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What is the definition of "Natural Selection"?
Natural selection is the differential survival and reproduction of individuals due to differences in phenotype.
Natural selection, a process that results in the adaptation of an organism to its environment by means of selectively reproducing changes in its genotype or genetic constitution.
Natural selection, then, can be defined as the differential reproduction of alternative hereditary variants, determined by the fact that some variants increase the likelihood that the organisms having them will survive and reproduce more successfully than will organisms carrying alternative variants.
Darwin's definition of natural selection his book "On The Origin Of Species By Means Of Natural Selection or the Preservation Of Favoured Races In The Struggle For Life" is:

The preservation of favorable variations and the rejection of injurious variations

In Evolution 101, natural selection is not defined, but rather the concept "evolution by natural section" is characterized as the outcome of variation, differential reproduction and Heredity, and a clarifying example is provided.
Clearly, the wording in each of the above is different!
I searched Biology StackExchange for any explicit statement of the definition of natural selection, I couldn't manage to find one. There are some discussions about whether it is a tautology or not, but even in those discussions, the definition of natural selection was not quoted.
I tried to search tags "natural selection" and "definitions" of biology StackExchange, and yet I didn't see any particular wording mentioned as the official definition of natural selection.
Actually, the tag [natural selection] mentions this definition in the tag information itself:
Natural Selection is a mechanism of evolution that leads to non-random spread of genes due to the effect that genes have on reproductive success
Natural selection is the process by which heritable traits that make it more likely for an organism to survive and successfully reproduce become more common in a population over successive generations.
Is there an official definition of natural selection that is adopted by biologists nowadays? and what is that definition exactly?

[EDIT] It came to my awareness that this question might be a possible duplicate of the following question: "How is Selection best defined", and indeed in the answers provided to that question the topic of definition of natural selection has been addressed.
I didn't know of this posting. I simply surfed for "natural selection", and not just for "selection", and I didn't notice it. But indeed what's presented in the answers does cover the question present here.
However there is some difference in the question itself from that present here. Here I wanted to know of what I thought would be an official definition, and I was asking in particular about "natural selection", while in the referred question, the question is more general, it's about what qualifies "any" force (apparently he means related to biology and especially evolution) to be labeled as "selection", including artificial selection, sexual selection, etc.., so it's a wider topic, at least as far as terminology is concerned.
Here in this question I've quoted the main results that one would see upon surfing the web for "definition of natural selection", and I wanted to know which one would be the official or as @Remi.b had put it, the most commonly used or referred to in biological research.
I still think, that for precision purposes, exact wordings are important, and such an extremely important concept like "natural selection", it would have been expected that it had an agreeable, kind of, official definition, by some convention or the alike.
Anyhow, I think, whether this question is a duplicate or not, can be better assessed by experts in evolution field present in this website, like those who provided answers, and others.
Thanks.

I think it's unrealistic to expect to find word-for-word congruence b/w definitions from multiple sources. All your definitions still describe the same phenomenon conceptually. From a broader viewpoint, no 2 textbooks (or at least few) define "simpler" biological concepts the same (e.g., even the word cell). The same can be said of common non-scientific words (e.g., see dictionary.com, OED, Merriam-Webster, etc. for any given word). In conclusion, there is no "official" wording for this definition or most definitions. This is why bio instruction emphasizes learning concepts not words...

Then there's the definition which pops up when you hover your cursor over the tag "natural-selection" at the bottom of this question.

@mgkrebbs, oh yes, thanks, i didn't notice that really. I'll add it.

Of all the definitions, I think the SE tag one is possibly the worst. Maybe @Remi.b would take a stab at editing it, if you agree?

As to whether it's a tautology: it's a tautology that the most fecund phenotypes will have more offspring, but it's not a tautology that there are more fecund phenotypes, or that heredity occurs, or that what qualifies as fit varies slowly (in fact, it might not). Nor is it a tautology that this is where adaptation comes from (or even primarily where it does), or that drift isn't also an important mechanism (which it is). These are all issues where evidence is key.

@J.G.: But fecundity, or reasonable lack thereof, really isn't a criterion for natural selection.  An organism can be extremely fecund, like the codfish with its millions of eggs, or humans (and other mammals) which only have a few offspring but make a large investment in post-natal care.  Either works: since both exist, they have obviously been selected for.

@Remi.b I think Bryan Krause was suggesting you to edit the the [tag:natural-selection] tag-info in SE.

@jamesqf Well, replace it with whatever you think succeeds under natural selection, but in any case I think you're conflating how species compare to how individuals in a species compare, which is what natural selection is all about.

Possible duplicate of How is "selection" best defined?

I think this is really related to the question linked above, and in this answer I name a couple of relevant sources to look at, and how to draw the line between natural selection and evolution by natural selection (which is sometimes fruitful).

Official definition

Is there an official definition of natural selection that is adopted by biologists nowadays? and what is that definition exactly?

I don't think there is such a concept as an "official definition" of any concept in science. There are common definitions though.
The definitions you cite
Let's go through your three definitions

Natural selection is the differential survival and reproduction of individuals due to differences in phenotype.

This definition lacks the idea that this fitness differential must be caused, in part at least, by genetic variation.

Natural selection, a process that results in the adaptation of an organism to its environment by means of selectively reproducing changes in its genotype or genetic constitution.

Part of the phrasing is about the consequence of the process rather than the process itself. The part that describes the process itself is "selectively reproducing changes in its genotype, or genetic constitution", which is a rather unusual phrasing and I would argue is slightly vague.
Note that while most authors refer to natural selection as the fitness differential, it is not impossible to refer to natural selection as the resulting change in allele frequency. I have never seen cases where this semantic difference matters though.

Natural selection, then, can be defined as the differential reproduction of alternative hereditary variants, determined by the fact that some variants increase the likelihood that the organisms having them will survive and reproduce more successfully than will organisms carrying alternative variants.

I have never encountered the expression "alternative hereditary variants". I think the author made it up. It sounds like the author tried to avoid the term "allele" by replacing it with "alternative hereditary variants". The author also seems to have tried to avoid the term "fitness" by replacing it with "likelihood that the organisms having them will survive and reproduce more successfully".
But overall the definition sounds correct to me. There is an important difference between the first and the third definition is that in the first definition, it emphasizes the fact that the genetic elements that explain fitness variance are doing so via its effect on the phenotype. The third definition just ignores phenotype. As such, I would consider the first definition more complete (and more compact).

Natural Selection is a mechanism of evolution that leads to non-random spread of genes due to the effect that genes have on reproductive success

Here, the definition is again very much based on the consequence of the process rather than the process itself. Only "due to the effect that genes have on reproductive success" refers to the actual process of natural selection.
I don't really like the term "random" here as the concept of randomness is somewhat unpleasant to define outside of a well-defined model. I don't really like the term "genes" either because selection doesn't only act on genes (but can act at any locus) and because the term "allele" would be more appropriate even if the phrasing would still remain unclear.
So in short, shame on us, the StackExchange definition is pretty bad!

The preservation of favourable variations and the rejection of injurious variations

I shall not talk here about how different is Darwin's theory of evolution from today's theory of evolution (which is called the "modern evolutionary synthesis"). I shall not talk either whether this single short sentence is a good summary of Darwin's representation of natural selection (see @Luaan comments for more information).
This definition is short and a bit vague. One would want to think of this definition as applying to a genetic variant, without regard to the phenotype, however, Darwin did not know anything about DNA.
My favourite definitions
Lewontin's recipe
A very simple way to think of natural selection is to consider Lewontin recipe. The Lewontin recipe says that natural selection occurs whenever:

Individuals in a population vary in terms of a given trait
This trait has a non-zero (additive) heritability. See this post for a definition of heritability.
The fitness varies (not necessarily linearly) as the trait varies

Single sentence definitions
If you prefer a shorter and simpler version I would personally suggest

Selection is the fitness differential among genotypes in the population.

This definition lacks the concept of phenotype but talking about the fact that an individual fitness is dependent on its phenotype (among other things) is, IMO, not required to mention in the definition of what natural selection is. Not that I also removed the term "natural". I don't quite like it because it leads people to think that natural and artificial selection could be fundamentally different. Same applies to sexual selection, IMO, but I shall not go down this slope now!
In a very similar post, I wrote the definition

Selection is a fitness differential associated to a genetic variance among individuals in a population.

I also like this definition because it highlights that selection acts on populations (and not on individuals or on species).
Mathematical modelling
You might want also to consider as a definition the mathematical modelling of the process. In absence of genetic drift (assuming infinite population size), assuming a bi-allelic locus with alleles a and A, one can model (haploid) selection as
$$p_{t+1} = \frac{p_t W_a}{p_t W_a + (1-p_t) W_A}$$
, where $p_t$ is the frequency of the allele a at time $t$. $W_a$ and $W_A$ are the fitness of the genotype with alleles a and A, respectively. Of course, you can extend this model to any kind of ploidy and any number of alleles. You can also extend this model to include genetic drift (typically done via the use of diffusion equations or via branching patterns).
For more information about these mathematical modelling, please have a look at an intro book in evolutionary genetics (see here for book recommendation).

@This is a very nice answer. I noticed that you skipped Darwins' definition?

@ZuhairAl-Johar Keep in mind that Darwin was simply defining his terminology for the book. This is similar to saying "James McKay (hereafter noted Defendant)...". The idea worked, the concept stuck, and the exact wording and semantics of the "definition" aren't important in the slightest - in general, in scientific thinking, the concept is far more important than the exact words you use to describe it. Scientists usually aren't language lawyers, they're just trying to communicate efficiently :)

@ZuhairAl-Johar It should further be noted that your cited part is the end of a whole paragraph where he describes what he means by natural selection (see https://counterbalance.org/evolution/direct-frame.html). And some of the definitions you showed focus on some mechanisms that we've found since Darwin's time - mainly, genetics (and the language of genetics). Darwin was talking about "individuals having any advantage ... would have the best chance of surviving", but that's equivalent to "some phenotypes promote survival" - just with more mature terminology and more insight.

