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How much energy we get from oxygen?
During a whole day breathing, how many kcal or watts do we get from the oxygen we breathe?

Why would you want to know something like that? What possible scientific interest does it have for you?

I'd say the only way this question would be answerable (see the comments and existing answers) is if we tried to transform it into "How much energy is produced via aerobic versus non-aerobic metabolism (in a human)?" - it's not really the same question, though, and might not really be what you were after, especially considering the content of the answer you hastily accepted. I think if you made this change it would be better to close this one and start a new question, rather than edit, given the existing answers here.

No scientific interest. It was an informal conversation and I am curious.

I know that you already picked an answer, but I found an alternative answer for you. On average a person consumes 550 litres of oxygen in a day. Now, our body could burn carbohydrates or fats or proteins to produce energy. Each litre of oxygen can produce 5.04 kcals if it burns carbohydrates, produce 4.68 kcals if it burns fats or produce 4.48 kcals if it burns proteins (reference). That being said, if I consider that all 550 litres were used to burn carbohydrates, a total of 550 x 5.04 kcals will be produced which is 2780 kcals.

It really does not matter very which answer the poster accepts as he generally is in the poorest position to judge. Not like Stack Overflow where you can test somebody's code. So do answer this question if it amuses you, but think how many significant figures it is useful or appropriate to cite. Six is absurd, especially as one of your figures has only four.

@David Where did I cite 6 figures? I just felt like answering it. Doesn't really matter who he picks or not

27.7585 kcal! Four decimal places, but six significant figures.

@David ah.. u can edit it as u seem fit.

OK. Have done that. Reduced to 3 significant figures as determined by values of 4.68 and 5.04. Anyone who doesn't understand this may be interested in my self-teaching web application on this topic at https://www.mvls.gla.ac.uk/Teaching/SLS-FTB/sigfigs.html.

I am not a biology expert (not even familiar with biology). I was just curious so I assumed all the answers are OK. But I like now this one more :) Thanks!
And come on, discussing for some decimals?

Just looking at the numbers, I get the impression that that 550L/day a number for males, because the resulting 2.7KCal number is pretty close to the average calorie consumption for males.

This question is not actually answerable.
Consider this.  Take a nice campfire.  It's warm and toasty.  How much energy comes from the wood you piled at the bottom.  It's a lot right?
Now how much energy comes from the oxygen the fire consumed?
We know that a fire needs three things to burn: fuel, oxygen, and heat.  How much energy comes from the heat?
Who creates a baby, the mother or the father?  Obviously the mother caries it to term, but the creation itself takes two, interacting.
These questions don't have clear answers because there's no natural division to be made.  We can't state how much energy came from the fuel or how much energy comes from the oxygen, because it is not the fuel nor the oxygen which provides the energy, but the reaction between the two.
In general, we find oxygen is more accessible than fuel.  We can always get oxygen from the air by breathing, but one has to find oxidizable fuel (food).  As such, we find it convenient to associate all of the energy of the reaction to the fuel, for bookkeeping purposes.  But that's just bookkeeping.  We do this because, if we're short on oxygen, we just have to breathe a little more.  If we're short on fuel, we have to go find fuel (food).

But in a combustion there is a clear amount of energy taking place, I do not care where it exactly comes from. What I wanted to know is how much energy does breathing give to our body in average.

@JaviV The human body burns roughly 2000 Calories a day (roughly 8.3MJ/day).  Thus, in exactly the same sense that "in a combustion there is a clear amount of energy taking place," breathing gives an average of 8.3MJ/day.

Of course, it's not the breathing that releases the energy.  The energy is released in the cells themselves, through the Citric Acid Cycle.  All breathing does is simply make sure there is oxygen available in the cells.  The cells do the releasing of the energy.

Also, note that that average does vary significantly based on food consumption, because the body regulates itself to avoid running out of stored fuel.  If you go on a diet, consuming fewer calories, your body will adjust the amount of oxygen it brings (by breathing less and/or using less oxygen from each breath)

@CortAmmon Roughly 8.4 MJ/day if you round the numbers correctly.

Oxygen does not provide any calories (energy) or watts (power), just the same as a water bottle states it contains zero calories.  Energy is held within glucose, or other macromolecules than can be broken down to supply electrons that generate ATP, or other similar molecules.

Well yes and no. The reaction of oxygen with the terminal electron acceptor of the electron transport chain provides the necessary Gibbs free energy change to allow the chain to continue, producing a chemiosmotic gradient from the oxidation of NADH and FADH2. Energy is not held within molecules. It is produced by their chemical reaction.

I would argue energy is held between the bonds of atoms, unless you are talking about quantum effects.  Thank you for correcting my knowledge ETC, but I nevertheless believe that ATP is not going to be produced with oxygen alone and in a biological sense and therefore does not biologically contain energy.  However I also think this question was poorly asked.

I didn't say that energy could be produced by oxygen alone — obviously it cannot. And yes, sugars etc are a potential source of energy because they have the potential to participate in reactions that are endo-ergonic. But to participate in the types of reaction we are considering — oxidation — they need a co-reactant that is also going to be changed. This is important. You can get round this to some extent by looking at the electrode potentials for the half reactions here, but it turns out that they are both +ve, so both are contributing to the –ve free energy change.


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Trying to identify an Ontario bird photographed in Spring in the Don Valley

Any help is appreciated! I think this may be a juvenile bird? I thought it might be a brown-headed cowbird, but the plumage and head markings don't seem quite right (compared to examples on the internet)? Any assistance is greatly appreciated.!
Rob aka orbitrob

Based on the location, timing and picture, this bird is a female Red-winged Blackbird (Agelaius phoeniceus)
In the spring in Ontario, it would be unlikely to have juveniles around, as breeding has just begun unless this photo was taken near the end of Spring. Male Red-winged Blackbirds would be in their dark black plumage with the yellow/red wing patch. Here is a photo of a pair with the male on the left and female on the right.

You can find more information about them here

That's very helpful. Thank-you! Makes sense as there were a lot of the 'showier' males around. :)

source: Stack Exchange

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

sort: votes


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Is this plant with very asymmetric leafes Aegopodium podagraria (aka ground elder)?
I found this plant in a city park in Germany. The leaves were about 20cm of height; the smell of the squeezed leaves was a bit like carrots. The stems were edged. So I guess it was Aegopodium podagraria (aka ground elder), but I'm not sure about it.

A man, collecting herbs, confirmed my suggestion about Aegopodium podagraria. Together with what I read about this plant, I can set my question as being answered with Yes.

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


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what is CpG coverage? DNA starting material?
referring to this quote from an article about predicting methylation states:

"Because of the small amounts of genomic DNA starting material per
  cell, single-cell methylation analyses are intrinsically limited by
  moderate CpG coverage"

can you please explain it to me?
What is exactly starting material? and why it's small per cell?

Please try to find the meaning of common English scientific phrases by an internet search. And think about how big a single cell is and how much DNA there would be in it.

Can you please link to the document you're citing from? Without a context, it sounds rather difficult to interpret this sentence.

https://link.springer.com/article/10.1186/s13059-017-1189-z

The comparison the authors are making is between bulk and single-cell sequencing.  Currently, single-cell sequencing is becoming very popular as it allows much finer grain analyses of the biological expression.  For example, tumor sub-populations can be determined.
However, single-cell analysis lose a great deal of genomic material, causing the resultant measures (expression most often) for each cell to have very minimal and sparse values.
Therefore the starting material is simply the DNA in each cell, which is limited by the single-cell process.

You write "the starting material is simply the RNA in each cell". Perhaps you can explain how you can measure DNA methylation starting with RNA.  The poster actually quotes what the starting material is: "genomic DNA" but appears unfamiliar with the English expression "starting material". As for "CpG coverage" it would appear that both his scientific knowledge and his English is deficient. But you ignore that part of his question.

I know the English meaning of the words "starting material". My question: what is that starting material? and why it's not enough?

specifically, is CpG coverage the number/percentage of C-G sites covered in sequencing? or it's something related to methylation?

CpG coverage is a general term, but thinking about it as the fraction of methylated CpG sites over the total number of CpG sites is accurate.  To get the number of CpG sites, accurate sequencing of the genome needs to be accomplished.  As I tried to explain, the single cell method limits the amount of DNA (edited the answer to be correct) able to be sequenced, and therefore the number of CpG sites is not well known, and the CpG coverage as well.

Also the question states "What is exactly starting material? and why it's small per cell?" nothing about CpG, therefore I did not include an answer about CpG.


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How is ATP converted to adenosine?
I am familiar with adenosine diphosphate (ADP) and adenosine triphosphate (ATP), how one relates to the other, and how each is formed in cellular respiration and photosynthesis, but I am confused as to how regular adenosine is formed.
I was reading an article on caffeine which stated:

Caffeine is structurally similar to adenosine, a neuromodulator, whose formation is dependent on the relative rates of ATP breakdown and synthesis.

From this I concluded that ATP can be changed to regular adenosine, and adenosine back to ATP, but I cannot find anything else on the internet to support my conclusion. I was also wondering when and why your body would change ADP into adenosine instead of ATP. I assume that AMP plays a role in all of this, and possibly ADA.
I only have a high school level education in biology, so please bear with me. If you do not mind, please include a source in your answer so I can further research on my own. Thanks!

Adenosine monoposphate can be converted to adenosine by a 5’-nucleotidase.

@canadianer that set me down the right track for the most part. I have one more question. Wikipedia says that ADP is converted to AMP like this: 2 ADP → ATP + AMP. What is the name of this process and where does it take place?

@CardinalSystem that reaction is called adenylate kinase and takes place in almost every living cell.

Perhaps someone could integrate these comments into a decent answer. Even the poster after he has finished his researches. I'd consider doing it myself but I know next to nothing about adenosine as neuro- signalling molecule, which seems to be the focus of this.

