is also possible that it got some kind of colony (pathogenic or not), and it died off before the food was consumed
in the case of a colony, it doesn't matter how much it got to consume before dying off. The spoon wouldn't have ended up clean under any circumstances, including the very unlikely "death by food going out" scenario
depending on the conditions in which the spoon is held, the colony which dominates the spoon can be bacterial, or fungal (mold, yeast), or you can end up with different species building their colonies in parallel. Still, the previous points hold under the "mold colony" or "multiple colonies" scenarios just as under the "single bacterial colony" scenario.

Thanks, I appreciate your patience with someone as ignorant as myself.  I am working on a different angle - that they simply didn't like the pasta :)

Wouldn't you think fungi would be better candidates than bacteria?

Heh, no problem - if I didn't have the patience, I wouldn't have written an answer. Also, you're raising an interesting philosophical question - can bacteria "like" something?

@AliceD both are possible, I suspect it's the circumstances which determine which ones will get the upper hand - I think it's mostly up to temperature, with bacteria being more likely at room temperature and fungi preferring it below 20 C. I can say from "standard food safety knowledge" (sorry that I can't point to a specific reference right now) that B. cereus is very fond of cooked starches, and can confirm from personal slob experience that you certainly can incubate a nice bacterial colony on pasta or rice - I didn't do anything to confirm that it's B. cereus, though.


text:
Why do some foods do not taste good when eaten together that eaten separately would taste great
The way I understand it, 'good tasting food' is evolutionary concept e.g to be able to distinguish between high nutritional value foods and ones that have no nutritional value whatsoever.
So if well-prepared fish tastes well and so does some other food (birthday cake/[put food that would not go along]) on its own why then when mixed together they might taste bad. The mix has the same nutritional value, same proteins carbs, and fats, but they just don't go along.
Why do some foods do not taste good when eaten together?

Here are a few recipes: Orange tilapia, Honey orange fish filets, Baked Fish in Parchment with Orange and Olives, White fish à l'orange, and fish with spices and orange juice. I am VTC as primarily opinion based.

Here is a list of surprising food pairings that people actually enjoy.

@Remi.b fish was just a (bad I suppose) example...

Can you find good examples?

@Remi.b I don't intend to... the question is not about some specific case. Also, your argument is defeated by yourself (by providing the link) as if some foods 'go together' that means that others don't...

My goal with this link was to show that even combinations that seem unintuitive might actually go well together. This link does not suggest that some food items fundamentally don't go together. I think that the fact that it is hard to find a good example shows that it is mainly a matter of culture preference and preparation. There is maybe nothing more fundamental than that. To me for example, sugar and meat were really the things that would be impossible to pair. My mind was changed when I started to travel a bit.

Your link is the other side of same coin... if something goes 'well' that can only mean that something does not...

If you could just come up with a few examples, that would clear up the argument. In all case, I'm done arguing on that matter. Good luck with your post.

Conditioning almost certainly plays a large role. Think of young children. Some are willing to put almost anything in their mouths (having been unconditioned), while others refuse to eat all but a select few foods until they're older (i.e after they've become conditioned either culturally or by what's available).


text:
Why doesn't pure fat taste better than pure sugar?
I mean looking from evolutionary perspective sugar tastes sweet and individuals that had this perception ate more sugar and survived and those that didn't perceive sugar as sweet didn't eat it and died from hunger.
So the better (more caloric) food is - the better it should taste so that one would be more likely to eat it and if choice had to be made between berries or lard (assuming that food is scarce) one should go for lard as this would increase his chances of survival
Out of all foods lard has the highest calorie content (898 cal per 100g) and therefore highest concentration of fat and yet it doesn't taste very nice.
There must be some explanation why fat doesn't taste much better than sugar?

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