@ZuhairAl-Johar You should consider reading the edit, which add discussion of the Lewontin recipe and add my own definition. Also, I quickly discussed "Darwin's definition" as you asked.

@Remi.b, why the first p in the equation is not in upper case?

@ZuhairAl-Johar It was a mistake. It is standard to use lower case p for allele frequency, so I changed all the Ps to lower case. Thanks.

I've adapted your definitions to another process that I think will be less controversial to you.

Eating is the intake of food by taking into the mouth, chewing, and swallowing.
Eating, the process that results in digestion by taking in food and chewing and then swallowing.
Eating, then, can be defined as the intake and digestion of food items, determined by the fact that organisms take in foods to the mouth and then chew and swallow them leading to digestion of those foods into nutrients used by that organism.

If you look up dictionary definitions of the verb "to eat" you will also get a variety of answers, but there is no controversy about what "eating" is: it's a concept you learn and agree on. Some of the definitions reach further, mentioning digestion. Some focus on the "just eating" part. However, they all agree with each other, there is no conflict. In fact, a lot of the words are just rearrangements of the same words into different grammatical constructs.
All of the definitions you cite are reasonable descriptions of the term; all of the sources you cite also go further into those definitions to describe the whole process. You should focus on that whole process rather than trying to find fault in the definition. Natural selection is not a tautology, and arguments that it is are misguided.

You've cited the same citation that I've cited. I'm not arguing that it is a tautology, I just wanted to know the definition, and all of your responses were great. Thanks

There is some variation as to whether it's thought of as acting on the phenotype or the genotype, although of course those two are interrelated.

As Remi points out there is not an official definition of anything as complex as natural selection in science. Science is a collective consensus, not a hierarchical structure, official things are rare and usually not directly connected to the science. The neo-Darwinian synthesis might count but that is far too large to be considered a definition, it is more a modern restatement of the theory.
I can offer the definition I use in class.
Selection: change in the heritable characteristics of a population due to differential reproduction of variations in said characteristics within a given environment
to break it down change in the heritable characteristics of a population... that's just a restatement of evolution essential for any consideration of natural selection.
...due to differential reproduction... so evolution happens because some things reproduce more successfully than other things.
...of variations in said characteristics within a given environment and this clarifies the cause of the differential, that variation in heritable characteristics exist and interact with the environment in different ways. Of course, it is important to understand the "environment" in this case is literally everything else, from other cells in the body to predators, to other genes on the same genome to abiotic processes.
Note authors tend to avoid the mention of genetics or related terms in the most fundamental definitions because natural selection is not reliant on nucleic acids it works with any form of heredity, an alien lifeform that has a different form of heredity will still undergo natural selection. Things like prions can also evolve via natural selection if a group of things has heritable characteristics that also vary in reproductive success natural selection will operate on those things.
Then you have the specification of "natural" selection. Which is simply selection not caused by human intervention. This has been an important piece of natural selection since the beginning mostly because people had little problem with the idea that humans could alter organisms by conscious choice but the idea that their natural environment could alter them simply due to survival and reproduction was not as easily accepted.
Differentiating natural selection and artificial selection is probably the vaguest part and has a tremendous amount of gray area. There is no Real difference between artificial and natural selection, it is all just down to human conceptual framing. Natural selection is just a response to an environment, but what makes up that environment covers everything from rocks, humans, members of the opposite sex, etc. Nearly anything can have an impact on survival depending on the circumstances. Because of this the only thing that differentiates natural from artificial selection is whether humans are the major environmental factor but that itself is vague, human mate choice and species that live around humans but are not domesticated( like cockroaches) make this imprecise. I have never found a satisfactory precise differentiation between the two forms of selection.

natural selection was an idea proposed by darwin a scientist. he said that nature select the fittest.
  he concluded following points after his research
  In a population, some individuals will have inherited traits that help them survive and reproduce (given the conditions of the environment, such as the predators and food sources present). The individuals with the helpful traits will leave more offspring in the next generation than their peers, since the traits make them more effective at surviving and reproducing.
  Because the helpful traits are heritable, and because organisms with these traits leave more offspring, the traits will tend to become more common (present in a larger fraction of the population) in the next generation.
  Over generations, the population will become adapted to its environment (as individuals with traits helpful in that environment have consistently greater reproductive success than their peers).

Quoted from the book
Darwin and Henslow
The growth of an idea
Edited by Nora Barlow

Thanks for this nice quote. But is this predictive? I mean suppose that it has always been a merry time for trait A and bad for trait B, then according to what you've said one would predict that trait A would prevail since it has more capacity to adapt to its environment and thereby survive and reproduce more. Now suppose suddenly an outbreak of a deadly disease spread that trait A happened to be susceptible to but not trait B, the outcome is final triumph of trait B, and the extinction of trait A.

What was usually the weaker trait, i.e. the less fit trait, prevailed in this example. Now a selection had been made, but for what? for what used to be the less fit trait? Its done by nature. So it doesn't appear that nature always select in favor of the most fit traits? isn't it.


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Reaction of the body to heat
In massage school we are being taught hydrotherapy -- applying cold and heat to specific areas.
It says that when applying cold, first the body goes through vasoconstriction, and then later vasodialation. That makes sense -- preserve heat through the former, but if the cold is applied for too long the body still has to keep the cells alive, thus the latter.
What doesn't make sense is this passage, in relation to applying heat:

Law of Action and Reaction: Initially blood will rise to the
  surface, applied for too long the blood will recede to the interior
  causing inner congestion to be greater than before

Is that true?

Local warming of a patch of skin will cause vasodilation. However, after prolonged warming there is a 'die away' phenomenon, is which blood vessels slowly constrict back to their normal diameter.

Johnson JM, Kellogg DL Jr. Local thermal control of the human
  cutaneous circulation. J Appl Physiol (1985). 2010;109(4):1229–1238.
  doi:10.1152/japplphysiol.00407.2010
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2963328/

You are right, it doesn’t make sense. No matter what, the inner organs have to function at some level, producing heat which the body has to transfer to the surroundings, otherwise the inner temperature will rise. The main physiological mechanisms for losing heat are to increase the blood flow to the skin (vasodilation) and sweating (evaporation). And the body will try to use these mechanisms, no matter how futile it may be in a high-temperature/high-humidity environment.
Actually, neither does the suggested responses in low temperature make much sense. Again, the body has to preserve its inner temperature, this time by reducing the blood/heat-transfer to the skin (vasoconstriction), shivering and raising the feathers or fur. Maintaining the core temperature is paramount, and eventually, the skin and extremities will be sacrificed if needed. Numerous examples can be found!
There is however a small amount of truth in the hypothermic response: people adapted to cold environments can control bloodstream to different extremities (fingers or feet), avoiding frost-bites or for dumping excess body heat after heavy exercise, avoiding to sweat all over the body (Ref.: Schmidt-Nielsen, Animal physiology adaptation and environment, Cambridge University Press 1990).

Welcome to Biology.SE! We prefer answers that are supported by references. Can you [edit] your answer to include references?

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How to isolate a high proportion of available helminth ova from animal faeces/feces without damaging them?
I need to isolate large numbers (tens to hundreds of thousands) of cat (and later dog) hookworm ova from cat/dog faeces.
I have a centrifuge, and various sieves with pore sizes of 20, 63, 75, 106, 125, and 180 microns as well as the ability to create various flotation solutions to any specific gravity
The specific gravity of the ova is 1.21 and they are oblong, their size is 50 by 38 microns varying by ±5 microns.
I have tried sieving the cat faeces after emulsifying them using a liquidiser. I pass them through successively smaller pore size sieves but the concentrated ova still contains a very large admixture of unwanted faecal material.
Flotation following sieving by bracketing the ova in successive flotations of iron sulphate results in too much contamination and many ova are lost.
My technique is self-taught and clearly lacking.
I need to remove 98-99% of the unwanted faecal material without damaging the ova, which are not very resilient.
My access to equipment any more sophisticated than that listed is unlikely but if costing less than a thousand pounds possible.
I am new to this area, so I am sorry if I have omitted anything required or failed to follow form and protocol.
Thank you very much in advance.

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Does our brain use up more ATP after smoking cannabis?
kind of an amateur here.
If the firing of the neurons' signals uses up some ATP, and smoking cannabis makes them fire off more quickly, do our brains use up more ATP to sustain that rapid firing?

The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. In particular, it's helpful to cite references for claims in your question.

considering that it can hasten heartbeat and breathing, https://medicalxpress.com/news/2017-08-brain-cannabis-oxygen.html

IV THC injection increases glucose metabolism in chronic cannabis users..see https://www.researchgate.net/profile/Linda_Chang2/publication/5944014_Functional_Imaging_Studies_in_Cannabis_Users/links/5431fc150cf27e39fa9f9880.pdf


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Do we posses technology to rebuild sequenced DNA?
Is there existing technology that would allow to rebuild DNA molecule from a digital file storing sequenced DNA?
If not, does there at least exist theory explaining how such device could be built?

This question is quite broad. Also see this: https://en.wikipedia.org/wiki/Artificial_gene_synthesis

Yes, in fact synthesizing short stretches of DNA and RNA is available through several commercial services. However this limited to tiny DNA fragments (say 120 base pairs or so). Longer sequences require custom laboratory work.

Making long sequences is possible too. The J. Craig Venter instistute synthesized an entire bacterial genome.