For a full understanding I refer you to the KEGG pathway map which is fairly comprehensive in showing all the metabolic processes that CAN produce Adenosine.
It's a bit daunting but if you find it on the map here it is interactive and you can see the enzymes and pathways involved. If you drill down it brings you to a host of papers and references in primary literature to back things up.
However the dominant process is as follows:
   2 ADP <=> ATP + AMP

enacted by an adenylate kinase then:
   AMP + H2O <=> Adenosine + phosphate

enacted by adenosine 5'-monophosphate phosphohydrolase (a 5'-Nucleotidases )

So the nucleotidase can reverse its own hydrolysis to produce AMP, and the adenylate kinase to produce ADP?

The kinase is certainly reversible with almost an equal balance of each reaction. The nucleotidase I believe is but i don't have a watertight source on it yet.


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What gives researchers a reason to test the Radiation Resistance of organisms?
I was reading about the Thermococcus Gammatolerans and its absurdly high radiation resistance, when something occurred to me.
What reason did anyone have in the first place to subject this thing to this level of radiation?
I'm very curious to find out about the process behind deciding which organisms to test the radiation resistance of. Is there an ongoing effort to test the resistance of every species yet discovered? Or are there other factors in determining which species should be subjected to this kind of testing?

OK. You cite the Wikipedia page on this organism. There is a reference to a paper about it on that page. I suggest you look at that paper (no need to read it all) and find out where this organism is found. That should give you an indication of why they chose it. Why should anyone be interested in (or fund research in) the resistance of living organisms to radiation? This is not Guiness book of records stuff — animal with the longest penis and the like — they are interested in the molecular mechanism. Ask yourself what use that might be. Learn to save your own life.


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Minimum age to reproduce
How old does one (male and female human) have to be in order to reproduce
Im thinking that it's 13 for a boy and 3 for a girl, is that right?

What is your definition of reproduction?  Does it just involve a female getting pregnant, or does it involve carrying it to term.  It seems highly unlikely that a 3 year old could carry a fetus to term.

Cross-posted at Health and underresearched.- please delete one post and refine the other, most of all add some prior research and correct the 3 years for a girl's reproductive age. That's just plain nonsense.

The youngest fathers recorded were 11 years old (see wikipedia >
List of youngest birth fathers).
The youngest mother recorded is L. Medina was 5 years, 7 months and 21 days old when giving birth, which is rather astonishing! Of course, she gave birth by a caesarean section. She had an extremely early puberty; she appears to have had her period when she was 3 years old only. You might want to have a look at wikipedia > List of youngest birth mothers. According to this article, a mother (L. Gryshchenko) became a mother at 6 years old and gave birth "naturally" (not by cesarian section).

Not propably but definitly :). But  it is nice answer.

@L.Diago Not probably, not definitely, but definitely not - in its current shape the question is unfit for any site in the SE network. Whoever upvoted the question should re-think their motivations to do so -1. The answer is fine but removed my upvote as it's an answer on a question that should've been improved first, or put on hold altogether.

Dear ALiceD i was on your side. I didnt mean it on that way. :D Btw thank you, because i have never noticed that mistake.


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Can herbs absorb harmful substances leached in water supply
I have small herb garden (parsley, coriander mint and basil) that is watered from below by a hydrophilic filter using capillary action from a reservoir. This filter allows water soluble nutrients to be fed to the herbs.
The manufacturer of the filter use a special propitiatory additive in the filter that allows for excellent water flow. I need to know the the harmful implications of the material as they have stated the unknown "additive in the filter is not FDA approved". They will not tell us what additive is to protect their intellectual property.
My question is that will the herbs absorb the additive regardless assuming the additive is leaching into the water. Say that 1 ppm (parts per million) of substance X is in the water. Will the herbs absorb that and propagate it to their leaves. If so how much of the substance? (very rough estimate will do)
TIA, Dave

You'd have to test it. Plant roots naturally pull poisons like heavy metals out of the soil through water. These are called metallophytes, and can even be classified into what're called hyperaccumulator plants. The use of plants to remove harmful substances from the soil, air or water is called phytoremediation.
The process of absorbing harmful substances, however, relies on the structure and size of the substances involved because the substances must enter cells. We know from elementary biology that cells only allow molecules of certain properties to pass their cell membranes. Since the filter additive in question is an unknown, it's hard to say if a plant would absorb it. It's also hard to say if it's harmful to you, or if it even gets into your water. Testing for a chemical of unknown behavior requires some analysis like mass spectrometry (fair example).


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Are there any anatomy books focusing on etymology?
I noticed that I can remember names for a very long time if I now their etymological background, the reason is easy I love etymology, especially when it is connected to mythology. However when I learn anatomy searching for the etymological background consumes too much time.
Are there any books or even preferably searchable online materials focusing of the etymology of anatomical nomenclature?

Though a little bit outdated looking this from the university of Sydney is pretty good and searchable.
I find it pretty useful for aiding memorisation or just a quick entertaining read.
Arnold's Glossary of Anatomy - The University of Sydney


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Relative rates of migration of circular, linear and supercoiled DNA in agarous gel electrophoresis
I have read the supercoiled plasmid DNA migrates fastest when subjected to agarose gel electrophoresis and this makes sense to me because it is small and experiences the least friction because of its supercoiled structure.
Linear DNA migrates faster than the circular form. I didn't understand why exactly. Shouldn't the circular one be considered to be smaller than the linear, and thus quicker?

First let me supply an illustration of the situation described in the question, together with a reference.

Although you can see this sort of thing, just by searching for “plasmid migration on agarose gel”, this is one of my own from the last millennium (plasmid pBR322), appearing in a text from the last millennium, Adams et al. The Biochemistry of the Nucleic Acids (11th ed).
The poster’s attempt to rationalize the results, though expressing the quandary, is marred by the loose use of the word small, and the absence of any statement as to why ‘small’ pieces of DNA should migrate more rapidly.
The different forms of the plasmid have exactly the same molecular mass, so what is meant by small? My own initial way of looking at this is to consider the agarose gel as a mesh or sieve through which the molecules must pass, so that the larger the volume they occupy in space, the less likely they are to pass through the ‘holes’ in the mesh. The volume that they occupy in space might be regarded as that generated by rotating them from their midpoint in three dimensions. On this basis the supercoils, in which the DNA is collapsed into a short fat pseudo-linear shape should occupy the least volume in space, and the long thin linear the greatest. The diameter of the circle should place it somewhere between the other two.
So, we reach the same conclusion as the poster: the faster migration of the ‘linears’ than the nicked circles does not fit this simple model. In the text accompanying the figure I wrote “…a result that is a little unexpected” without attempting to explain it.
Am I able to explain this somewhat unexpected result now? An internet search produces either hand-waving or evasion (I stand to be corrected on this), so that I can only imagine that the result has something to do with the linear molecules having a greater chance of their ends being directed to the holes in the ‘mesh’ than the nicked circles, because of the open nature of the latter. One can perhaps imagine an hour-glass shaped portion of the sphere for the rotation of the linears that allows the ends to be directed at the holes.
More waving of hands? Perhaps. But the main point is that the physical explanation for the migration of molecules of different shapes during electrophoresis is more complex than a mere biologist might have hoped.


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What are ECT parameters?
ECT or shock treatment is used to treat psychological disorders. How much voltage,  current and duration is used for this? Wikipedia mentions a treatment of 0.8 Ampere for 5 seconds.

Peterchev et al. (2010) reports

The current amplitude is [... ] held fixed at the device maximum (e.g., 800 mA or 900 mA)...

and that

[constant-voltage devices are] now obsolete

The total stimulus duration as I understand is a pulse train of a few seconds (Peterchev, 2010). The duration of total treatment is about 20 minutes in the treatment room and up to an hour including recovery (source: Hopkins Hospital).
Note that the total stimulus duration depends on the total amount of injected charge. This in turn depends on stimulus frequency, stimulus shape, frequency and so forth (Fig. 1). For an excellent overview see (Peterchev et al., 2010).

Fig. 1. Sample ECT waveforms: (a) sine wave, (b) biphasic pulses with indicated parameter definitions, and (c) monophasic pulses (Peterchev et al., 2010)
Reference
- Peterchev et al., J ECT (2010); 26(3): 159–74


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Where does the human brain drain to?
When a brain has a aneurysm and the patient survives untreated then   where does that blood drain to or how is it absorbed? How is the pain perceived?

if you mean the pain in brain during the operation, It doesnt, because there is no nocireceptors in brain. I actually doubt about the aneyrysm survivel without threatmeant, and i hope someone is going to answer that part soon.


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Identification of snake
Can someone identify this snake? Photographed in a home in Los Lunas, NM, USA.

Check out the Desert Kingsnake (Lampropeltis getula splendida).  It is native to New Mexico.

Source: Desert Kingsnake (wikipedia)


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Need help with insect identification
Saw this bug in my hallway tonight, crawling alongside the baseboard, it didn't seem like it could crawl up the wall despite trying to countless times. Google wasn't much help, although I saw a weevil that looks sort of similar to it.
Location: Augusta, Georgia, US

It would help if you could edit the question and add the location where you took this photo. City/state and country is usually sufficient.

@Chris It's updated now.

I don't know about weevil, those usually have a long snout looking thing. https://en.wikipedia.org/wiki/Weevil#Gallery Almost looks like a type of ground beetle, but that's because ground beetles are typically black and boring looking. Plus, it's shaped a lot like this north carolina ground beetle: https://en.wikipedia.org/wiki/Brachinus#/media/File:Brachinus_spPCCA20060328-2821B.jpg

That is definitely a ground beetle. Family Carabidae. These are running predators. They are rarely found in homes, and are not pests. It must have gotten in by accident.