@user137 While it's true that long sequences can be made, this most often requires 'manual' stitching of several smaller fragments. However, current technology can already generate fragments of a few 1000bp (see e.g. here)

Thousands of base pairs is trivially possible with current technology - it's an off-the-shelf order from many companies. Tens of thousands becomes tricky. More importantly, although the question doesn't specifically ask this, this could not be used to re-create extinct animals (other than perhaps bacteria) because among other things epigenetic information would be missing.


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Red and yellow insect found in kitchen in Conrad, Montana (USA)
Beetle found in our kitchen in Conrad, Montana (USA) on 3/13/19:

This appears to be a stink bug in the superfamily Pentatomoidea of the true bugs (i.e., order Hemiptera).
Specifically, your specimen appears to be Perillus bioculatus or the two-spotted stink bug.

 Photo Credit: Margarethe brummermann (2008)
You can see additional photos including those demonstrating the species's various yellow vs red color morphs here.
According to the Integrated Plant Protection Center at Oregon State University [my emphasis and links]:

Mature nymphs of the two spotted stink bug are about 8 to 9 mm long. Adults range in length from 10 to 12 mm. Nymphs may [be] pale yellow or reddishorange with a distinct black "Y-shaped" marking on the pronotum and two black spots on the thorax.

According to Wikipedia, this species is usually a beneficial predator (especially of the Colorado potato beetle), but early nymph stages feed by sucking on potato stems. The trade-off, I would guess, is worth it.

In fact, the color variation in this species (namely the shift from white/yellow to red) that my earlier link shows photos of is a result of a higher diet of potato beetles. [Source, taken from p 99 in McPherson's 1992 book The Pentatomoidea (Hemiptera) of Northeastern North America].

 Source: bugguide.net
Their range, according to bugguide.net is southern Canada, the U.S. and into Mexico.

I was gobbling cherries one day and I ate a cherry with a stink bug which defended itself on my tongue. It was a bit hot and a bit indescribably chemical. wasn't a major worry though, i had forgotten about it after a while. don't eat them :D their defense works you spew them out haha.


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Can the human body survive in a zero sugar diet strictly through gluconeogenesis?
I read an article a while back about athletes (I believe cyclists) being exposed to a 0 sugar diet and their blood sugar levels stayed relatively constant, which prompted the question whether people could survive strictly off a no sugar diet.


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Multiple numbers in the Ishihara test?
When I was in high school (30 years ago), I took a biology class, and the instructor showed us an Ishihara color test for color-blindness. (This is the "hidden numbers" test.)
What I thought I saw once or twice was two different numbers* that had been embedded in the same slide. Were there slides in the test that had two or more numbers, or was I hallucinating?
[EDIT:] * "Two different numbers" means "different numbers in different colors."

I got a chance to look through the actual images, and it appears I hallucinated the third number.

The Ishihara Color Test consists of plates containing one number. But that number may consist of two digits (Fig. 1). After scouring the internet I have also found variants of the test where the each of the two digit had a different coloring (Fig. 2), but these tests may not all be validated/standardized or used by health care professionals. The plates may also contain one or two wiggly lines that have to be traced (Fig.1). In all, my conclusion is that there are many variants of this specific test around, at least on the web. I am not aware whether there are certain standardized versions being used by health care professionals. In all, my answer to your question...

Were there slides in the test that had two or more numbers, or was I hallucinating?

...is that there might have been two digits of different coloring in the plate, dependent on the specific make of your teacher's plates. You might, or might not have been hallucinating. To give a more affirmative answer, the specific test with the specific make would have been dug up by your teacher.

Fig. 1. Ishihara test with a plate containing one number of two digits (left) and one or more wiggly lines (right). source: Colour Blindness

Fig. 2. Ishihara variants, showing two digits with different shades in the middle panel. source: allinesnowmop, a personal web page, credibility questionable

@user237650: Once again, I consider that one number. Maybe I need to add: "the second digit wasn't lined up with the first one"?


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What determines the duration of larval stage?
Why do insects have very long pre reproductive periods and very short reproductive periods? Is there a common characteristic that can indicate the duration of these stages or offer an explanation for the same?

I honestly find the question a bit too broad, since insects are a very diverse group that use a wide variety of substrates and environments. Is there a group of insects that you are particularly interested in? Generally, development time is often a function of food substrate quality (i.e. the food niche of the larvae) and temperature (especially for insects in a temperate environment). In the case of e.g. saproxylic (wood-living) beetles, development time is shorter for species that use the phloem of rather fresh wood and long for species that use dry core wood.

Also, in colder climates development times are longer due to shorter larval activity periods, so development times between individuals can differ e.g from 1-3 years depending on climate, location (open/sunny or closed) and substrate quality.

I actually see two different questions in your question. The first is "what determines the duration of the larval stage ?", the second is "why is this duration longer that the adult stage ?"
A) What determines the duration of developmental stages?

First, you must note that not all insects follow the same development process. Holometabolous insects (e.g. butterflies) have four life stages: egg, larva (with several instars), pupa and adult (or imago). On the other hand, hemimetabolous (e.g. bugs) only have three life stages, and some insects are ametabolous, i.e. no metamorphosis. Development time thus greatly depends on the mode of development. Of course, there can also be a huge variation within insects that have the same mode of development.
What else determines the duration of developmental stages ? (i.e. eggs/larva/pupa) A large combination of factors. Before they reach the adult stage, insects need to accumulate enough energy to undergo every developmental step and become mature. Resource quality and availability of course influence developmental "speed", but abiotic parameters such as temperature or humidity are also of prime importance. Actually, development time of many insects can be measured in degree days, which corresponds to the accumulation of temperature over time. For instance, larval-pupal development of the codling moth Cydia pomonella can go from 1 to about 6 months, according to temperature conditions.

B) Do insects have longer pre-reproductive periods that reproductive periods ?

It depends. There is a huge variation a) in the lifespan of all insect species, b) in the relative length of their developmental stages.
Some insects indeed have a very short adult life stage, relatively to their developmental stages. Mayflies are a classical example, but it's also true for many butterflies and moths of for mosquitoes, for instance.
On the other hand, it's not true for many other insects. Many Coleoptera (e.g. beetles, cockroaches) can have several-month long adult lives, sometimes way longer that their life as a larva. Bees are a more extreme example: bee queens need three weeks to become fertile, and can then reproduce during several years (same for ants).

C) Why do s̲o̲m̲e̲ insects have short reproductive periods ?

To my knowledge, the reasons are mainly ecological. Insects that have short adult lives are often fragile, flying insects that disperse a lot. They face an increased risk of predation as well as environmental fluctuations (weather, etc.) against which they are poorly protected. Besides their resources (e.g. sugar) may be scarce or poor-quality - some even do not have the ability to feed, e.g. mayflies.
What about evolutionary reasons? Developmental stages need some time because, as I said earlier, insects need to acquire a lot of energy to pass all developmental steps. I didn't even talk about metamorphosis, which is a complete cellular re-organization -that takes some time. On the other hand, adults just need to mate and/or lay all their eggs before they die. They don't need to live too long as they'll probably die soon anyway. Think about mayflies: they are less protected as free flying adults that as underwater-protected nymphae. And they'd better try to maximize egg laying in a reduced time.
Besides, note that there is a difference between potential lifespan and realized lifespan. For instance, parasitoid wasps can live up to 30 days in safe, food-abundant conditions - in the wild however, they often live just a few days.

References
https://www.terminix.com/blog/bug-facts/how-long-do-bugs-live/
Harvey, J. A., Cloutier, J., Visser, B., Ellers, J., Wäckers, F. L., & Gols, R. (2012). The effect of different dietary sugars and honey on longevity and fecundity in two hyperparasitoid wasps. Journal of insect physiology, 58(6), 816-823.
Müller, T., & Müller, C. (2015). Behavioural phenotypes over the lifetime of a holometabolous insect. Frontiers in Zoology, 12(1), S8.
Rafoss T, Saethre M-G (2003) Spatial and temporal distribution of bioclimatic potential for the codling moth and the Colorado potato beetle in Norway: model predictions versus climate and field data from the 1990s. Agric Forest Entomol 5:75–85


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Does the theory of evolution fail to explain people sacrificing their lives for their enemies?
Monika i Marcin Gajdowie, "Rozwój. Jak współpracować z łaską", the very beginning of the book:

Przede wszystkim jednak, niektórzy z nas są gotowi oddać życie z miłości do nieprzyjaciół, a to zaprzecza instynktowi przetrwania. Ten absurdalny krok nie daje się wytłumaczyć teorią Darwina.

My translation:

And above all, some of us are ready to forfeit their lives from their love to their enemies. This contradicts the survival instinct; such an absurd act cannot be explained with Darwin's theory.

To give some context: As is evident from later sentences from this book, what I quoted above is one of the few arguments the authors present while trying to support their claim that men "also belong to the supernatural order" (they write from a Christian POV).
This is not, however, what I'd like to focus on in this question.
Instead, my focus is: Does the theory of evolution indeed fail to explain the cases when someone sacrifices their life for their enemies?

The question is not very well worded. It's a good evolutionary psychology question. It's paralleled with human ability to commit suicide, which goes against the survival instinct. The fact that humans invent lots of deadly weapons and tortures and also go to war does not place men in the supernatural order, it's animalistic. The creation of simian deadly weapons is recent in evolution, and it's artificial, not supernatural, so it facilitates intra-species killing. Defensive suicide is very rare vs deserters, it's actually either last ditch attack or a brainwashed kamikaze/suicide bombing.