@Karl Kjer agreed, and I believe that the out-of-focus photo will not let anyone go deeper than you have (had the palps--the short antenna-like appendages at the front of the head--been in focus we might have eliminated tribe Bembidiini [where the last segment is abruptly narrowed and shortened], but that isn't possible with the evidence at hand).


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Is happiness or pleasure an evolutionary programming for survival?
I think that whenever we feel some kind of happiness or pleasure it is always related with improving our chances of survival, that might be temporarily or in long term, might be of only of an individual or his/her relatives or all human beings or all living beings as a whole.
I find that a sense happiness or pleasure is linked with the survival (might not be true as it's based on personal observation).
 We crave for things like attention & being cared, beauty & physical health, power (& money). Attaining them gives us a sense of pleasure, and these things improves the chances of our survival. People having power & money dont die out of scarcity. People having beauty & physical health get to pass their genes more often(keeping whole human history in mind). Dogs developed their behaviour around humans so as to get more attention & care thus improving their chances of survival. We also feel happy helping other people, we feel happy making more friends.
  But there is no simple answer to this one as we also have tendencies to hurt ourselves and some people derive pleasure in hurting others.
So is pleasure or happiness evolutionarily programmed into us to better our chances of survival?

"Evolution" and "programmed" together sounds a bit strange.

Please do not post to this site as a new user without consulting the help to find out what the scope of the site is and what sort of questions are acceptable here. This sort of question based on a "feeling" and asking for answers that can only be subjective are off-topic and a waste of everybody's time.

@David I fail to see how is this a subjective question. Please let me know where I made the mistake.

Describe an experiment or study that would provide an objective answer to your question.

I don't know of any experiment as such but there is definitely a correlation between pleasure/happiness and our improving chances of survival

Look at the things we crave. Being caref or loved, getting attention, power, having beauty/physical health. All these give us some sense of pleasure when we get them. Why so? When we help others why do we feel good? So my question is that does improving our chances of survival the cause of our happiness or pleasure.

Please @ me in if you reply to my comments. This is a scientific site. Statements like "there is definitely a correlation…" without citing any research in support is scientifically worthless. And as you devote your following comment to arguments in favour of this idea it would appear that your question is not an attempt to test it with scientific evidence but to solicit others of like mind to say "yes you're right".

@David I have no problem if you think my question is unscientific. I don't know the standards used to measure the worthiness of a question, and I believe such standards (if exists) are mostly subjective. I was thinking about the reason why we feel pleasure and happiness and couldn't figure anything  more than this. I don't belong to the field of biology and couldn't find any research or experiment related to it. The purpose of the question was not to put forward what I think to be true rather to know where I am wrong. And for that reason I am totally open to discussions and criticism.

Our current understanding is that pleasure is one of the major ways your brain gets "you" to do things, it is the basis of positive reinforcement of behavior and associative learning. It can almost be thought of a a tag for an individual behavior that says "do this again/more". That pleasure alone can motivate animals to do things has been understood since way back in the Skinner box experiments where a wire to the pleasure center was inserted in rats and said rats would keep doing whatever behavior they associated with stimulation via the wire foten to the exclusion of all else. The basis of our learning could be summed up as do things that elicit pleasure, don't do things that elicit pain. tying many complex behavior to a single signal seems to make it easier to control and even prioritize very complex behavior, just do whatever yields the most pleasure, of course humans and many other animals have many more competing emotions and other factors, like metacognition. But for simpler animals it is easy to see how this system is efficient, it is easy to tag new behaviors or experiences into this system, at its simplest form just connect (possibly inhibitory)a few neurons triggered by the behavior or memory of the behavior to the pleasure center.
Of course it is not perfect, few things that evolved are, behaviors that are not beneficial can trigger the system, especially novel or extremely rare behavioral options, especially ones created by technological advancement, drug addiction being a great example. Evolution is very poor at preparing organisms for novel conditions like the modern technological world. And the our brain did not evolve under conditions where cocaine (as an example) existed. Just because something is pleasurable does not mean it is beneficial.  The full range of behaviors that can elicit pleasure would be well beyond the scope of a single question but it is quite clear pleasure itself is an evolutionary advantage, it is one of the major reasons we learn to eat, drink, reproduce, and make social connections.
Happiness, is more difficult, mostly because it is a poorly defined term in biology, it is unclear if it is distinct from simple pleasure.

All features of life have evolved in order to better the chances of reproduction, the feeling of happiness is included.  After all, happiness is just the release of various molecules such as dopamine, oxytocin, and endorphins, that cause the body to more likely produce a certain behavior.
These chemicals can produce advantageous behaviors by promoting deep friendship, mating bonds, and gratitude in an investment paid-off.  However, they can also provide bad behaviors if jealousy or laziness emerges.  All emotions exist in a tug of war in evolution, in fact Darwin wrote a book entitled: "The Expression of the Emotions in Man and Animals".  While I have not read all of it he probably states how fear, jealousy, anger, etc. all can promote both good and bad behaviors.
More recently, scientists have tried to study specifically the evolution of happiness two publication are by Nesse and Buss.  Both are not very sure, but note the evolutionary advantages of evolution.
So the short answer to your question is yes, with the caveat too much, or too easy a sense of happiness has its downsides, and that all other emotions and measures of the body are effected by evolution.

All features of life have evolved in order to better the chances of reproduction This is wrong. It is too a panselectionist view of evolution. You might want to summarize the two papers you linked to, they are probably of interest. I would love an answer that highlights the difficulty to define the concept of happiness and how much it may be culture specific.

Yes I generalize evolution and remove the random aspects, but if natural selection is not selecting for features that enable better reproduction then what is going on?  Also an answer that branches into cultural aspects would appear an anthropological answer, not a biological one.

Your arguments amount to an assertion of belief, and as such have no more value than those opposing ones based on religious beliefs. Indeed they are worse as they purport to be scientific but are actually anti-science.

My answer is about belief?  I try to cite chemical pathways, Darwin, more recent work, and generally give an answer that is not very confident but based in logic.  If you have a problem with my answer, then please point to it, but don't just say I am anti-scientific outright with providing any supporting feedback - it is not helping anyone, and instead insulting.

You might be better off saying "pleasure and the brain reward system is too widespread an adaptation to not expect an evolutionary advantage". not every feature organisms have are evolutionary advantages. An actual sourced description of the system would also be a big improvment, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491543/


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What does "molecular" mean in the context of anatomy, for example the molecular layer of cerebral cortex
The first apical layer of the cerebral cortex is also called as the molecular layer, I could not find the exact reason of the naming.
What I found:
Molecular alongside its primary meaning in chemistry can also mean:
of or relating to individual or small components
source
And if you only stain the neuron somas, you can only see some scattered neurons in this layer. Maybe this is the basis of to the naming.
What does molecular exactly mean in this context?
Is this adjective used widely in anatomy with the same meaning?


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Is it possible for a prey to become its main predator's predator?
This is actually for a worldbuilding project, but I thought I'd just ask it here as it is solely about biology.
Anyway, would it be possible for a herbivore, let's call him X, that is predated by a predator, or Y, to evolve to become a specialized hunter of Y?
For example, wolves hunt deer. Imagine that in millions of years, the deer has evolved into the main predator of wolves.
If that's not possible, is it at least possible for X to evolve adaptations for fighting/killing Y (Not for food)?
If you require any further context or clarification, please let me know.

Humans, compared to everything ("Lions and tigers and bears, oh my!") that used to eat them.

@jamesqf Mine is a question more about evolutionary traits. Humans can hunt and wipe out those large predators because of their advanced tools.

Also it should be noted as you move from prey to predator, there is less energy to be had. This is why we often do not have a predator of a predator species. There simply isn't enough food at that level of a predator to support another predator above it.
That said, I am assuming you are thinking of an alien ecosystem. In which case you might be able to sustain such a system if there is a massive flux of bio-matter through the ecosystem. Ie plant food is extremely abundant and animals within it reproduce at an extremely fast pace. We can see such an environment at the bottom of a marine ecosystem in the polar regions during summer (near constant sunshine, and an up welling of minerals from the deep sea.

If that's not possible, is it at least possible for X to evolve
  adaptations for fighting/killing Y (Not for food)?

Happens all the time. While lions do hunt cape buffalo, cape buffalo can and do kill unwary lions.

I guess that the Cape buffalo can kill lions because it's just a dangerous animal in general. But if there was, for example, a rodent that was preyed on only by snakes, is it possible for that rodent to, say, become bipedal to have hands to grasp their serpentine predators? I don't mean "is it physically possible", that was just an example, but can anti-predator adaptations be that specialized?

Well the mongoose is immune to cobra neurotoxin because the molecular structures of acetylcholine receptors of the mongoose has an altered shape that prevent the neurotoxin. So yes, the anti-predator adaptation could become fairly specialized, especially if the prey has only a single predator.

As most prey are herbivores, becoming a predator requires large adaptions to the digestive system. I therefore think becoming a predator is unlikely.
However, some animals are able to defend themselves very well against their predators. The best example I know, is the African buffalo. This animal is capable of defending itself against all predators, including lions. I've once seen a documentatory where buffalo attack and kill young lion cubs.


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Compare affinity to potency h1 receptor
This quote from Miller (2004) makes it clear that the affinity of drugs for the H1 receptor does not correlate to sedation:

Although both dosage and affinity for histamine H1 receptors play a part in the sedative effect of a medication, what ultimately determines sedative effect is the amount of the drug reaching the histamine H1 receptors in the central nervous system. For example, quetiapine, which has little affinity for the histamine H1 receptors, is a less potent antipsychotic medication and requires many more milligrams to be effective than do higher-potency medications such as risperidone and ziprasidone. Because of this, quetiapine has a greater sedative effect on patients in clinical use than do risperidone and ziprasidone.

Is there a mathematical way to compare affinity to potency between different drugs?

There are a few important things to consider as you interpret these data.
Here potency means Chlorpromazine equivalents
When your linked review refers to potency, it is likely referring to the old concept of chlorpromazine equivalents. The table in the article cites Jibson and Tandon in a review in CNS news special report from 2001. This is not a standard peer reviewed article, and I can't access it, but it lists relative potency in mg, with chlorpromazine set at 100mg and haloperidol at 2mg:

This is almost certainly chlorpromazine equivalents. You can read a discussion of the limitations of this understanding of antipsychotic potency here, but these numbers are not based on a mathematically rigorous pharmacodynamic analysis. They are not consistent, especially for atypical antipsychotics, and are estimated based on clinical data of the minimum effective dose among other methods.
So, where the affinity in this article, $\frac{1}{K_D}$, has a rigorous pharmacodynamic definition, potency does not. Here it is, effectively, shorthand for how much of a drug you have to administer in order to get a therapeutic effect.
Antipsychotic drugs act at many CNS receptors
To understand exactly what Miller means when he says:

For example, quetiapine, which has little affinity for the histamine H1 receptors, is a less potent antipsychotic medication and requires many more milligrams to be effective than do higher-potency medications such as risperidone and ziprasidone.

You need to understand that $H_1$ receptors do not mediate the primary clinical target. So the lower potency of quetiapine means you have to give more of it to have a clinical effect. Because of the higher typical dose of quetiapine, even though the affinity for $H_1$ receptors is relatively low, you're going to get more binding to $H_1$ than with, e.g., risperidone, which requires a lower dose.
Take a look at the chart in the Richelson and Souder article Miller cites to see the different receptor targets for these antipsychotic drugs.

The primary therapeutic targets (used to characterize the general clinical potency) are (probably) the $D_2$, $5HT_{1A}$, and $5HT_{2A}$ receptors. The action at the $H_1$ receptor is primarily an adverse effect. Miller is trying to say that the sedation effect does depend on affinity at $H_1$, but you also have to consider the dose required to get an effect at $D_2$ and the relevant $5HT$ receptors.
A rigorous definition of potency involves simplification
There is a rigorous definition of potency for an agonist (and also of inhibition for an antagonist, and antipsychotic drugs are antagonists). Potency is both distinct from and dependent on affinity.  I'd recommend Goodman and Gillman Chapter 3, if you'd like to learn more. It's not particularly relevant to understanding this article, in part because Miller doesn't use this definition of potency, and in part because the model involves a single ligand-receptor interaction that directly mediates a desired effect. It's based on the following equation, where $LR^*$ is an activated ligand-receptor: $L + R \rightleftharpoons LR \rightleftharpoons LR^*$.  Because both desired and adverse effects of antipsychotics involve actions at many different receptors even beyond those in Richelson and Souder, the simple model falls short.

Thank you for the response.  I just saw your comment.  I need to get a hold of the book to try to understand more before I assume you explanation isn't adequate.

@William what do you need help understanding?

@William the basic idea here is that the article is talking about a general clinical concept of potency, and the clinical (side) effect of sedation for drugs that are given in very different doses. This is not a single receptor system, and Miller is not talking about the relationship between affinity for $H_1$ and potency at $H_1$. I've studied this a good deal, in and beyond medical school. I'm happy to help answer your questions about it if you need more help. Just ask.

I'm trying to compare the drugs and from what I have gathered from reading your post is that there is no way to rank their sedation except with clinical trials and comparing sedation described by the patient.

I am asking for an equation I don't see where potency is plugged into the equation. Can you please post a Mathematical example walking though either Zyprexa or Seroquel.

Hi @William. If your goal is to understand this article, there is no equation that is going to relate chlorpromazine equivalents (potency in this article) to affinity, $\frac{1}{K_D}$ at the $H_1$ receptor. They are different things all together, with no known mathematical model connecting them. If your goal is to understand potency, olanzapine and quetiapine are not very good places to start. They are inhibitors at  many different receptors. I'm not sure what you would want in a mathematical example walking through either of them. Were you able to get a copy of Goodman and Gillman?

Okay ignore my last question.  According to Wikipedia the h1 receptor of seroquel is a neutral antagonist which means it does nothing on the receptors which seems to be at odds with miller?

@William all of these antipsychotics are antagonist, as I've said, and this is not at odds with miller at all. Affinity has to do with the strength of binding, not with the downstream effect. It seems like someone may have taught you something different along the way.

I guess I assumed h1 antagonist mean neutral antagonist and this answer states neutral antongists bind but don't alter the response https://biology.stackexchange.com/questions/73706/inverse-agonist-vs-neutral-antagonist

@William Affinity describes binding, not the effect of binding. Anything that binds will have a dissociation constant, no matter how binding effects the receptor, and the inverse of that dissociation constant is the affinity. Also, neutral antagonists do have an effect on the receptor. They prevent binding and activation by an agonist.

"In each of these studies, the atypical antipsychotic (risperidone, olanzapine, quetiapine, and ziprasidone) caused less sedation than did the conventional antipsychotic used for comparison, haloperidol, except in the highest doses. " This seems contrary to evidence in the article"


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What could an increase in systolic blood pressure and decrease in diastolic mean?
Sorry if this is a really simple question but my academic background is in completely different sciences. I recently made a computer game for an experiment that was related to anxiety and relaxation. One of the ways that I measured for success was to record participants blood pressure before and after they played the game.
There was a slight increase in systolic BP after playing the game, but not by a statistically significant amount. However the data shows a decrease in diastolic BP that is statistically significant. I've been trying to figure out why this might have happened but can't seem to find any answers. My brief overview of search engines and journals only seem to relate these changes to certain types of exercise. Which doesn't help as the participants of the experiment were asked to remain seated for 20 minutes by the time the second BP recording was made. Just wondering if anyone has any information in relation to relaxation techniques that might result in this pattern?
If it helps heart rate has mostly uniform throughout the experiment.

This is a question better suited to Health.SE.

First, a couple of considerations

Heart rate (HR) is lower when seating, and even lower when lying. I assume that participants were seated when the first measure was taken.
Cardiac output is not constant during the day. Depending on the moment, some factors such as digestion have an impact in Cardiac output, so take that into account when carrying out the experiments.

Normal walking may cause that blood pressure pattern. I think that you should not consider the increase in systolic pressure if it is not significant, as something as simple as crossing your legs when seated can increase your systolic pressure and normally diastolic pressure provides more information for physicians. Relaxation techniques usually decrease heart rate, which can affect the blood pressure. However, the point in this case seems to be that HR remains constant. I suppose that Mean Arterial Pressure $(MAP)$ has decreased.
If we part from:
$\textit{MAP} = (CO \cdot SVR) + CVP$
where $CO$ is cardiac output, $SVR$  is systemic vascular resistance and $CVP$ central venous pressure.
$CVP$ is usually depreciable. $CO$ is defined by $SV \cdot HR$, where $SV$ is the stroke volume. Then, if the HR is constant, only $SV$ or $SVR$ could have changed. Maybe the heart is pulsating more vigorously, or a vasodilation is decreasing $SVR$. I find the latter more likely. However, I don´t know why the smooth muscle could be relaxing. Make sure that heart rate is not changing and consider your sample size.
I hope it helps, at least to focus you search on cardiac regulation. It is difficult to conclude anything without seeing the data but I tried to answer from my limited knowledge since I am not specialized in cardiac physiology.


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Specific Neurons that Require Glucose
I've been doing a bit of armchair biology lately, and have been interested in the metabolic flexibility of neurons. My understanding is that, besides glucose, many neurons can metabolize lactic acid or ketones. However, some reports point out that some neurons can only metabolize glucose, without ever indicating which, or in what regions of the brain. (It may be that the following exert is suggesting that each individual neuron is using a mix of fuel sources. I have not been able to find much via the Google.)
From the linked book:

When changing slowly from a carbohydrate diet to an almost completely
  fat diet, a person's body adapts to use far more acetoacetic acid than
  usual, and in this instance, ketosis normally does not occur. For
  instance, the Inuit (Eskimos), who sometimes live almost entirely on a
  fat diet, do not develop ketosis. Undoubtdly, several factors, none of
  which is clear, enhance the rate of acetoacetic acid metabolism by the
  cells. After a few weeks, even the brain cells, which normally derive
  almost all of their energy from glucose, can derive 50 to 75 percent
  of their energy from fats.

Which neurons and regions of the brain can only burn glucose?

Although PsychologyToday might look like a reasonable source, it's just a blog. Anyone can post there. There is no peer review of the content.

I've seen it somewhere else, too... I just can't find the link again... (grumbles something about wishing someone would organize the internet)

@NonSecwitter Can you reproduce the text here in text form from Guyton Hall?

@BryanKrause - I opened a meta psych question

OP this is why I wanted you to find a better source - see that the book says nothing about certain cells can only use glucose, it just says normally use glucose. That is, brain neurons (all of them I believe) use glucose when it is present. The bit in your other source about some neurons can only use glucose sounds like complete bullshit to me, I've never heard of such a thing and can't find any peer reviewed source making that claim.

The source you link does not report that certain neurons only use glucose, and I am unaware of any reputable source that makes this claim.
Neurons do tend to use glucose as an energy source when it is available, and the brain does not tolerate sudden drops in glucose. However, as your source notes, other energy sources can be utilized given enough time to adjust, such as during starvation/fasting as well as suckling.