You might ask yourself some more pertinent questions, like "what did the theory of evolution attempt to explain?". Not altruism (or why people vote the way the do, which is generally selfishness) but something about how different species arose, I believe. And "does the evidence support the actual theory?". On a different level, you might ask yourself why the vast majority of biological scientists accept the theory and wouldn't waste their time arguing about it.

Possible duplicate of Why do some bad traits evolve, and good ones don't?

And above all, some of us are ready to forfeit their lives from their love to their enemies. This contradicts the survival instinct; such an absurd act cannot be explained with Darwin's theory.

There are two problems with this statement, which make your question whether evolution might actually explain such behaviour, essentially meaningless:
1) The statement assumes that certain actions (which are just assumed/proposed to occur) of individuals go against a 'survival instinct' and therefore contradict the theory of Darwin.
There are a lot of problems with that assumption:

the 'theory of Darwin' is quite far away from our modern theory of evolution
Evolution acts on a species, not on individuals. Therefore even if some individuals show a behaviour that is not favourable, evolution still works as normal (and that behaviour may or may not be selected again within a couple of generations).
Acting against a 'survival instinct' can in principle be beneficial to the survival of the species, even if detrimental to an individual (think of parents sacrificing themselves for their offspring).

2) An 'enemy' is an utterly human concept and has no meaning in the context of evolution or biology.
From a scientific standpoint something like "forfeit their lives from their love to their enemies" makes absolutely no sense.
An individual can sacrifice themselves in certain situations, this may just end their life and therefore be an evolutionary disadvantage. However, - in other situations - it might also help their offspring or other individuals of the species in survival and therefore be an evolutionary advantage. There is no way determine a priori whether such an action will always be beneficial or always negative - both options are possible depending on individual context.

Re "From a scientific standpoint something like "forfeit their lives from their love to their enemies" makes absolutely no sense."  It also doesn't make much sense linguistically, either.  You might also consider that it's seldom a straightforward case of sacrifice, but of risk.  The individual who e.g. risks his life to defend the tribe from a sabertooth may die, but he also may live, be hailed as a hero, and have lots of opportunity to spread his genes around as a result.

If you're asking if evolutionary explanations of suicide have been proposed... they have e.g.:

The altruistic suicide hypothesis posits that the presence of low reproductive potential and burdensomeness toward kin can increase the inclusive fitness payoff of self-removal. [...]
Altruistic self-destructive behavior has been found in a wide variety of organisms, ranging from unicellular organisms and parasites to social insects, and is debated in mammals. Self-destructive defensive behavior has evolved independently in a number of social insect species in response to natural enemies. Self-sacrificing behavior has mainly been found in the context of nest protection. Defensive self-sacrifice persists in social insects because of its positive impact on the fitness of the colony’s reproductive individuals. As with other forms of altruistic traits, the genes involved will pass on to subsequent generations.

One interesting paper proposed (using simulation) that

Altruism-benefiting fellow group members at a cost to oneself-and parochialism-hostility toward individuals not of one's own ethnic, racial, or other group-are common human behaviors. The intersection of the two-which we term "parochial altruism"-is puzzling from an evolutionary perspective because altruistic or parochial behavior reduces one's payoffs by comparison to what one would gain by eschewing these behaviors. But parochial altruism could have evolved if parochialism promoted intergroup hostilities and the combination of altruism and parochialism contributed to success in these conflicts. Our game-theoretic analysis and agent-based simulations show that under conditions likely to have been experienced by late Pleistocene and early Holocene humans, neither parochialism nor altruism would have been viable singly, but by promoting group conflict, they could have evolved jointly.

And I'm not sure people sacrifice themselves for their enemies often enough for that to be worthy of constructing an (evolutionary) explanation for. It might be like asking what's the evolutionary explanation for the moon being made of cheese. Even assuming that this phenotype (sacrificing for their enemies) does occur with some low but non-zero probability (that onus is on you prove it's higher), that doesn't invalidate the theory of evolution for a couple of reasons:

Selection doesn't act instantly to produce a perfectly fit population, instead fitness increases over time more like a power law, at least in microbes where it's easily quantified. Various loci may be under different levels of selection pressure, depending on the environment. Even assuming the mutation that causes the phenotype is uniformly detrimental to fitness (which might actually not be the case, depending on variations in the environment), weak selection can cause it to linger for a long time; see Huntington's disease as an example of weak selection. (And more recently it's disputed whether the mutations that cause Huntington's provide no fitness advantage whatsoever; the technical term for a tradeoff being "antagonist pleiotropy".)
Current estimates put the percentage of human genome that evolved due to chance alone to around 5%. Random occurrences of "weird" phenotypes can thus happen with some fairly low probability.


text:
Is spiders building webs on plants an example of mutualism or commensalism?
In one section of the GED study book I'm looking through to prepare myself for exams, they define parasitism, mutualism, and commensalism, and give examples.
One of the examples they give for mutualism is ants living in an acacia tree. The ants get a home, and they defend the tree.
One of the examples they give for commensalism is a spider building a web on a plant.
Is this actually an example of commensalism? This seems more like mutualism to me. The spider benefits from being able to put its web somewhere, and the plant benefits from protection from bugs (as the spider's web will catch them).
Is this relationship an example of commensalism or mutualism?

You're thinking too broadly and rigidly about these concepts -- both commensalism and mutualism are types of interspecific interactions.
Commensalism is when one species in a given interaction is benefited while the other is neither benefited nor harmed. In a mutualistic interaction, both species benefit from their interaction with each other.

Like any interaction between two organisms, these interactions can vary between individuals. Although some species pairs will consistently undergo the same type of interaction (e.g., shark and prey -- predation), some groups of species may vary in their paired interactions. This variation may result from two different scenarios:

Variation in interaction type between different species within a taxonomic group

E.g., one type of spider catches insects that don't harm the plant -- commensalism -- while another spider species catches insects that would harm the plant -- mutualism. In other words, not all spider-plant interactions are the same, and the interaction type may be dependent on the species involved.

Variation even from the same individual in different circumstances.

E.g., A spider catches an insect that doesn't eat the plant it's growing on (commensalism) but at another time it catches an herbivorous insect that does eat the plant the spider has built its web on (a mutualistic behavior). In this scenario, the interaction type between the same two species (even the same individuals) can vary based on circumstances.

Put differently, commensalism, mutualism, etc. are not behavioral traits, but interactions, and so are dependent on not only the species involved but the circumstances as well.
Note: To further complicate things, each given interaction can be qualified in various ways. For example, from Wiley ELS:

Positive interactions can be trophic and nontrophic, can act directly or indirectly (mediated by a third species) and can be symmetric (species have equal effects) or asymmetric (species have unequal effects).

For the scenario you laid out, the short answer is yes.
Like @theforestecologist pointed out, interactions can be complex and contingent.
Although, in the example you give, it can be easily tested: grow plants with spiders and without, and see if there is a difference in plant fitness. Fitness can be measured directly by looking at, for instance, the number and quality of seeds the plants in each group produces. But fitness can also be measured indirectly by looking at the amount of herbivory on the plants (e.g., scars), the number or area of leaves before and after the spider treatment, photosynthetic rates, etc.
If a fitness benefit can be demonstrated with both species involved, then it is considered a mutualism.

Great experimental/application point! +1. Very clear that this fitness experiment could be used to begin getting at the predominant interaction type. Thanks


text:
Calculating Possible Combinations of Bases in a DNA Strand of a Given Length
In my Biology class we were asked this question:

This DNA strand consists of eight pairs of nitrogenous bases. How many different sequences of eight bases can you make? Explain how you found your answer.
I guessed either 28 or 8!. Apparently, the answer is 8! ÷ 24. I asked my teacher, but she did not know the answer. Does anyone know why this would be?

The answer your teacher gave you might be the answer to the question of how many sequences of 8 bases can be formed using only the bases shown in the diagram, each one can be used once. The factorial comes from the fact that once you pick a base there are n-1 options left and so on. 2^4 is 222*2 which accounts for there being four duplicate bases so that count only unique sequences.

Don't guess! You need to learn to approach this sort of simple statistics logically as laid out by @Remi.b. The relevence of this sort of problem to biology is more in relation to the frequency of restriction sites, which are smaller and a better place to start. You can find lots of practice questions and an explanation of how to answer them on a self-teaching resource I put up for students at my own university. Give it a try.

At each base, you can have 4 different bases (A,T,C or G). Therefore for the first base there are 4 possibilities, namely

A
T
C
G

For the first two base pairs there are $4^2 = 16$ possible combinations
(I'm no good with math but the premise below is in error. If there is an A then it can only be paired with a T if there is a T it can only pair with an A C with G and G with C. So many of the below listed options will not occur - changed to italics)

AA
AT
*AC
AG*
TA
*TT
TC
TG*
*CA
CT
CC*
CG
*GA
GT*
GC
GG

For the first three bases, there are $4^3$ possible combinations. For 8 base pairs, there are $4^8 = 65536$ possible combinations. $2^8$, $8!$ and $8! + 2^4$ are all wrong.

I think the problem asks combinations with bases in the given sequence. There is 2 of each of A, T, G, and C. So the combinations come out to 8!/(222*2) which is the answer their teacher provided.