Cahill, G. F., Herrera, M. G., Morgan, A., Soeldner, J. S., Steinke, J., Levy, P. L., ... & Kipnis, D. M. (1966). Hormone-fuel interrelationships during fasting. The Journal of clinical investigation, 45(11), 1751-1769.
Hawkins, R. A., Williamson, D. H., & Krebs, H. A. (1971). Ketone-body utilization by adult and suckling rat brain in vivo. Biochemical Journal, 122(1), 13-18.
Nehlig, A., & de Vasconcelos, A. P. (1993). Glucose and ketone body utilization by the brain of neonatal rats. Progress in neurobiology, 40(2), 163-220.
Owen, O. E., Morgan, A. P., Kemp, H. G., Sullivan, J. M., Herrera, M. G., & Cahill, G. J. (1967). Brain metabolism during fasting. The Journal of clinical investigation, 46(10), 1589-1595.
Pollay, M., & Alan Stevens, F. (1980). Starvation‐induced changes in transport of ketone bodies across the blood‐brain barrier. Journal of neuroscience research, 5(2), 163-172.


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Is urban beekeeeping harmful or are there good practices to follow?
I have found several newspaper articles on how good could be urban beekeeping both for the bees and for agriculture.
Today I read this one: Urban beekeeping is harming wild bees saying that urban beekeeping is harming wild pollinators. I did not find a direct link to the paper, but it is probably referring to Conserving honey bees does not help wildlife. Unfortunately I only have access to the summary of the paper.
Are there good practices that could be followed to practice urban beekeeping without harming wild life (for example avoid placing hives close to a forest...) or is it harmful in any case?

Did you read the article?  Did you read the article cited in the article?  Did you read the comments?

@swbarnes2- I couldn't find the original. Did you? I'd be interested in reading it.

@swbarnes2 I could not access the cited paper. Today I finally managed to download the paper cited in the article. It looks like the problem (if real) has little to do with urban beekeeping and more relevant for beekeeping in protected areas.

AFAIK, any monoculture or similar practice by humans reduces the diversity of resources available to wild animals... That said, compared to pesticide use, which is massively depleting wild insects found rurally, beekeeping is of much lesser concern.

You can sidestep the entire issue and raise native bees, https://www.sare.org/publications/managing-alternative-pollinators/chapter-five-bumble-bees/raising-bumble-bees/

Beekeeping in urban areas often require that beekeepers supplement their colonies with feed since urban areas have, on average, very little forage available to sustain a colony year-round. There are usually very little in terms of wildlife (or wild pollinators) when it comes to urban settings. In contrast, suburban areas would have more to offer as there are often backyard gardens and unmanicured lawns that could provide food throughout the season.
The wild pollinators within suburban to rural areas are probably under the biggest threat from managed colonies, but the impact is also usually very difficult to assess. Even with the limited range of managed colonies forage (around 5km), there's usually not enough of the colonies stretched out across a wide area in such big numbers that it would out-compete with other wild pollinators. The wild pollinators are often solitary, with much greater foraging capacity. As such, they would just move away from any competing resource if they're unable to defend it themselves until the threat subsides.
Regardless of the location (urban, suburban or rural), best practices still include protecting your colonies against diseases and pests. If you don't you may end up losing your colony, or spreading diseases to other colonies or wild pollinators. Probably the most significant threat nowadays globally (except for Australia) would be Varroa Destructor. So, best practices here would include keeping on top of these mite loads to avoid it from spreading and/or overrunning your colony.
As reference, here is a visual capture of the article:


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complete DNA transfer across different organism zygotes
Consider we have a monkey zygote (i.e. single cell just fused) and a tiger zygote. If we extract the nucleus of monkey zygote and place it into tiger zygote where nucleus of tiger zygote is already removed. Is there any chance of zygote to survive and finally turn into a monkey offspring ? I tried Google for any such experiment ever conducted but seems like biology is googol to Google, no close result at all.
For more clarity it can even be considered all chromosomes transferred  instead of nucleus.
As far as I think this could be possible as all 20 amino heads must be present in zygotes of both the mammals and thus synthesizing protein should not be a problem. However I can't say anything about their respective immune system response.
This question came to my mind considering Darwin hypothesis/theory(interpret as you wish) of evolution, where even if some mutation changes the DNA sequence how much chances are there for a completely new organism if cells don't support growth natively.

Unfortunately the answer is no. Similar experiments of cross species nuclear transplants into enucleated oocytes have been attempted. Rat nuclear transfer into activated denucleated mice oocytes, rabbit oocytes etc.
The primary stumbling block appears to be incompatibility between mitochondria proteins derived from the donor nucleus and proteins derived from the host mitochondria. Mitochrondria proteins are encoded from two DNA sources, the genome within the nucleus and the genome within the mitochondria. While mammalian mitochondria proteins are very similar, there are differences. These small differences between species appears to be enough to kill a developing embryo if there is a miss match.
Attempts have been made to replace both host nucleus and host mitochondria. However complete replacement of host mitochondria has not been successful. Partial replacement of host mitochondria (mouse oocyte as host and rat nucleus with rat mitochondria as donor), appears to marginally prolong the life span of embryo. But death is still the outcome.
PS: nuclear transfer between subspecies and very closely related species does produce viable clone.  Coyote (Canis latrans) using dog (Canis lupus familiaris) oocytes. (Bos gaurus) adult nucleus donor cells and bovine (Bos taurus). My guess is that if a hybrid is possible between the two species, nuclear transplant between the two species should be possible

Can you provide me some pointer to any such research. google sending to animal cloning even when I use words cross species nuclear transplants.

https://www.ncbi.nlm.nih.gov/pubmed/21556135 Here is a started article.

The fertilized tiger ovum probably has some tiger mRNA in its cytoplasm already, those are not going to interact properly with the monkey DNA.  That is going to be a problem long before there is any development of the immune system.

Doesn't mRNA has same structure across multiple eukaryotic cells? I don't know specific exception but heard there are exceptions.

"Structure" isn't enough.  Lots of genes are controlled by mRNA binding to matching sequences upstream.  If those sequences don't match well enough, the cells won't develop correctly.


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What do bats do if played ultra sound?
If there are bats flying in the cave, and I play the same pitch they use to echolocate from a speaker, what would the bats do?

they shouldn't be able to orientate...

Depends completely on how good ultrasound you are producing.
Will they interpret your signal as an obstacle ?
Not really until you produce signals exactly calculated for the distance and speed of bat from obstacle. Here something known as dopler effect will come into play which will make bats understand probably thats not their sound. Otherwise every bat would have made a noise to divert another bat.
Is just making sound good for dislocating
Well, till this date we don't know what humans are speaking from their sound waves what you can guess for bat for what they did just speak. If you listen closely to bat sound you will find amplitude variation at non-constant duration.
Here is a detail of what else bats use . Its harmonics that takes sleep of physicists.

I don't understand the second section

its hard to explain in much detail the second point but just understand that bat get reflected voice from multiple incident points. Replicating such voice using single source generator won't be any effective. More simply, have you  ever been tricked by mobile sound as real human voice at some distance?


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Is this a bedbug? Found in my bathtub
I found this bug crawling in my bathtub

Yes it seems like bedbug. If you want to make it certain put it on your skin and let it suck some blood. After sometime kill that bug by pressing it against your nails. If your nail is smelling awkward then it is definitely a bed bug.
Try comparing your bug against this post.


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How was Crisper Cas9 function discovered?
What paper outlines the discovery of how the CRIPER DNA, CrRNA, and Cas9 interact?

The two "classic" papers cited in terms of Crispr/Cas9 discovery include the Doudna/Charpentier initial discovery, and the Feng Zhang application to gene editing.  There is an ongoing, famous patent dispute as to whom really discovered the Crispr/Cas9 gene editing technology.
As a quick timeline that better answers your question, a good publication is Cell Paper and there is actually a great podcast, but I will summarize:

Yoshizumi Ishino et al. in 1987 Discovers Crispr mechanism - the authors simply noticed the odd regular repeats of DNA in bacteria and noted: “no sequence homologous to these has been found elsewhere in procaryotes, and the biological significance of these sequences is not known.”
Francisco Mojica in 1993-2005 - Furthers research into CRISPR, at this time the terms has been coined by Jansen, however it is Mojica who really notices the Crispr pattern in several bacterium and suggests that it is involved with an immune response.
Alexander Bolotin in 2005 - Looking into the bacteria Streptococcus thermophilus, Bolotin discovers that the genetic material in between the spacers is viral DNA, providing definitive evidence of the Crispr hypothesis.
Marakova in 2006 - First proposal that the protein Cas9 can be used in a bacterial adaptive immune response, although Bolotin is also credited around this time from noticing the use of Cas9.
Koonin in 2006 - The first one to piece the Crispr storage of viral DNA and the Cas9 reports of an immune response together as a related system that might be able to use the Crispr DNA with Cas9 in an immune system.
Marraffini in 2007 - Studying the Crispr-Cas9 system further, he provides the first definitive microbiological evidence that Cas9 is a programmable restriction enzyme, and that it targets DNA not RNA. At the same time Philippe Horvath, Danisco France also provided the best evidence yet of the adaptive immunity system.
Doudna and Carpentier in 2010 - Through sequencing, definitively put the Crispr and Cas9 system together as complete unit that is able to cut DNA, they also described tracRNA as the RNA piece that join with Cas9 to program DNA cutting.
Feng Zhang in 2013 - While Doudna previously suggested that the Cas9 system could be used to target mammalian DNA, Zhang was the first one to actually that it was possible and therefore open to the door as the Crispr/Casa9 system as a tool that easily edit genomes.

While I definitley missed several key steps, and did not fully explain the actual mechanism of Crispr/Cas9, I think this provides a decent timeline.  For more information about the actual mechanism see: Harvard, Wired, Science News.