Unfortunately @Remi.B is wrong. His answer allows the choice of any base for each position. This includes arrangements such as AAAAAAAA which is not possible as there are only two A bases. User40950 is correct in his comment. Here is a little more expanded version of his comment.
If we label the bases as A1 A2 C1 C2 G1 G2 T1 T2 then there are 8! possible arrangements. Notice however that interchanging A1 and A2 while leaving everything else unchanged yields the same arrangement, hence we divide the answer by 2. This same argument applies to each of the other duplicate pairs, so we divide the answer by $2^4$. Thus the final answer is
$8!/2^4$


text:
How does the body detect irreversible binding to receptors?
I have read an article on Wikipedia about irreversible agonists and antagonists. These permanently bind to a target receptor on a cell. However, the receptor protein is then internalized and recycled by the body after the binding occurs. How does the body detect when a protein has been irreversibly bound in such a way? Is there some pathway involved in that or are proteins simply regularly recycled by the body?
Article: https://en.wikipedia.org/wiki/Irreversible_antagonist

I've edited your question to, I think, clarify what you meant by "damaged". Usually, "damaged" proteins refers to, e.g., oxidative damage, or some change other than that of a ligand binding (even if irreversibly), and "how does the body detect damaged proteins" is, i think, a different question from the one you are asking.

The process of downregulating a receptor by internalizing and degrading it in response to (sometimes prolonged) activation or (sometimes prolonged) failure to activate is what pharmacologists call desensitization (in either context). You can read about this generally in Goodman and Gilman's Pharmacological Basis of Therapeutics, Chapter 3, under the subsection "Receptor Desensitization and Regulation of Receptors". There are a number of mechanisms, not all well understood, but the basic idea is that when a signal is constant (either always on or always off), it no longer has any value as a way of providing information. Receptor regulation, or desensitization, is a mechanism for, effectively, resetting the cell or tissue. Removal of the receptor can be followed by recycling, or protein synthesis and return of new receptor to the site.
One well studied mechanism for desensitization is seen in G protein coupled receptors (GPCRs), such as some Dopamine receptors. It is well reviewed here.
To answer your specific question, binding that leads to desensitization is detected the same way any other binding is detected. A receptor produces a signal on binding (or stops producing a signal). The downstream effect of that signal includes a process that involves internalization of the receptor from a location where it can receive signal.
Here that process is mediated by phosphorylation by GRKs (GPCR kinases), which allows for binding of arrestin, and so on...

It would be great if you can provide some information on whether this feedback is thresholded (like sigmoidal kinetics or similar dynamics).

@WYSIWYG i don't happen to know the dose response relationship here. I'd welcome an answer that adds this information.


text:
What cell types comprise the median eminence and the tuber cinereum?
I have tried pretty hard to get a detailed description of what exactly the median eminence and the tuber cinereum are but to no avail. I am very familiar with their anatomical relationships (spatially) with the hypothalamus, 3rd ventricle, mammillary bodies, etc; however, I still do not quite understand what they are or what cell types comprise them.
Are they areas of grey matter? Are they some sort of modified ependymal cell layer of the 3rd ventricle floor?
Or are they areas of connective tissue that merely "house" white matter projections from the hypothalamus to the pituitary? So, to repeat the inquiry from above:
What cell types comprise the median eminence and the tuber cinereum?
And, moreover, what's the actual function of the cell types that comprise them?

Have you read the Wikipedia articles on both structures?

I do not see anything in the articles that even remotely talks about cell type...and seeing as that is the topic of this inquiry.

The tuber cinereum is the "swelling" at the ventral surface of the hypothalamus (Subarachnoid space surface) at the base of the infundibular stalk. The median eminence (a circumventricular organ) is an elevation on the ventricular surface of the infundibular recess of the 3rd ventricle.

Welcome and thanks for your answer. Unfortunately it doesn't answer the question as OP specifically says they are familiar with anatomy of said structures.

Since the question title asks specifically about the cell types, could you maybe edit your answer and add this information?


text:
Is it PSI-BLAST or BLASTP if I use PSI-BLAST for only one iteration
In my case, I used PSI-BLAST in the local BLAST+ to search queries against the self created database. After the first search, I added the searched result to the database and then conducted the multiple sequence alignment myself with MUSCLE to get the conserved parts. Then, I searched the queries against the consensus sequence obtained from the multiple sequence alignment (without gap). In this process, I did not calculate a PSSM, while the first iteration of PSI-BLAST uses a constant matrix, which is much similar to BLASTP. So what did I actually use in the process – PSI-BLAST or BLASTP?

You simply used BLASTP against a consensus sequence. The first iteration of PSI-BLAST is identical to BLASTP.


text:
Why do fruit flies go so close to large reservoirs of liquid when they are likely to fall in due to surface tension?
I had accidentally left out half a glass of red wine by the windowsill when I went to sleep. As anyone knows, if you do this with a window cracked you will get quite a few fruit flies near it in that time(region dependent obviously).
I noticed that many of them had simply fallen in as there was nearly nothing on the sides of the glass. What causes this behavior in a likely death scenario? Is it only exhibited during extreme hunger? Would this also not likely be an evolutionary cost or is that outweighed?

Fruit flies are attracted to the smell of alcohol (~rotten food). Large reservoirs of liquid alcohol in which they could drown seem rare in nature. There are some (selectable) reasons why flies are drawn to the smell of alcohol. Anecdotally, never seen a fruit fly drowned in liquid water suggesting that they cope fine with more frequently occurring liquids.

@tsttst Even just the time we've been industrialized would be reasonable to start to be negatively selected for in a species like this no?

Might as well ask why they like to land on solvent-borne paint... and permanently get stuck in it. I suppose they can fly off the surface of liquid... under normal circumstances.

As indicated by their name, fruit flies can be found on fruits, where they prefer to lay their eggs. Since the larvae feed not on the fruit itself but on microorganisms found on rotting material, they will especially target overripe fruits. Therefore fruit flies have evolved to identify and respond to odors emitted from ripe fruits. Red wine similarly emits odors that are attractive for fruit flies. Since fermentation is a form of controlled rotting (in both cases material is decomposed by microorganisms), the resulting compounds can be similar, which includes ethanol and 2-phenylethanol.
So, fruit flies are attracted to the smell of wine, that's why they approach the glass. Due to their small size and the surface tension, they should be able to land on water without drowning. But wine isn't water. With an ethanol concentration of 12% we see a reduction in surface tension from ~72mN/m to ~45mN/m, which is comparable to adding some detergents.

This explains, why the flies are not able to escape and drown after landing. I would nevertheless argue, that the selection pressure isn't strong enough for an evolutionary adaptation. In their natural environment, they usually would not encounter large bodies of liquid which they are attracted to and which are not able to hold their weight.
In evolution and behavior we have to consider the entire species. While a few unlucky animals will die in wine glasses, most other flies will not. For them being attracted to the smell of overripe fruit and ethanol is an advantage. It's a cost and benefit calculation. For the species, the costs of a few individuals dying is outweighed by the enormous benefit of finding a good place to raise their offspring (laying eggs into rotting fruits). Therefore, the attraction to these smells and approach are positively selected for, even though this results in death in wine for some members of the species.
Watching fruit flies at a trap, you see that mostly flies land on the container rather than on the liquid, indicating that they already avoid touching down on liquid. On the other hand, fruit flies don't seem to be very acrobatic, with a part of their landings being "crash landings". Hence, some of these flies might just accidentally end up in the liquid or by walking down to the edge of the liquid and being caught up by it when touching it. Even though I couldn't find hard data on this, "landing on liquid reservoirs" doesn't seem to be necessarily a strong behavior in fruit flies, that evolution could negatively select for.

Although this is from  a popsci article, a biologist says that fruit flies can normally land on liquids and take off from them thereafter:

However, simply leaving a shot glass full of fruit-vinegar will only serve to feed the flies. The surface tension of the liquid [Ed. note: You remember surface tension, right?] allows fruit flies to land on liquids but not drown.
To break the surface tension you’ll need a tiny bit of dish soap. Dish soaps contain surfactants, which are molecules with a head that likes water, and a tail that doesn’t. Because of this property, the surfactants tend to situate at the interface of air and water, forming molecular “cliques” that disrupt the surface tension of water.
By putting a tiny bit of dish soap on your finger, and touching it to the surface of the vinegar in the shot glass, you will add enough surfactant to break the surface tension. (Add too much and the molecules in the dish soap will alert the fruit flies to danger).
Now fruit flies will unknowingly attempt to land on the vinegar for a little sip, then, before they can react, will break through the surface tension and begin to drown.

So if this is true/confirmed, then they do have enough of an evolutionary adaptation to the [surface tension of the] usual liquids of their diet. Just not to [trace] dish-soap contaminated liquids.
And I can confirm from a peer-reviewed paper that dish soap is indeed used even in science trapping experiments:

The cup trap (figured by Beers et al. 2010) is a 946-ml clear plastic
drinking cup with a clear plastic lid (Solo, Urbana,
IL), with four 1-cm-diameter holes in the sides of the
cup near the top. A drowning solution or drowning
solution plus bait was placed within the cup. Forty
grams of boric acid and 0.5-ml liquid dishwashing
soap (Palmolive Pure and Clean Spring Fresh Dishwashing Soap; Colgate-Palmolive Company, New York, NY, USA) were added to a batch of 3.8 l of
water or aqueous bait to make a drowning solution
used in all traps. Boric acid served to inhibit microbial
activity of baits and captured insects, and soap
reduced surface tension to promote capture and submersion of trapped insects. For both types of traps
and all treatments in all experiments, each trap contained either 300 ml of drowning solution or 300 ml
of bait in drowning solution

0.5ml of soap to 3.8l of water is very little, but that's all it takes to drown the little flies. It seems entirely plausible to me to have this level of trace contamination on glasses that have been dishwashed.
And as a complementary survival mechanism, fruit flies can apparently survive 12 hours of drowning at room temperature (or more in lower temperature):

Flies submerged at 23°C did not survive after a submersion time of 12 h whereas flies submerged at 3°C survived up to 72 h of submersion.

@Frieke may be on to something, namely that ethanol lowers the surface tension of the solution (with water) by itself, significantly. At 20-25 degrees C, pure water has a tension of about 72 mN/m. Adding 10-15% ethanol lowers that to about 47-42 mN/m. Also, the trapping science paper does mention that

Very few flies were captured in traps baited with 10% ethanol in water.  Traps baited with a combination of acetic acid and ethanol in water captured more SWD flies than traps baited with acetic acid or ethanol solutions alone.  These results indicate a synergy of the two materials, and of the two chemicals, as lures for SWD.

Interestingly wine has substantially higher attractive effect than an equivalent ethanol solution though:

Wine is about half as effective a vinegar and about a quarter as effective as a combination of wine and vinegar. On the other hand, a 10% ethanol solution was 20-50 times less effective than alcohol 10% plus acetic acid 2%. So there's more to wine than ethanol that attracts the flies.
So the flies probably do avoid the higher alcohol concentrations... unless there's also vinegar.
Another paper finds that wine's surface tension is mostly determined by its alcohol content.

So it does look like:

Fruit flies are fairly strongly attracted to wine (on the same order of magnitude as to vinegar).
The surface tension of wine is substantially lower than that of water.

I'm still not sure what the surface tension of (2%) vinegar might be, in comparison. Pure acetic acid has substantially lower surface tension compared to water, about 27 mN/m at room temperature. And if Wikipedia is correct, 10% acetic acid solution has about 55mN/m around temperature. So acetic acid lower the surface tension less than ethanol, but not by much less. On the other hand, fruit flies are much more attracted to acetic acid than to ethanol (alone). So perhaps that's enough to explain why they drown easier in wine.
Actually it look like Wikipedia is wrong here. From an authoritative source, acetic acid has nearly the same effect as wine on surface tension; at 11.4% it has 43.5 mN/m; just 3.2% is enough to lower the tension to 55.6mN/m; at 1.6% it's 61.7mN/m.

So probably just the fact that acetic acid is much more attractive to flies than ethanol is the only factor (other surfactants excluded). Perhaps they "confuse" a higher concentration of ethanol to a lower concentration of acetic acid, which they would be able to handle as far as surface tension goes.
Yet another source (actually quoted in the previous one, on the next page) gives even lower values for ethanol surface tension.

Apparently determining surface tension is a hard problem, both experimentally and theoretically. So I'm not sure we can properly compare figures reported in different sources. Alas no single experimenter has done both ethanol and acetic acid in the same paper/setup. But what was observed about their relative attractiveness to flies is probably sufficient...
And for ballpark comparisons, a similarly or lower surface tension as that of 10% ethanol (or acetic acid) i.e around 30-40mN/m can be obtained by a adding a few ppm (parts per million) of a surfactant, such as LAS or AE.

And as related fun fact, it's sex-starved males who prefer alcohol, in fruit flies too! https://www.nature.com/news/rejected-flies-turn-to-booze-1.10227

I appreciate this answer but it doesn't really address why something like this hasn't been and isn't being negatively selected for. For example, one could easily imagine adaptations by which melanogaster evolve aversion to certain liquid smells of those in which the suface tension cannot support. This could even occur via simple reinforcement. Wrt the work on psuedo suspended animation in fruit flies this makes sense as a general survival mechanism but I wonder why a more nuanced model has yet to be selected for.

@hisairnessag3: not enough evolutionary pressure for that until now, apparently, at least at the trap concentration. See https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont The first quote does mention that they can detect the detergent at higher concentrations. Perhaps some lab experiment will [try to] evolve a line of flies in that direction.

0.5ml in 3.8l is a 0.013% solution of soap. In half a glass of wine of, let's say, 1/8l=125ml, that would account for about 16microliters of soap. I have not tried this, but I would guess you would taste that if there is that much soap left on your glasses after washing. Therefore it does not seem plausible to me that soap contamination levels would be high enough for drowning the flies. Do you have any idea about surface tension of alcoholic solutions compared to water?

@Frieke: apparently alcohol has lower surface tension than water: https://en.wikipedia.org/wiki/Tears_of_wine That might also explain it, since the science paper also mentions that high alcohol concentrations don't attract flies much. Small amounts of alcohol mixed with vinegar have a better attraction effect. And since alcohol also seems to affect the nervous system of the flies (see 1st comment), it's possible they also get "drunk" which might contribute to them getting drowned easier in the presence of alcohol.

@Frieke: However, the wiki link also says that in an alcohol solution the alcohol evaporates faster at the surface, so the surface tension of the solution is probably close to that of the solvent (water).

Thanks for the edit. I still think you can delete or shorten the soap part, since this is in my opinion not relevant for the issue. you have covered the attraction to wine (and fair enough, some of it might have turned into vinegar over night) and the lower surface tension that would contribute to the flies drowning, but you haven't touched on the evolution part of the question.


text:
What exactly is this small puffer fish doing and how did it manage to accomplish such a feat?
I recently saw a video on youtube  where it shows a puffer fish making intricate designs in the sand:
OZZY MAN VIDEO
The puffer fish made this design on the sand:

What exactly is the puffer fish doing and how is it capable of accomplishing such a feat?  Is this behavior learnt, or innate?

A tiny Japanese puffer fish creates a grand sand sculpture on the featureless seabed by using his fins to dig furrows. He uses this to attract the attention of passing females.

Why do puffer fish build sandcastles? (BBC)

Further observation revealed that this “mysterious circle” was not just there to make the ocean floor look pretty. Attracted by the grooves and ridges, female puffer fish would find their way along the dark seabed to the male puffer fish where they would mate and lay eggs in the center of the circle. In fact, the scientists observed that the more ridges the circle contained, the more likely it was that the female would mate with the male. The little sea shells weren’t just in vain either. The observers believe that they serve as vital nutrients to the eggs as they hatch, and to the newborns.

http://www.spoon-tamago.com/2012/09/18/deep-sea-mystery-circle-love-story/

Here is the source of the video:

Puffer Fish Constructs A Masterpiece of Love - BBC Earth (YouTube)

The following papers analyse said structures and the ethology in more depth:

We report that male pufferfishes (Torquigener sp., Tetraodontidae) constructed large geometric circular structures on the seabed that played an important role in female mate choice. Males dug valleys at various angles in a radial direction, constructing nests surrounded by radially aligned peaks and valleys. Furthermore, they created irregular patterns in the nest comprising fine sand particles. The circular structure not only influences female mate choice but also functions to gather fine sand particles in nests, which are important in female mate choice. Strangely enough, the males never reuse the nest, always constructing a new circular structure at the huge cost of construction. This is because the valleys may not contain sufficient fine sand particles for multiple reproductive cycles.

Role of Huge Geometric Circular Structures in the Reproduction of a Marine Pufferfish (2013)

Here, we examined the process of the outer ring construction, and extracted the ‘rules’ followed by the pufferfish. During construction, the pufferfish repeatedly excavates ditches from the outside in. Generally, excavation starts at lower positions, and occurs in straight lines... A simulation program based on these data successfully reproduced the circle pattern, suggesting that the complex circle structure can be created by the repetition of simple actions by the pufferfish.

Simple rules for construction of a geometric nest structure by pufferfish (2018)

Ok thanks +1. But this only answers the first part of the question. How is such a puffer fish capable of doing this?  Is this knowledge learnt or ingrained?

@user35897 I've added a quote from a paper which simulates the construction. It appears we don't yet know if it is learned behaviour, but in any case it only seems to require a small number of simple movements, repeated.

i would bet that the behavior is instinctive but also influenced (perhaps) by the structure the male rears the young in. note how hard it would be as hatchling to learn the patterns in this way --seems like if the pufferfish do learn from their dads this is unusual intelligence. not hard to test this by comparing fish removed very early from nest vs those reared the normal amt of time. also, testing of intelligence (like maze navigation which i bet both sexes would be good at) might reveal some surprises.

This "nest" is created by a male pufferfish for both courtship and for rearing young.
The male puffer fish uses its body and fins (a combination of pectoral, anal, and caudal -- see here) to break up the sand into fine particles and to move it around into the pattern seen above. It swims in channel-like (or furrow) patterns to create the ray pattern seen:

You can see a more complete video of this action through this BBC video on Youtube.
According to here and here this male puffer fish does all this to attract a female. National Geographic adds:

The circles, scientists say, are actually nests created by male pufferfish, which spend about ten days carefully constructing and decorating the structures to woo females. What’s more, this industrious pufferfish is thought to be a new species in the Torquigener genus, according to the study, published July 1 [2013] in the journal Scientific Reports....
When a potential female partner arrives on the scene, the male stirs up the fine sand in the nest’s inner circle. If she deems the nest, and the male who built it, satisfactory, she lays her eggs in the center of the nest and leaves.

Scientists are not sure why building intricate sand nests attract mates, but perhaps a larger, more-intricate nest (i.e., one that took a long time) could indicate to the female that the male is stronger or more fit.
All this effort does not stop at courtship however. Again from Nat Geo:

Once the female splits, though, it’s the male who does the parental chores: He remains in the nest until the eggs hatch six days later.