This paper will tell you about it.https://www.ncbi.nlm.nih.gov/pubmed/?term=A+Programable+Dual-RNA-Guided+Endonuclease+In+Adaptive+Bacterial+Immunity
I am not allowed to seee the full text,but there it is.
Here is a full text link of that paper
http://science.sciencemag.org/content/337/6096/816.full


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What tree has three balls
I have seen this tree in Spain and Portugal. Its leaves and bark bring to mind the American Sycamore or London Plane Tree, but not exactly. Also, it has three spherical fruits, an arrangement I am unfamiliar with. Like an idiot, I left my tree identification book at home and the Internet has failed to satisfy my curiosity in this matter. Any help would be appreciated.

As you noticed this is definitely tree from Platanus order.

The London plane which is Platanus acerifolia, which is more casual is actually a hybrid of two platanus. Those two names are Platanus occidentalis and Platanus orientalis.

Frankly, I think the one of what are you looking for is that Platanus orientalis. See it on a picture of seeds taken from Wikipedia.

What a useful and interesting answer! Thank you. Additionally, the links you included made for fascinating reading. I am charmed even more by these magnificent trees.


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Why do humans enjoy spices?
It seems that many flavor and food preferences can be explained in the context of regulating feeding behavior. Generally, organisms tend to enjoy those foods which are optimal for them to feed on and provide the best nutrition. There are well-known exceptions to this, such as:

Artificial chemicals (eg. the supposedly sweet-tasting but deadly polyethylene glycol) which are very rare in nature, thus there was no opportunity for an appropriate taste perception to evolve
Nutrients which are desirable in moderation but dangerous in excess (eg. sugar), but have only become readily available recently thanks to technology (thus once again moderated consumption has not had opportunity to evolve)

But humans in particular also seem to enjoy consuming a large variety of foods that one would expect to be unpalatable or mildly harmful. For instance various peppers, spices, hot sauces, wasabi, mustard and so forth, don't appear to provide much of a nutritional benefit. Indeed their chief property of interest, the spicy flavor, is a defense mechanism: The plant attempts to make itself unpalatable or toxic to deter predation. Why is it then that this very defense mechanism has ironically become prized as a food ingredient by humans, to such an extent that wars have been fought over access to spices? And why is it that humans do not consider (for instance) pure, fresh, raw meat to be more delicious than meat with seasoning or condiments?

There has been a similar question (see comments) on here but that has also not attracted a good answer. I think this exemplifies the enduring interest in the subject and as such I'd like to keep this question open to stimulate a better response from more recent visitors.

I don't know enough of this, so I won't answer. However, I know that one hypothesis is pathogen avoidance. I don't know how much truth there is to it, but it is sometimes claimed that spices help against pathogens. Proponents of the antimicrobial hypothesis (as it is called) point for example to the fact that spicy food is more common in warmer climates as evidence for the hypothesis (the point, of course, is that pathogens are more common in warmer climates). However, I don't know whether there is something to the hypothesis or not.

@John Incidentally, also unanswered.

actually there are two answers


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Who/where has the advocado genome been sequenced?
I have read several places that the genome of the advocado has been sequenced in mexico but i am not sure at what university or persons involved.

Although it does not matter much for this question, please never just say I have read several places without correctly referring to where you read that.

You can search for genome sequences at the National Center for Biotechnology Information (NCBI) site.
Here is a link to Persea americana (avocado) from NCBI. It states on the page the submitter for the genome was Hainan University.

I found all the sequences they did here: https://www.ncbi.nlm.nih.gov/Traces/wgs/?display=contigs&page=1   However they are 5000 different short sequences.  How to combine them or view them in a searchable manner?

@Dale            You can access the entire genome via: https://www.ncbi.nlm.nih.gov/Traces/wgs/?val=NXHZ01 and then go to the Downloads tab and you can download the FASTA file. This will have all the 5000 contigs together in a ~130MB file. If you do not have software to open the file type, you can change it to a .txt file and open it that way, although you might want to use a good text editor for that. https://en.wikipedia.org/wiki/FASTA_format


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What mushroom species is this?
Found in garden ,Brisbane Australia at base of trees and amongst plants in open ground

you need a decent mushroom book m8. flipping through the pages of a well photographed book always leads to a close ID, and good ones have spore drawings too.

Could you describe the substrate they were growing on? For instance were there wood chips under the plants, or were the fungi growing on soil? Did you get any photos of the stipe (stem, if any) and a clear shot of the pattern of the gills?

These look like they fall under the description of 'gilled fungi with lateral or no stipe' (there looks to be a lateral stipe on at least some of the fruiting bodies), so it should be in https://www.fncv.org.au/wp-content/themes/field-naturalist/publications/fungi_in_australia/fia-8-pg-lateral-stipe.pdf. Crepidotus crocophyllus sounds like a close match, but the pictures don't seem to agree as closely...


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Finding out the best concentration for my plant extract to be used as drug for diabetes
I am using plant extract of Ajuga parviflora and found out that it possess anti-diabetic properties by using alpha-amylase inhibitory assay. I used various concentration 250 µg/ml(29% inhibiton of alpha-amylase), 500µg/ml(37%),750µg/ml(46%) and 1000µg/ml(63%). Basically, alpha-amylase results in increase in glucose level after eating food. So  i wanted to know that how could i find out that what is the best concentration of my plant extract to be used as drug.

This sounds like a homework question. Is it?

No, i am in my final year of my btech working on a plant and when a plant report some property then it is better if we can also give its best concentration.

You have to try to determine the best concentration.
Usually there are multiple clinical trials, first in animals, then in humans to

figure out the effective dose
look for side effects
compare the new drug's efficacy with existing drugs

I think this is better as a comment as it doesn't answer the question which in any case looks very like a homework question.

@David Actually I started writing a comment first and was expecting a "please don't answer in comments" response :) And it didn't occur to me this could be homework.

@David Owh, and the answer was: You have to try.

"humen"? spelling is human...

@SolarMike Yeah, was confused by the man/men and woman/women plural.


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What is the earliest point at which one can detect pregnancy?
Imagine a woman gets pregnant on day X. What is the shortest interval (like a day, a week, a month) after which she can detect she is pregnant?
Example: Let's say that she keeps track of her menstruations and the next one should occur on 2018-05-01. On 2018-04-29 she has sex without protection and she doesn't take birth control pills. On 2018-05-02 she hasn't got her period. Is it reasonable to assume that she is pregnant based on these facts?
Note: I need this information for a fiction book. It doesn't need to be 100 % accurate, just believable.

Is it reasonable...? I don't think so, based on this limited data. A lot of variation is normal in the length of a cycle, and OCP can themselves alter the cycle's periodicity, at least in the close aftermath.

What if the woman gathered a lot of data and knows (based on past data) that her period comes with the precision of a Swiss train?

It is then, only speculation in my opinion. For the purpose of a sci-fi setup it might be sufficiently plausible, but not otherwise. Plus, the fertility window of menstrual cycles is limited, and late in the cycle, the chances of a successful fertilization drop. A better premise might be to make her realize her pregnancy during the cycle before she has missed a period, using some biomarker or hormone or something.

It's not a sci-fi setting. Maybe I expressed myself incorrectly. After what time after conception can a woman know that she is pregnant? One week, two weeks, a month, two months, more?


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Sound produced by muscle tightening
If you are at some quiet place, you will hear some mild noise when you tighten your jaw. Why is this? Is this sound produced by face/jaw muscle?

You can do something similar with your ears as well What causes “ear rumbling”? and What is official term for contraction induced muscle “vibration”?


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Is there a specific terms to describe variant of existing genes in bacteria?
I have a question regarding a specific term that describes the variant of existing genes. I am analyzing whole-genome sequencing of a bacterial isolate. I found there are a large number of genes that have partial sequence identity or subject/query coverage to the known reference genes.
Now I know that by looking at sequence identity and coverage may not be enough to analyze the genes. I know some gene can have 30% sequence identity and still folded the same way as the original genes. However, let's say these genes are truly variant of the existing genes based off sequence identity. What is the term to call them?
My PI told me they are rapidly evolving genes. I searched some paper and found rapidly evolving genes are genes that are subjected to positive selection. While I agree for some of these are rapidly evolving genes as they probably subject to positive selection, I cannot see that all of the genes actually undergoes selection at same time. I am wondering if there is another term to call these gene variants. If there is any paper to define them that will be great.
Thanks

Allele
From wikipedia > allele

An allele is a variant form of a given gene

I somewhat disagree with this definition in the sense that it is not general enough. An allele is a variant at any locus (locus = position in the genome). You can talk about allele at non-coding sequences. Also, if you are talking about a coding sequence, you can define different sequences as belonging to different alleles whether or not their protein products differ in function or not. The proteins might even be the exact same one for two different alleles if the only difference between these alleles concerns a synonymous mutation (or a mutation in an intron).
You can feel free to define that different sequences as being different alleles by any kind of arbitrary threshold measure. You will just need to define it. For example, you can define that different sequences are different alleles only if they have at least 5% pairwise differences or if you found out by some biophysics computation that they ought to fold differently or for whatever another arbitrary measure.
The term allele is used very often in evolutionary biology and you'll find its usage in any intro course to evolutionary biology.
Rapidly evolving genes
As far as I know, there are no commonly agreed upon definition for what a rapidly evolving gene is. To me, a rapidly evolving gene is simply a coding sequence which evolved more rapidly than other reference sequences. Per se, although it would very likely involve positive selection, I don't think it is a requisite by the definition of rapidly evolving genes. It could, for example, be caused by a very high mutation rate at this particular sequence or by balancing selection causing any new rare alleles to be beneficial.

Thank you for your answer. Yes, I am mainly talking about coding sequences. I will try to find a better definition of rapidly evolving genes.
The reason I don't want to use positive selection as definition for rapidly evolving genes because it make it sounds like there are over half of my coding sequence are under positive selection which doesn't make sense to me. If they are under selection and are mutating fast enough that should be better.


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Can anyone help to identify this fruit?