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If bacterial resistance randomly occur, then why limit broad-spectrum antibiotic use?
If there is importance to study some discipline, then one of the main matters is its applications, so besides the primary goal of knowing the truth of the matter regarding what that discipline is investigating, applicability or usefulness of that study in other fields or in the field itself is a very important matter. I'll direct my attention here to Evolution, and its mechanisms. So accordingly if something that I personally want to come up with is application of that knowledge to the field of my work.
In reality we don't study evolution extensively at college level in medicine, since it doesn't have a direct clinical impact on the diagnosis and treatment of patients in most of the cases. However, one possible area of interaction is "bacterial resistance to antibiotics", since this is related to "mutations", and generally viewed as a mechanism whereby the bacterium adapts to its environment.
Now all of my life in medicine from college through specialty and academic teaching, we've never ceased being reminded about not dispensing antibiotics liberally, and the main concern outlined is "emergence of resistant strains of bacteria" due to this liberal use of antibiotics itself. There are other reasons of course, like side effects and cost, but they are not the main concern most of the times.
During my recent review of Evolution, looking at the introductory courses that were cited to me by many participants here, in particular this page of Evo101 titled "Mutations are Random" I was really shocked to know that even the mutations that resulted in bacterial resistance were not "directed mutations", i.e. it is not the case that the exposure to the antibiotic caused the bacteria to have that mutation in the first place, actually the page mentions Esther and Joshua Lederberg experiments showing that those resistant bacteria were already there before the population was exposed to the antibiotics?
So why have we been always reminded by bacteriologists of limiting our antibiotic usage if emergence of drug resistance is not due to exposure to it?
Actually, its not only that, many lectures we attend, which are pretty much delivered by official bodies, does mention of emergence of antibiotic resistance as a DIRECTED mutation response to exposure to the particular antibiotic, that almost most of us we clinicians became to think that this is a fact. For example hospital bacteria are of the most resistant ones, especially those in intensive care facilities. The association between exposure to antibiotics and emergence of drug resistant bacteria to them is almost hammered in our brains, that to discover that the mutation was already there before exposure to the antibiotic seems quite shocking, at least to me in person.
My question here is the following:

Is it a scientific fact that emergence of bacterial resistance through mutations is always random, i.e. in the sense that it is not a directed response to exposure of the population to that antibiotic?

For instance this seems to be a counter-example.
If that is the case then why bother about liberal use of broad-spectrum antibiotics? I mean as far as emergence of bacterial resistance is concerned!
I mean its not the case that I'm going to eradicate the "useful bacterial" that could rival the pathogenic resistant bacteria, by that liberal use of broad-spectrum antibiotics. If that happens temporarily we can in principle replace them back, like with the use of probiotics.
During my surfing of the web I found that page addressing the same point, but the responses are not that explicit, and far from being convincing?

See related questions https://biology.stackexchange.com/questions/55372/have-bacteria-evolved-antibiotic-resistance-in-a-laboratory-setting https://biology.stackexchange.com/questions/28379/does-long-term-use-of-antibiotics-in-humans-actually-lead-to-a-greater-risk-of-i https://biology.stackexchange.com/questions/14350/can-antibiotic-resistant-bacteria-compete-with-normal-one-in-an-antibiotic-free

Also see https://biology.stackexchange.com/q/48724/3340

You're correct, this is extremely relevant, and it's unfortunate that your medical education didn't include good instruction about evolution.
You point to some very useful and interesting studies. I'm particularly fond of the studies that demonstrate the early existence of antibacterial resistance genes, e.g., in ancient permafrost.
Now to your question

Is it a scientific fact that emergence of bacterial resistance through mutations is always random, i.e. in the sense that it is not a directed response to exposure of the population to that antibiotic?

I think the issue here is a conflation of two separate concepts. Mutation is one mechanism for producing variation. Mutation can be understood as a stochastic process, causing changes in the genome of an individual by chance.
Evolution occurs because of existing variation. Evolution is not a stochastic process. It is a biased process, a change in the distribution of existing variation.
The emergence of antibacterial resistance is evolution that results from selection acting on existing variation. Emergence here refers to emergence of a resistant variant within a population. Selective pressure (application of antibiotics) causes a predictable change in the frequency of genes that would allow reproduction in that environment, the frequency of existing resistance genes increases in the bacterial population.
Though there is evidence for important antibacterial resistance mutations pre-dating the use of antibiotics, this does not rule out the occurrence of spontaneous mutations, as demonstrated in the article you linked. The production of genetic variation by random mutation can be followed by a rapid increase in the frequency of a new genetic variation that is selected for in a given environment. This can be particularly likely in organisms with high error rates, short generation times, and large numbers of individuals. The spontaneous mutation isn't directed, as you say. It is random. The selection of that particular random mutation is directed, though.  Once the random mutation occured, then we can say the variation exists. Then selective pressure acts on existing variation, allowing evolution, a change in the frequency of the, in this case, gene for resistance.
Goodman & Gilman, one of my go to pharmacology references, actually has an excellent discussion of these concepts as they relate to antibacterial resistance, in Ch. 48, under the subsection EMERGENCE. There is a good discussion of the various mechanisms of emergence, but this general statement is helpful:

Mutations are not caused by drug exposure per se. They are random events that confer a survival advantage when drug is present. Any large population of drug susceptible bacteria is likely to contain rare mutants that are only slightly less susceptible than the parent. However, suboptimal dosing strategies lead to selective kill of the more susceptible population, which leaves the resistant isolates to flourish.

I think most medical schools around the world don't have a meticulous course on evolutionary biology. Actually the trend is going more and more towards clinical based teaching with reduction of most of what is used to be taught in basic sciences in colleges before, only those parts relevant to clinical practice are highlighted nowadays, the others are actually selected against and they are vanishing with time. I don't know why evolution was already minimal, and even in the future it would most be mentioned  in relation to possible applications only.

@ZuhairAl-Johar there is a lot to teach in medical school. In the US, it's in the prerequisites for admission, and taught in this context in microbiology and infectious disease.

Yes in where I live its also taught in secondary schools but not that deep anyway. I'm speaking about matters related more specifically to medicine. I see that Remi.b had pointed to evolutionary medicine. which unfortunately never been even heard of in most medical schools

The mutations are random, the survival and spread of bacteria with said mutations is NOT random.
Evolution and selection are situational.
The careless use of antibiotics causes those mutations and bacteria to spread because they out compete others without resistance. However, often these will not outcompete without antibiotics being present. Often mutations that produce resistance are detrimental when antibiotics are not present, or more precisely the downsides of the mutation are more than offset by the benefits of resistance when antibiotics are present.  Meaning even when they occur mutations the produce resistance die out quickly without antibiotics.
Even when they offer no advantage of disadvantage without the presence of antibiotics normal genetic drift can eliminate them, but when antibiotics are present and a mutation occurs the mutation then offers an advantage and spreads. That means a person is more likely to catch a strain that is resistant than if their was no antibiotics present in the bacteria's environment.
Note the "environment" can be anything from the greater ecosphere down to an individual patient. and population can be the population inside an individual or the population of bacteria across the globe.
lets try a pair of scenarios
In each the mutation for resistance occured in 1% of the population of bacteria.
Scenario 1  no antibiotics. You have a 1% chance of catching a resistant strain.
Scenario 2 Antibiotics present. Now selective pressures quickly change the population so that resistant strains now make up the majority (we'll say 75%). Now you have a 75% chance of catching a resistant strain, and worse those resistant strains now have a high chance of meeting other strains with other resistances or of having another resistant mutation occur (now 1% of 75% instead of 1% of 1%) this means the population becomes even more resistant and it does so rather quickly until no antibiotics work.
So emergence, AKA exposure of humans to resistant strains, IS due to use of antibiotics.
Careless use of antibiotics include.

Use of antibiotics on people/animals/things who do not need it.
Disposal of antibiotics in the environment.
Incomplete courses of antibiotics.

But there is a hidden forth and fifth concern, that is the one your paper is concerned with. Patients and doctors are humans and each of these things will inevitably happen, patients fail to take drugs, or impure drugs are improperly disposed of or a hundred other errors expose bacteria population to antibiotics. So a further concern about having useful antibiotics, by limiting which antibiotics we use, that is by only using common ones unless absolutely necessary, we are minimizing the chances of resistance to those less used antibiotics so we have something that works when we run across a resistant strain.
Lastly people already have bacteria present in their system so these microbes can be exposed to antibiotics targeted at other unrelated infections, thus encouraging resistance. Some are even protected by natural barriers that reduce exposure to antibiotics used to treat other things, like bacteria on the outside of the skin for internal antibiotics. Worse, bacteria can transfer resistance horizontally so these microbes can then share resistance with later infections. So even using  antibiotic A correctly on a patient to kill microbe X can lead to microbe Z developing resistance just because the treatment for X is not enough to kill all Z. Staph is particularly prone to this since it is everywhere. So even if you use antibiotics correctly you can still produce resistant strains of other bacteria.
As a side note some confusion is caused by is a quirk of language and terminology in the study of evolution. If X produces an environment in which a mutation that produces trait Z is favored causing that mutation and thus Z to spread in a population often scientists will just say X caused Z, just to save time. humans are lazy and typing out "X produces an environment in which a mutation that produces trait Z is favored causing said mutation to spread in the population and thus Z to spread in a population." takes much longer and uses more space than "X causes Z to spread" or just X causes Z. Other evolutionary scientists know what they mean but it can be confusing for everyone else. It is not a great practice but jargon creeps into all science.
As a personal note it has always been a concern for me that medical schools don't require an understanding of evolution at least for research fields; infection, cancer, and a million other weird quirks of anatomy and physiology are caused by evolution or evolutionary baggage. Heck infection and cancer ARE evolutionary competitions, and some of the most predictable ones.

I see what you mean. But still there is some difference! The argument is: if the use of a particular antibiotic itself is not the direct cause of a mutation causing resistance to it. Then we shouldn't be afraid form using it for that concern, because simply its not there! As for the argument you've presented what we can do is to simply use broad spectrum antibiotics but with subsequent replacement of the NON-Pathogenic bacteria that are sensitive to that antibiotic. This way we'd change the bacterial environment towards the non-pathogenic bacteria, and try eliminate the pathogenic ones.