It stays the same color when ripe. It's about the same size as a pear. Grows in sub tropical climate of Meghalaya, India.

It seems like cutting it open and showing the inside would give us more insights

Will cut it open and check if it is indeed Solanum Muricatum as suggested.

I think this looks a lot like a pale variety of Solanum Muricatum or Pepino dulce/melon/pear.

It's native to South America, but I think that it would be able to be cultivated in India as well.

Thank you so much. This very much looks like the plant I have as well.

@JamesSyngai Did you know already that you can mark an answer as accepted, if it answers your question? You just need to click the check mark symbol next to the up and down arrows of that answer.

It looks like Tinda (Praecitrullus fistulosus), also known as round melon, Indian round gourd, Indian baby pumpkin, apple gourd, or Indian squash.

Source: https://www.bigbasket.com/pd/10000372/fresho-tinda-250-gm/

Source:  http://fruitspecies.blogspot.com/2008/10/tinda-indian-round-gourd.html

I am not fully sure but in my opinion the leaves look more like chili pepper leaves and it resembles a tomato or eggplant in the fruit, with a similar stem. It's likely a member in the nightshade family (also known as Solanaceae) https://en.wikipedia.org/wiki/Solanaceae .
For reference, a green eggplant:

However, I am unsure what the specific species might be as the leaves don't match the typical eggplant pattern.


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How to generate protein graphics for illustrating articles?
The structure of insulin shown below appears in a Wikipedia entry.
What software was (or can be) used to create pictures of this type?

Have you tried to Google protein 3D visualization?

Please give a reference to this particular example. You are surely aware that Wikipedia's contributors (not users) are completely independent and thus use whatever software they choose to create molecular images. This is hardly a question about biology, and, as @Remi.b  said, you can find out about different molecular graphics software. You might also wish to look at the PDB site, which used two alternatives in their displays. But none are simple push-button programs, but require you to learn proprietory scripting commands.

I really appreciate your comments

there are plenty. Try autodock for a start

All comments are great, there are numerous software programs that allow you to make such images.

Gathering information about the insulin structure
By simply clicking on the image in wikipedia it will provide you with  valuable information:

Created by Isaac Yonemoto created with en:pymol, en:inkscape, and
  en:gimp from NMR structure 1ai0 in the en:pdb. Ref: Chang, X.,
  Jorgensen, A.M., Bardrum, P., Led, J.J.

So the creators used pymol, inkscape and gimp, but let's dig a bit deeper. Unfortunately Isaac Yonemoto, the editor of this wiki, did not provide a direct link to the original publication (see wiki file history). However by searching the author names in combination with insulin we quickly find the article: Solution structures of the R6 human insulin hexamer. In the first paragraph we see:

The atomic coordinates of the 20 refined hexamer structures and the
  NMR-derived restraints have been deposited in the Brookhaven Data Bank
  (PDB ID codes 1AIY and 1AI0 for the symmetric and the nonsymmetric
  hexamer, respectively)

You can find the structure that was depicted in this wiki article by searching the PDB id.

Creation vs visualization
You can interpret 'create' in your question in two ways here:

Creating this whole structure from nothing
Visualizing a structure someone else determined

If you refer to the former you should look at the article corresponding to this structure. Note that this is quite detailed and requires  knowledge of several concepts, such as molecular dynamics and NMR spectroscopy. If you refer to the latter than you should take a look at the programs mentioned earlier such as pymol, inkscape and gimp

Not generalizable
This boils down to what @David already said in his comment:

You are surely aware that Wikipedia's contributors (not users) are
  completely independent and thus use whatever software they choose to
  create molecular images.

Just to add, the author of that specific image did cite the PDB ID which allows you to find the structure, paper, etc in RCSB.


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Is there recent info about the hypothetical ancient two-codon genetic code?
Here is the latest I have found. link
This is the basic idea: Evolution does not look ahead and make plans. It would not create a system of mRNA with giant ribosomes to create proteins, until proteins were already useful. There must have been a simpler way to create useful proteins before, that got complexified after it was already useful.
Since enzymes can be made of RNA, presumably early life made just RNA enzymes and no proteins. It didn't matter whether RNA enzymes were as efficient as modern ones because protein competition hadn't evolved yet.
And since we now make peptides off an RNA template, probably early proteins were also made off an RNA template. It is hypothesized that particular amino acids would be attracted to particular RNA pairs, and they would be put in just the position that would help them link to neighboring amino acids. This could be slow and inefficient compared to modern protein production because again the competition was not stiff back then.
Between two pairs of coding bases, the RNA needed a noncoding base for spacing. Possibly the noncoding base might be particularly good for catalyzing the joining of amino acids.
The system did not have to use the same amino acids we use today. It could use amino acids that were good at attaching to RNA, and later after the system got changed around the modern list of 22 amino acids could have developed.
There are various ways this is a satisfying idea. For example, the machinery to make proteins is largely made of RNA. The mRNA carries the message. tRNAs decode the message. Ribosomes are giant machines which transcribe proteins efficiently, and they are largely made of RNA with a lot of little proteins that help them hold their shape etc. Presumably the first protein-building machinery was itself built entirely from RNA -- because that's what was there to build with -- and over time evolution found ways to improve that machine with protein scaffolding.
This 2005 paper link describes a reasonably plausible way it could have been once. They imagine a few alternate amino acids which might have once been part of the genetic code -- ornithine. Homoserine. 2,4-diaminobutyrate. They imagine ways that the crevices between pairs of bases could be like the binding sites of enzymes. They fit the ideas together.
Have there been advances since 2005?

I doubt it, and I doubt whether you'll find anyone here who is even familiar with the idea. However I suggest you try to answer your own question yourself by looking for papers that cite the 2005 paper.  The online PNAS site may have this, otherwise I am sure that there are tools for doing so.

@David I don't think your comments are fair or constructive. They don't help improve this valid and interesting question. The paper has been cited 75 times so it seems like research continued after 2005. The question seems like it was written after J Thomas put effort into getting an answer.

@Michael_A — On the contrary, my remarks were absolutely constructive. I told the poster how to get an answer to his question, assuming that my subjective view of the likelihood of his getting an answer here was correct. (A view based on my experience of responses to questions on protein synthesis.) You confirm that this approach will bear fruit. The poster may well have tried to get an answer, but had been adopting wrong approaches. As an educationalist on this list I try to help people to learn how to learn, rather than spoon-feeding them. (In this case I have no spoon.)

I don't find this advice insulting, and it is of course a valid approach.
I wanted to ask the question first because if someone is following the topic, they may point to great research that many of us would like to know about. While I would like to eventually study all of the literature since 2005, there is no harm in getting tips about important links.
And second, I thought that some people who are unfamiliar with the topic might like to hear about it.


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Is this a worm or snake?How to get rid of it?

Hi! I found this thing in my bathroom. I killed it but still it's friends keep on reappearing. It moves slowly , is it a snake? How can i get rid of them? I live in Mumbai, India. It's rainy season here and the size of animal varies from 5 cm to 15 cm approximately.

This animal moves slowly. Have a look at this video https://youtu.be/IDhxsmuRq3w

If it's dead you should be able to get some closer pictures? (Looks to skinny to be a snake, but really hard to see anything)

Hi! I just got a clear video of its young relative. Can you tell me what is it? https://youtu.be/gOsNf-jtppM


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What is the evolutionary or biological origin of apathy and indifference. Is it uniquely a human thing?
I believe that social apathy is one of the main reasons why changes cannot easily be brought about in contemporary society due to the general lack of interest of the public, and this has ties with many mental diseases
But does the act of indifference and apathy actually has an evolutionary advantage and more curiously, do animals known how to demonstrate that in some manner?
A Google search on "evolutionary origins on apathy" returns no relevant hits other than the links to schzophrenia and other related neuropathies

Are there known studies on apathy and indifference in animals and their evolutionary origins?

I have edited your post, partly to correct the English, and in particular the misuse of the word disinterest, which means lack of bias from having an interest (financial etc.) in something. I have also changed "We knew" (presumably meant as We know) to "I believe". I believe it is bad practice to make unsupported assertions of this sort, attributing them to others, rather than taking responsibility for them yourself. I personally neither know what you assert, nor do I believe it.

You need to ask the reverse question why would a species evolve to care about individuals not related to it, the only examples are reciprocal altruism which has so strict requirements.

one has to try to define "apathy" and thats tricky, but maybe you really are looking for "low altruism" where altruism is well explored in evolutionary theory. on other hand maybe you are overthinking this, what you are really describing is "survival of the fittest" which involves/ or is at core an individual-centric drive to compete/ survive ie "zero sum game". there seems to be some interspecies altruism where for example in africa, sometimes different animal species will occasionally assist each other evading predators. so there seems some tradeoff between altruism and survival-of-fittest.

While I'm really unsure as to what you mean by "social apathy". even a cursory observation of animals will show that they're apathetic about many things.  (For instance, of my two dogs, one gets excited when I throw a tennis ball, the other could care less unless I throw it into water.)  The parts about changes to contemporary society might be better addressed on the Politics site, though I must say that it's quite possible that large numbers of people like society the way it is better than they do your proposed changes :-)


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Will humans ever evolve to cope with the rising temperature of our planet?
I am a complete layman of this field(Biology).I went through an article about global temperature rise and i wanted to ask this question.

Federal science agencies announced Wednesday that 2016 was the warmest year on record, beating the previous record of global temperature set in 2015, which had beat the previous record set in 2014.

(As seen in the graph temperature is rising rapidly and will increase even more in the near future.)
Can we evolve to cope with high temperature?Will we evolve?Is mutation the only answer?
(Frankly not looking for an answer saying by natural selection,the last thing i want to hear)

The graph actually shows that the temperature has risen although over the last few years it is constant. What it does not, and cannot, show is the direction it will take in the future and, if there is a change, how rapidly it will occur.  There may be other reasons for thinking it will change, but as a layman you should learn that it is unscientific to attribute these to the graph you present. This should be evident from the fact that previous downward trends did not continue.