Let me specifically present my argument further so that you get the exact context of what's going on in medicine. A clear example is staphylococcal aureus resistance. You hear a lot of call's from bacteriologists not to use the strongest guns against them, the idea is because resistance to even those powerful guns would rise, and this would render us defenseless.  Clearly this is not due to the situation you described, since it would be applicable to lower guns as well. What we often hear is that exposure to this strongest antibiotics itself will cause a mutation causing resistance to them!

for example see this link https://www.ncbi.nlm.nih.gov/pubmed/16271060

@ZuhairAl-Johar Are you saying that's simpler to constantly replace the environmental microbiome than judicious use of antibiotics? What?

@Cell, of course not. I'm saying that we can do that sometimes if we are pushed to. Of course judicious use of antibiotics is already needed for many reasons, not just the emergence of resistant strains.

Let us continue this discussion in chat.


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How do I efficiently develop a plant cultivar?
Or, perhaps: how do I develop a cultivar at all?
First off, my knowledge and experience on the subject is close to nil. I've got a decent enough knowledge of gardening concepts, but have done precious little plant breeding, and nearly everything I know about genetics comes from the reptile hobby and the breeding of various morphs (also haven't done any of that).
But I wanted to try my hand at plant breeding - at least, get started somewhere.
I've decided to go for something simple - a dandelion. Hardy, easy to grow, flowers quick and I know will definitely reproduce for me. Contamination from external sources might be an issue but there's several easy fixes for that. I could probably wait around and inbreed them until some funny traits pop up but for now I want to try some obvious changes - wider leaves, bigger flower, maybe both.
All I (think I) know is that I'll have to keep track of my individuals and their ancestry and select for traits based on their current expression and genetic pedigree. On the surface that sounds pretty simple but I don't know the details of the execution. Is there a specific way plant breeders do it? Software that would make the management easier?
I tried looking this up, but Google isn't very extensive on this subject. Any advice or resources that can get me started would be greatly appreciated.

You have made quite unlucky choice by picking dandelion. Most dandelions reproduce by apomixis. The seeds produced (without polination) are clones of mother plant. It would be hard (if its even possible) to force them to cross, which puts many classical breeding techniques out of your reach.

@BagiM Wow, didn't know that. I know there are already dandelion cultivars which is why I thought it would be possible. Are there any other simple plants you'd recommend?

Creation of cultivars of species that reproduces only vegetatively or through apomixis is possible by accumulation desired mutations (mutagenesis). What you cannot do is cross two plants with desired traits and create homozygots  or double mutants. You would have to start with cultivar closest to what you want and try to mutate it then pick one plant with best properties and try to mutate it further. What you also cannot do is to segregate undesired trait from desirable one.

... It is hard to tell you which plant to choose. It depends on what you want to do. I would recommend to read as much as possible on plant genetics and specific genetics of plant you choose. Breeding is application of the genetics theory and is included in some plant genetics textbooks. Once you are well versed in plant genetics it will be clear to you what you can do, what outcomes to expect and you will be able make this decision for yourself.

@BagiM Thanks. I'll definitely keep trying to study plant genetics. As for dandelions I don't think it's a complete loss - just a matter of making sure I have diploid plants. The cultivars I have came from Europe, which even though they're still T. officinale much of the dandelion population is diploid (except for Northern Europe). I just want something quick and easy to breed so I can easy tell if I'm doing something right or not.


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Valence electrons in DNA nucleotide addition
Can anyone explain the movement of valence electrons during the nucleophilic attack that occurs during DNA synthesis? The 3' oxygen starts with two lone pairs of electrons but what happens during the formation of the phosphodiester bond?


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Evolution of scratching
Is scratching (aka the scratching reflex) thought to be inherited from a single vertebrate ancestor or is it something that evolved several times e.g. in birds, mammals etc., i.e. is it a case of convergent evolution?
I suppose this question may be somewhat subjective (what level of scratching is homologous) but since more recently the neurochemical basis for it has become more clear namely that

a molecule known as neuropeptide natriuretic polypeptide b (Nppb) that is released by nerve cells far from the actual itch site triggers an electrochemical cascade that ultimately tells the brain it’s time to get scratching.

perhaps one can ask (the same evolution question) about the signaling cascade for itch-scratch.


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Depolarisation of post synaptic neuron
When the post synaptic neuron begins to depolarise as positive sodium ions move into it and it reaches threshold- does the inside of the neuron actually switch to being more positive than the outside?
I thought depolarisation meant that the inside became less negative but still remained more negative than the outside, hence having a voltage of -55mV. If the inside became more positive wouldn't the voltage be 55mV?

How does relatively positive and positive make a difference, since what propagates is the change in voltage difference, which will be positive in both cases?

When the neuron reaches threshold, this is the trigger that leads to sodium channels opening and this creates a positive feedback process causing the neuron to become less negative and more positive, triggering more sodium channels to open until it is inevitable an action potential will be reached. During an action potential, the neuron cell becomes more positive compared to the outside for a very short period(ie, 1 millisecond or less).
Yes, depolarisation does mean the inside becomes less negative in this context.
You would expect the inside of the neuron to be at +55mV (or perhaps more) during an action potential, as the depolarisation of the neuron grows closer to reaching the sodium equilibrium potential which is estimated to be around +58mV. However, during the phase leading up to an action potential, potassium channels also remain open. The diffusion of potassium ions can lead to the cell becoming more negative. In other words, it limits the voltage of an action potential to around +33mV instead of +55mV.
Sources:
(1)https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/depolarization-hyperpolarization-and-action-potentials
(2)https://opentextbc.ca/anatomyandphysiology/chapter/12-4-the-action-potential/


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Which aspects of evolutionary biology are most relevant to medical practice?
I'm not pretty much sure if this question suites this forum. But I think its important.
In what aspects evolutionary biology can be seen to be very helpful in medical curricula?
Clearly infection and drug resistance seems to be relevant, also pointed are Cancer evolution.
Are there some interesting output on Neurology in particular?

wikipedia > Evolutionary medicine

ah thanks, I never heard of this term in all of my medical life. I see that there is a whole discipline addressing this question, that is actually never even been mentioned in medical schools unfortunately.

I see that there is evolutionary neuroscience as well. Good!

https://en.wikipedia.org/wiki/Evolutionary_neuroscience


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Does eating nonsalty food with MSG make you thirsty?
Assume that you're thirsty after eating food  that didn't taste salty while you were eating it.
Quora posts and https://msgdish.com/msg-problems-and-answers/ still impute the thirst to salt:

The Problem with MSG Problems - MSGdish
“Chinese food makes me so thirsty—it’s the MSG.” — Well, chances are, if you’re thirsty after eating Chinese food (or any food), you’ve probably consumed a good dose of sodium in the food or you’ve not had enough liquids recently. And, while MSG does contain sodium, it has only 1/3 the sodium of table salt. Chinese food contains a lot of high-sodium ingredients, including soy sauce, broths and other sauces. In fact, there are lots of foods (snack crackers and flavored chips, condiments, soups and sauces, commercially-prepared entrees) we eat all the time that typically contain much more salt than MSG. It’s time to stop blaming Chinese food (and MSG) for your thirst. Many Americans are chronically under-hydrated, and a salty meal of any ethnicity can send us all racing for water afterward.

But Hungry Onion

But since the food didn’t feel overly salty at the time, the only reason I can think of for the thirst is MSG.

and Wired.com impute the thirst to the MSG respectively:

The exact flavor MSG confers is difficult to describe, and many just say it increases the "taste intensity" of food. One thing is certain: It makes people thirsty, encouraging them to eat and drink more. Americans consume about 28,000 tons of MSG per year, according to one estimate reported in the June 1995 Journal of Environmental Health.

MSG also contains sodium. So does soy sauce. The final "taste" depends on the food composition. Did you try a controlled experiment on your grandma? ;-)

Eating food makes you thirsty, digesting most macromolecules consumes water.

MSG (monosodium glutamate) can trigger thirst simply because it's a spice or because foods with MSG often contain other spices.
Relationships between human thirst, hunger, drinking, and feeding (PubMed, 2008)

Drinking may occur at meal times to facilitate chewing and swallowing,
  improve sensory stimulation and food palatability, reduce aversive
  sensations evoked by irritants such as spices, or in anticipation of
  physiological deprivation.

Thirst after ingestion large amounts of MSG is described here as part of Chinese restaurant syndrome; the mechanism involved is a transient release of acetylcholine:

symptoms experienced by individuals following intravenous MSG were
  similar to those experienced by individuals following intravenous
  acetylcholine (ACH).

So, does MSG trigger thirst? It may, but not necessary.


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Spider Identification (UK)
I found this spider (~10 mm body length) indoors on a wall (South-East England) and I was wondering what species it was.

My first guess is false black widow, but I can't be sure.
I'd be grateful if anyone could help me out.

Yes, it's Steatoda, probably nobilis, the False Widow.  The white band curving around the front of the abdomen is a good Steatoda diagnostic, and the light-colored abdominal pattern is pretty variable in this species - only hints of it here, but the pointy front end and the bits of a skeletal 'shield' pattern are there.
The spider is pretty harmless, although it is supposed to sometimes give a bite that's like a very mild Widow bite.  Not at all dangerous, but a little more potent than the usual harmless spider bite.
Below are a couple of pictures of nobilis, showing a range of markings:

Here is a citation describing the effects of S. nobilis bites that's not a fear-mongering tabloid story:
https://www.researchgate.net/publication/320623444_Envenomation_by_the_noble_false_widow_spider_Steatoda_nobilis_Thorell_1875_-_five_new_cases_of_steatodism_from_Ireland_and_Great_Britain
The images were taken from a random survey of Steatoda nobilis images from the internet, as a broad selection was desired.  However, this note (below) discusses some of the features I mention, along with photographs that support my comments.
https://cisr.ucr.edu/european_spider.html