No, for two reasons.  First, the time scale of human evolution (10K-100K years) is much longer than the time scale of the athropogenic temperature increase (100-1000 years).  Second, if the rise continues, humans will become extinct, along with most multicellular life.

A change in temperature of 1 degree, or even 4 degrees, is less than the variation in temperature that is seen between different areas that are inhabited by humans and less than the variation which is seen annually in those areas. Accordingly it seems that humans are already adapted to these differences in temperature and that our response to the temperature changes are more likely to involve habituation and cultural changes in behaviour and technology use than evolutionary change.

The difficulties for human are not so much a direct effect of the few degrees difference but the effect that temperature will have on ecosystems in general and on our agriculture and its repercussion to us.


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For long term survival of a species in a harsh environment which is more important-mutation or evolution?
The environment is the ultimate cause of population stabilization. Considering the environment to turn harsh for the survival of a species.How to adapt better to this change-by evolution or by mutation?

Considering mutation is part of evolution this question does not make a lot of sense.

maybe because i am not related to this field

One of the central requirements of evolution is that individuals of a species vary. Natural selection acts on variants. Mutation is the source of variation upon which evolutions works. Variation is then increased through sexual reproduction and recombination. Variation in the environment is the reason that variation among individuals is so important for the long-term survival of a species. Otherwise, it would be best to fix on a single optimal genotype. But with variation in the environment, the optimal is a moving target. So your question is complex. Variation in the environment requires a mechanism for species to adapt to change. That mechanism is mutation, amplified by sexual reproduction and recombination.

To operate for many generations evolution needs a process that adds variation (mutation) and a process that removes it (natural selection). Evolution can operate without mutation but not for very long the process will exhaust the available variation rather quickly.


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Recognition of snake (image)
I would like some help with the recognition of the snake shown in the image below. I was doing a fieldwork in a forest in Slovakia when I found it.
I was thinking it could be a water snake but I am no expert in snakes.
Does someone know what kind of snake is this?

Aesculapian snake (Zamenis longissimus). Common european species, non venomous, rodent/egg eater.
edit1: they can swim and can be found next to water bodies but are terrestrial.


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Can the environment affect genes and adaptation in offspring?
I recently read several articles that believe that environment can affect gene expression and this change will transfer down to the children. Some theorists believe that random mutations are more rare and time consuming than a mutation that develops as a response to change of the environment the organism is in.
Epigenetics could be the key to how animals adapted and evolved so fast.
So does this mean a couple living in say, Siberia (both of whom migrated from say, Congo) will have higher probability of transferring gene variations to their children or grand children that will allow them to adapt better to the cold (as compared to the offsprings randomly developing mutations that help them adapt to the cold, and then passing it on to future generations)
Does that explain how humans were able to evolve quickly to their travels from Africa to the rest of the world and still survived the drastic changes in environment, rather than conclude that random gene variations led to adaptation?
Is this genetic adaptation as a response to the environment  biologically proven?
http://dukemagazine.duke.edu/article/big-question-can-your-environment-change-your-dna

Welcome to Biology.SE. I am afraid your question is very unclear. I have not read the linked popular article but I suppose you are talking about epigenetics. If yes, you should make this clear. random mutations are more rare and time consuming ... than what? gene expressions could be the key to how animals adapted this is very unclear. Does it mean mutations to regulatory sequences or are you still talking about epigenetics? higher probability of transferring gene variations to their children higher than what? I am VTC as unclear.

@Remi.b , edited the question with clarifications.

Offspring has no plural. (Oh, and the answer to your question is NO, but until you provide evidence to refute, this cannot constitute a SE answer.)

Generalities
You have misread the articles (or read misleading articles).
Epigenetic modifications are, by definition, any modification to the DNA and proteins attach to DNA that does not affect the nucleotidic sequence (note that I here ignore some of the difficulties defining the term epigenetics). Such modification include methylation of histon tails for example (a histon is a protein around which the DNA is wrapped). Those epigenetic modification can appears in reaction to the environment and can be passed on to the offspring giving it a seemingly Lamarckian style of inheritence.
A mutation is, by definition, a change in the sequence of nucleotides. An epigenetic modification is therefore not a mutation (and a mutation is not an epigenetic change).
Comments in the text

Some theorists believe that random mutations are more rare and time consuming than a mutation that develops as a response to change of the environment the organism is in.

You might want to avoid calling "mutations" "random mutations" because it feels like you might not understand how unclear this phrasing is. Have a look at the post Are mutations random?
Epigenetics change are NOT mutations.
The claim is too general and unclear and is impossible to comment about it without knowing what process you are interested in. One might claim that most genetic variance in populations is caused by epigenetic variation or make other claim that can be discussed but the above claim is too broad and unclear.

So does this mean a couple living in say, Siberia (both of whom migrated from say, Congo) will have higher probability of transferring gene variations to their children or grand children that will allow them to adapt better to the cold.

I don't understand what you mean here. And it feels to me that explaining everything that is unclear and going through all possible ways of understanding this sentence would take too much time!

Does that explain how humans were able to evolve quickly to their travels from Africa to the rest of the world and still survived the drastic changes in environment, rather than conclude that random gene variations led to adaptation?

You are really not using the term random correctly, which makes your question hard to understanding. Also, instead of gene variation I suppose you might want to use the term allele.
It is possible that epigenetics has played a role to allowing faster range expansion / range shift of human populations. I don't know if this is the case and I don't how important of an effect it would have.

Is this genetic adaptation as a response to the environment biologically proven?

Epigenetic, not genetic. Yes, epigenetic modifications do exist. We have plenty of evidences. I don't know how much we know about their impact on population range shift and survival but I would notice that it depends upon what mechanism exactly we want to consider into the broad term of epigenetics. For example, everybody will consider histon modification as part of epigenetic modifications. However, not everybody will want to consider fat content in the egg as an epigenetic modification. There is also a blurry border between what would be environmental effect (such as maternal effect) and epigenetic effect. But this is a discussion for another time.

Epigenetic modifications may exist in bacteria and in the differentiation of cells, but I have yet to see a study that shows environmental conditions can cause e.g. histone modifications in humans, and that these can be inherited. This seems to me to be the sleight of hand in all these popular articles. So no, this is not biological proven.


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what species moth is this?

found in garden in wiltshire, england. about 15mm-20mm long. Resting at 6pm on raspberry plant.

You have found Smerinthus ocellata, the Eyed hawk moth. It is name comes from the eyes on the hindwing, which do not show at your photo. It is known to show these eyes if disturbed, to scare of attackers.
Photo from wikipedia commons:

The forewing shows considerable variability, as you can see here


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Failed attempts at changing ecosystem in order to preserve it?
Have there been any notable tries in the recent past (think 20th century or later) to purposefully change any ecosystem in order to save it or some particularly species in it, but which have instead produced the opposite effect? I am sure there must have been, but can't bring any to my mind at the moment.
Like, for example, if you have an island that has some large felines, which frequently attack sheep that are becoming scarce, so the felines are starving and becoming scarce, too. So you introduce feral goats, which were supposed to provide meat for felines, however, goats were (a) too nimble for felines to hunt well due to, eg. geography of the island (too many rocks that goats can prance about, but cats not so well), and (b) ate all the grass that sheep still had. So the net effect was that sheep died out, cats died out and there remained a few goats.
I am aware of a number of cases, where these things could have happened due to humans not aware or not caring about the problem (eg. introducing rabbits in Australia), but I am wondering specifically about misplaced efforts to save/stabilize an ecosystem.

Perhaps not quite what you had in mind, but it seems like the introduction of the mongoose into Hawaii is close. In the late 19th century sugar planters introduced mongooses into Hawaii in an attempt to control rat populations. It turns out that rats are mostly nocturnal, and mongooses are mostly diurnal, so the two species rarely interacted. The mongoose population boomed and had a huge negative impact on native bird and turtle populations, since the mongooses would eat the bird and turtle eggs.


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Is this a Wolf Spider?

I live in Illinois and this came running across my living room floor.  After I stopped freaking out, I threw a bowl over it and called someone to come get it.  It was about 5” across.  My son thought it was a wolf spider but I didn’t think they got that big.  I hope someone can help to identify it.  Just the thought of there being more around is making me want to book a hotel!

That's not a Wolf Spider, although it's often mistaken for one.  The long, jagged-edged-banded legs, splayed out in a characteristic flat posture, and the large, round carapace are pretty characteristic indicators of a Dolomedes fishing spider - one of the terrestrial ones that have moved into drier, upland areas and hunt more like Wolf Spiders do.
There are two species this could be, but the fact that you don't see a full white underline beneath the 'w's on its abdomen tells you it's not Dolomedes scriptus, but its common relative Dolomedes tenebrosus.
These spiders are actually pretty mild-mannered and can make good pets (as spiders go), but they will bite if bothered too much (how much "too much" is seems to be different from spider to spider).  The bite can be painful because of their size and large fangs, but the venom is not particularly effective against humans.  I'd rate it as a lot less painful than even a mild wasp sting, although of course every individual spider and every individual human is different.
Here's a link to the Bug Guide page, which has more information and lots of photos..
https://bugguide.net/node/view/2011
I should also add that these guys eat beetles and other relatively large insects and small animals that you might or might not want to share your home, if that makes any difference.  I can't see its pedipalps clearly, but the large cephalothorax and relatively small abdomen make me suspect it's an adult male, just wandering around looking for love.  It's unlikely that you have all that many individuals living with you - unless you have a dirt cellar, of course; they seem to like places that are a bit cave-like.
I also forgot I'm supposed to include an image: