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Why does high-voltage mostly shock a person, and even small current kill?
This may be the wrong forum to ask.
For instance several people are known to have survived a direct lightning strike; albeit the number of fatalities are probably far larger. Anyway, I found myself wondering why high-voltage may shock a person and throw them off whereas high-current even small current is, purportedly, a killer.

Related questions on Skeptics and on Physics: http://skeptics.stackexchange.com/questions/1664/it-is-not-the-voltage-that-kills-you-it-is-the-current http://physics.stackexchange.com/questions/7911/why-can-different-batteries-with-the-same-voltage-send-different-currents-throu

@nico: Thanks! An answer on the linked skeptics post links an article that answers the question

These statements are not true, simply speaking. Currents as little as few microampers can kill a person if, for example, applied directly next to the heart. A few seconds of 220V can kill a person even if the current is in miliamper range (Biksom, cited below, mentions 4s at 120mA). However, it is true that it is not the voltage alone that kills, that there are other factors (most importantly, the effective current, which, however, normally increases with voltage).
Look, Ohms law states that R = V / I (resistance equals to voltage divided by current). Given a constant resistance, a higher voltage produces also a higher current, full stop. Given a voltage of, say, 24 V, and the resistance of our bodies being 1000 - 4000 Ohm, the current will not exceed 6 - 24 mA. Note that in case of 220V this largest current would be less than ten times these values, so well below 1A! Yet, this is sufficient to kill an adult.
What's more, extremely high voltage can actually break the skin and effectively lower the skin resistance, which results in an even higher current (see formula above).
So where does this popular knowledge come from? Well, we know that things like electric sparks can have very high voltage, but are harmless. They are harmless not because the current is low, but because the duration and the total energy is low, since the total energy is given by power (in watts) times seconds, and power P = V * I (voltage times current).
Also, it comes from anecdotical evidence, since being shocked by thousands of Volts and survive can make you famous... precisely because it is extremely rare to get into contact with a high voltage line which can supply a steady flow of the current and survive.
Another reason became apparent in the comments: confusion between the factual current of the jolt one is getting and the nominal amps on the fuse. The former is given by the resistance and voltage; the higher the voltage, the higher the current. However, an 1A fuse is likely to blow quicker than a 10A fuse, thus cutting the line before the current penetrates our body to reach the heart and bring it into fibrillation.
It is a similar story with lightnings: duration is extremely short, but more importantly, in most of the cases the lightning did not run through the person who survived -- because if it did, they would be dead (also, see this fascinating bit). It either run over the skin, seeking the path of the lowest resistance, or through a material nearby.
Also, high frequency currents are less likely to penetrate the skin.
Literature links:
Biksom, "A review of hazards associated with exposure to low voltages"

Sorry I'm not sure abou this.... can you provide references? I think 220V with milliamps is not usually, or even commonly fatal.  Most of us have gotten shocks from home outlets (110V 10+ amps) and not had to go to the hospital or anything.  Do europeans die when they get home electrical shocks - their standard voltage is 220-230V?   Anecdotes aside, if i had to choose, I think there's reason to prefer a high voltage jolt with low current vs lower voltage with lots of amperes.

110V 10+ amps would have killed you on the spot. However, the point is that these 10 amps are nominal, the most current that can be provided without blowing a fuse. The real current is given by the resistance and voltage. Also, the physics is such: given that your resistance remains constant, you do not have the alternative "high volts, low amps vs low volts, high amps".

My mistake. I did indeed mean even little current fatal rather than large current fatal. Whereas several kV may even be survivable. I'll just make the correction

I come in touch with several kV every day (static electricity).

@January you said 'milliamps'.

It depends entirely where the current passes through. If the circuit is completed through your hand, you are unlikely to die no matter what the current. But it it completes across your chest, you run a much higher risk of fibrillation and heart attack.


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How are there multiple varieties of the potato?
The potato appears to propagate by growing an 'eye'/'bud' which eventually grows into a new plant. So there would probably be single representative of the potato species in the world with all others being genetically identical.
Yet wikipedia indicates there are several closely related species of the potato; apparently as a result of selective breeding. To my understanding (which is probably wrong) there is only a single potato that grows the eyes without the need for a second parent - so there should probably only be the same genes repeated in each potato/plant.
What am I missing here? Why are there multiple varieties of the potato?

Spontaneous mutations?

This question is more interesting that first meet the eye (ho-ho).

You're missing that potatoes also reproduce sexually.
They're flowering plants, and they produce seeds that are not genetically identical to their parent plants.

I've never seen them flower ... and i missed it on the wikipedia page too.

Wikipedia describes the flowers, fruits, and seeds, and goes on to say "All new potato varieties are grown from seeds, also called "true seed" or "botanical seed" to distinguish it from seed tubers."

Well, uvesten is correct in saying that potatoes are flowering plants and as such they can reproduce sexually. However, as everyone mentions potatoes can, like many plants, reproduce asexually by putting out clones.
Since clones are (by definition) genetically identical to the parent plant, this would seem to rule out the possibility of producing different varieties (or even species) from clonal propagation.
But! this very interesting study by Jiang et al. looked at Arabidopsis lineages (Brassica family). They found:

"in vitro regeneration of Arabidopsis plants results in a high frequency of heritable phenotypic variation "

That is, regenerant Arabidopsis plant lineages displayed extensive phenotypic somaclonal variation - the cloned "offspring" were not genetically identical. They attributed most of this genetic variation to an increased base substitution frequency in the regenerant offspring but there may also be unknown epigentic factors as well.
Jiang et al. summarise:
...

... somatic mutation rates are characteristically higher than germline rates in multicellular organisms [26] and has important particular potential consequences for the evolution of plants, given that they frequently adopt life cycle strategies that involve regeneration from somatic tissues.

So, perhaps some of the variation we see in plant species which commonly propagate asexually actually arose during this process and not via sexual reproduction ... ? This would be good news for houseplants which are nearly always propagated asexually.
However, I am not sure whether this extends to potatoes.
Jiang et al. 2011, Current Biology, 21, 1385, Regenerant Arabidopsis Lineages Display a Distinct Genome-Wide Spectrum of Mutations Conferring Variant Phenotypes

Thank you, Poshpaws (+:
This is what I seem to experience as the potato plants hereabouts spring from the bud on the tuber

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Does the DNA sequence of a butterfly match that of the caterpillar it used to be?
Just had this thought occur to me.
If one were to take a DNA sample(or is it RNA?) of a caterpillar before it became a chrysalis, and attempt to match the sample against one taken after the chrysalis matured to a butterfly, would the two samples come up identical?

By 'signature' do you mean sequence? Is the sequence of caterpillar DNA the same as the sequence of butterfly DNA? And if you do mean this you probably need to differentiate between somatic cells and germline cells in the butterfly.

@AlanBoyd: DNA Sequence is probably what I had in mind. That thing the Ministry of Law use to definitely identify a person...

Sometimes a caterpillar turns into a wasp rather than a butterfly. But then its DNA Is very different! (And it doesn't go on to make more catterpillars)

The genome (entire DNA sequence) of the butterfly would be identical to that of the caterpillar in all somatic cells.  A caterpillar has the genes to produce wings, for example, however at that stage in it's development they are not 'switched on' to make the necessary proteins.
If you were to sample the mRNA produced from transcription of the DNA in the caterpillar and butterfly stages, there are likely to be many differences.  As in the example I previously used, the mRNAs that are translated into wing-forming proteins are more likely to be apparent in the butterfly than the caterpillar.  When saying this, please be aware that I'm assuming that the regulation of these genes is pre-transcriptional - I'm not an expert of butterfly physiology!

Forgive me, but would it be possible for you to elaborate on 'pre-transcriptional' ?

@Everyone there are several points in protein production where regulation can happen to stop it being produced - this happens naturally (for example there is no benefit to producing chlorophyll in root cells where there is no light).  Some of these points are before the DNA is transcribed into mRNA (pre-transcriptional) - if the gene is being suppressed here then there should be no template mRNA produced that could be detected.  If it was being regulated post transcriptionally then mRNA would be present (though likely in small amounts before being degraded).

Alan Boyd's Answer suggests that there is more going on than just gene suppression/expression, however.

@Rory M
Here is evidence for developmental genome rearrangements in Hymenoptera. I have emphasised the relevant section of the Abstract. It is probably premature to assume that similar changes might not happen in somatic cells of some Lepidoptera.

Bigot Y, Jegot G, Casteret S, Aupinel P, Tasei JN (2011) DNA modifications and genome rearrangements during the development and sex differentiation of the bumble bee Bombus terrestris. Insect Mol Biol. 20:165-75.
Abstract
Bombus terrestris is a bumble bee that, like most hymenopteran species, exhibits ploidy-specific sex determination controlled by a single sex gene. Depending on their ploidy and the queen pheromone repression, the imagoes differentiate into three castes: males, workers and queens. Here, we focus on the differences of genome organization that occur during development and sex differentiation. We found that cytosine methylation is a significant epigenetic factor with profiles that can be correlated with both processes. We also showed that two kinds of genomic rearrangement occur. The first consists of important DNA amplifications that have sequence profiles that differ in the different developmental instars and sexes. In the second kind, DNA losses also occur, at least involving the mosaic transposable element B. terrestris mosaic repeat 1 (BTMR1).

True, but the genome sequence is still the same.

@nico I don't understand what you mean. If two cells differ because in one of them a region of the genome is  amplified (e.g. single copy > tandem repeats) then the genome sequences are different. There may be no appearance of DNA with a novel sequence, but I don't think that anyone would argue that the two sequences were identical.

sorry, forget my comment, I had read the quote too quickly and thought it was just speaking about epigenetics.

@AlanBoyd I imagine the germline cells' DNS remains the same?

I would like to expand on Rory's answer.
You can think about the DNA like a very complex book of recipes (genes) for constructing cellular machinery (e.g. proteins). Every genome has a large repertoire of machines that it can construct. For a given organism, all its somatic cells will have the same DNA (more or less, but let's put that aside) since it starts out as a single cell. In spite of this, you can see that cells can have completely different shapes and functions. For example, look at how different a neuron is from a muscle cell or a blood cell in terms of shape and function. In addition, cells can change in reaction to their environment.
Then how is the repertoire the same but the cells completely different?
The solution is choosing which genes to activate. This is the called gene regulation and is an extremely complex system as you might guess. It is to some extent the "brain" of the cell, with which the cells can make decisions and gain its plasticity in biological function. This system operates on many levels, one of them being by controlling transcription, i.e. transcriptional regulation, which controls how much RNA to make from each gene, which will later translate into some level of activation (no RNA means the gene will not be active). This is why the RNA will probably vary widely according to the cell type and cellular state.
In general, each species have a similar DNA sequence give or take some minor variations. The sequence of family members will be even more similar, and the sequence of clones (e.g. identical twins) will be virtually identical. This type of variation is random and thus will not be used as a control system. From this you can already guess that the change from caterpillar to butterfly will be controlled by its gene regulation program, as it is a developmental change, in the same way as a human grows from a single embryonic cell.
That said, it is always possible that some random changes occur somewhere along the way and would cause differences, as biology is stochastic. However, for these to be consistent between all cells in the organism, they would have to happen when the organism is a single cell, which is not the case when transitioning from caterpillar to butterfly.

Here's an interesting story from npr.org, Are Butterflies Two Different Animals in One? The Death And Resurrection Theory.
Apparently some people are proposing a theory that says (heavily paraphrased) that a butterfly is actually two different ancestral species rolled into one. This is the relevant quote:

The old view was that over millions of years, animals evolved this habit of switching from one set of instructions to the other. The new view is that this is not one animal gradually changing shape, but rather instructions for two different animals sandwiched together and this change is so radical, says Bernd, "with no continuity from one to the next, that the adult forms of these insets are actually new organisms."

Far out.

And a chicken is a new organism, radically different than an ovoid, calcium-covered egg.

That's a bit different of a scenario ... or do you look at a carton of a dozen eggs and classify them as 12 living and breathing organisms sitting on a shelf?

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Are all healthy animals more likely to defecate near the end of a rest-cycle?
Just what the title states.
It stems from observation & personal experience that a person/dog/cat/monkey is more likely to relieve oneself immediately after it wakes up from the peak-sleep cycle of it's body-clock. Is this observation true? What causes this behaviour ?

I think we can actually go farther than mere behavioral argumentation. The separation of the autonomous nervous system into parasympathetic and sympathetic is, one the one hand, associated with the sleep/wake cycle, on the other with parasympathetic/sympathetic activity (low/high epinephrine secretion). This duality certainly applies to all vertebrata (i.e. big animals), as fight & flight is associated with all vertebrata, see e.g.
http://en.wikipedia.org/wiki/Fight_or_flight_response
In other words: from the existence of fight or flight in all vertebrata I infer the existence of a dual autonomous nervous system (parasympathetic and sympathetic) in all vertebrata, although there may be other proof. Since in sleep the parasym. NS is active, the bowel moves. Conclusion: the bowel moves in the sleep of all vertebrata.

I'm sorry, I don't understand your answer. Could you elaborate please?

I have added a reformulation. Better now?

I'm prefixing this one by saying that I don't actually agree with you (also, I think the old nut that the plural of "anecdote" is not "data").
That having been said: wouldn't the simplest explanation just be "because it was likely a long time since the animal's last 'relief'" since it's been sleeping for XXX hours? Or would you argue that this observation is also true after, say, a 20 minute nap?
Also, what does this have to do with a nervous system?

Accepted this may be anecdotal; I'll update the question on this & remove the note on the nervous system too. But I would argue the second paragraph with the clarification that an animal/being is more likely to defecate after the typical 'night/rest' cycle which is the 'deepest' such sleep cycle.

Digestion is an energy consuming process. It is, therefore, often followed by a period of rest. Animals will, consequently, often digest during sleep. It follows that they will eliminate the waste products of digestion upon awakening.
Given the above, I doubt there is a causal link between sleep or rest and the need to commune with nature, water a tree, appease the porcelain god, or whatever your preferred euphemism happens to be, soon after awakening.


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Can paper/plastic currency serve as a medium for pathogens?
http://www.nytimes.com/2009/12/15/health/15real.html seems to indicate for a surface, to serve as a medium, the following properties are relevant

animation
humidity
temperature

The article however does not elaborate on the properties a surface must possess to serve as a medium - albeit i would figure it may vary from one virus/bacterium to another.
The same article also states
... when objects in a hotel room — light switches, telephones — were contaminated
with a  cold virus, 60 percent of healthy volunteers picked up the virus when they
touched one of the objects an hour later. Eighteen hours later, the transmission rate
was cut in half.

When currency changes hands we rarely ever know whether it may , within a reasonable timespan, have passed through an agent/carrier.
Sir Dumpty loves to sneak off with a currency note to get me to chase him. He is protected; another member of his species may not be so protected. For that matter a person infected with, say, the common cold virus may have passed a note/coin/card to the vendor at the store within a minute of sneezing/coughing into his/her hand. What if the same person , instead, suffered from TB?
So ... can currency serve as a medium for transmission of pathogens?

It's going to vary wildly, for example Hepatitis B can survive 7 days outside of a host.  Furthermore, some bacteria such as Bacillus antracis can produce endospores and survive for years.

its always a good idea to wash your hands when you handle money.

TB is perhaps a poor example as it is actually quite difficult to contract without spending extended time with someone actively infected.

Who the heck is Sir Dumpty?

@arboviral: That's my canine son

@Everyone Ah, that makes sense.

@Everyone While you're around - is there anything else you wanted to see in the answers?

TB is an extremely poor example, because as has been mentioned, it usually requires prolonged contact.
But lets go with something with a low required infectious dose, that's friendly to surface contamination, and persists in the environment: Norovirus.
Can norovirus serve as a medium for pathogens? Absolutely. To be blunt, almost anything will serve as a medium for the right pathogen with some level of efficacy. This is a presentation from the New York Federal Reserve on what contaminates money, but given the outlandish things that can be contaminated with infectious material, there's no reason to suspect money isn't among them.
Wash your hands.

Yes. Salmonella, Staphylococcus aureus and Escherichia coli have all been isolated from paper money. There is a review article here on money (paper money and coins) as a source of infection but it's unfortunately behind a paywall.
Exactly how important money is as a source of infection and for which pathogens is more complex. As you note in your question, material will be important too, making answers to this question also relevant to the subject (although it hasn't been answered yet).


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What is the life-span of the various organs in the human body?
It is possible for a person to donate the harvestable organs (kidneys, eyes, and such) posthumously. Let's assume for a moment that the technology exists to kill rejection, and maintain the organ in excellent shape after it is harvested.
Could the organ/s ( e.g. Eye ) (assuming a decent life-style) travel for centuries from one donor to yet another donee? What is the typical life-span of the various organs in the human body assuming a healthy, and low stress life?
p.s. It's a curiosity question; my eyes even millenia after my death would continue to see.

Perhaps you can infer relative lifespan from the age at which organs start declining in someone of average health.
Skin, muscles, bones, eyes, and ears start to visibly decline around age 40.
Kidneys become smaller and their ability to filter blood starts to decline around age 30.
Brain function begins to decline around 70, even in the absence of neurodegenerative diseases such as Alzheimers.
I don't think any organs can be passed through people for centuries, since decline of virtually every organ is observed even in individuals in perfect health. There may be two exceptions: The digestive tract and liver seem to be the most long-lived and are very little affected in healthy elders, probably because they regenerate their cells.
Reference


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Food Intake versus ability to flee among birds, particularly the hummingbird?
Logically speaking, if a hummingbird drinks too much nectar, it will be temporarily overweight and less able or unable to fly to escape danger. However if the same hummingbird doesn't drink enough nectar, it will suffer the same problem of not being able to flee danger, but for the different reason of it wouldn't have enough energy to do so. Hummingbirds are incredibly small, so I would assume they would have the most problem with this issue due to the fact it would have very little margin for error. I am not sure how much that margin is though or the marginal percent of body weight, so I'll ask that question too.
What mechanisms do (humming)birds have to regulate and control their body weight and their energy needs and scouting and timing the acquisition of their next potential food source? What is their margin for error and how do they meet it and how did they meet it in the past?
EDIT: I want a more concise question, so hopefully this is answerable:
Alternatively and optionally, Can you describe to  me a general day in the life of a Hummingbird? I want to know what good decisions it makes over the course of its "perfectly average" day to survive. Such things as what it does to avoid dangers, and how it finds its time to eat and how much it eats and at what intervals, and what it does with the rest of its time?

Okay someone who knows a bit about this told me that like shrews, hummingbirds are always less than two hours away from death. If they do not find a meal in that two hour window they die.

It is not specific to hummingbirds, but this topic is treated in the book Modelling for Field Biologists and Other Interesting People by Hanna Kokko: http://www.cambridge.org/us/academic/subjects/life-sciences/quantitative-biology-biostatistics-and-mathematical-modellin/modelling-field-biologists-and-other-interesting-people


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What chemicals and structures control the *direction* of plant growth in leaves, stems and roots?
If you want a specific plant, let's say the snap peas I am growing that I bought at Agway. I noticed that they grow towards the light source through the nearby window. Also I think roots work the same way for water/minerals. also don't various kinds of ants find food conceptually identically?
How much of this is true? Please correct:

I think analogous to ant colonies, plants will attempt to grow every which way initially, and will only continue growing in directions that give the most/enough light/water/minerals. If a direction is or becomes unfruitful, that section withers. After the initial state the plant will start branching in directions off of locations on still growing sections of plants and that cycle continues until none of the plant can be supported and the whole thing withers (perennials) or slows its metabolism down to the point where it could survive those conditions until they picked up again (such as winter seasonal survival of tree species). Also, it is not as if they decide which direction to go in. that type of decision would forgo going in another direction. And not sure, but I don't think plants have decision capabilities anyways. they grow in directions they grow best.

Your title is unclear.  Is the last question the question you would like answered? If so, I would recommend changing the title.

I don't unfortunately have time to write a full answer right now, but you will want to look at tropism on Wikipedia, particularly geotropism and heliotropism

PART 1 : Phototropism
The movement of plant shoot towards light is called phototropism. This process is mainly stimulated by the blue light. The photoreceptor involved is called Phot1 (Phototropin 1) or JK244.
Auxins such as IAA (indole acetic acid) are plant hormones, expressed highly in meristem, which cause shoot growth. On illumination this phototropin, through currently unknown messengers, causes inhibition of polar Auxin transport in the illuminated side. This causes the non-illuminated side to grow more and thus bending the plant towards light.

The image represents an older model which proposed lateral movement of auxin. The mechanism mentioned in last paragraph is the currently accepted model. The below figure illustrates 'polar auxin transport'

For details refer to this nice review on phototropism.
PART 2 : Geotropism and Hydrotropism
Geotropism or gravitropism is movement of roots towards earth (gravity) and hydrotropism is movement of roots towards water. Both phenomena interact with each other and share some common pathways. But hydrotropsim can inhibit geotropism and it is evident in conditions when root goes towards an adjacent water source.
Ethylene and Auxin signaling is involved in root growth both in geotropism and hydrotropism. In geotropism the auxin is stimulated by statoliths (clustered and membrane bound grains of starch) in the amyloplasts- the organelles which store starch. The model suggests that amyloplst sediments under the influence of gravity and thereby affect auxin polar transport (the second figure co-incidentally illustrates polar auxin transport in geotropism).
The exact moisture sensor is unknown but Abscissic acid (ABA), which is well known for its involvement in drought tolerance, is known to affect hydrotropism.
MIZ1/2 are some proteins uniquely involved in hyrdotropism.
Both pathways are dependent on Calcium as a secondary messenger.
To conclude, these pathways are not as clear as those of phototropism.
Reference:

http://www.academicjournals.org/ajar/pdf/Pdf2006/Nov/Dexian%20and%20South.pdf
http://www.sciencedirect.com/science/article/pii/S1360138504002717
http://www.plantphysiol.org/content/133/4/1677.full

Thank you :) .. and Thanks to the asker for making me revisit plant biology:)

Your statement is partially correct, but not entirely.

As an animal embryo, the seed, still closed, is already formed, with the distinction between root, stem and leaves. Tiny but already there are.
All the rest of the seed (in this case two cotyledons) is a kind of food dough, and serves as a food reserve for the seedling, until the time of rooting and the achievement of energy independence.

As animals, the plant seeks, first of all, water. The first need of water is determined by the need to break the skin that closes the seed. If there is no presence of water,  the seed dried and does not sprout.
If it "feel" the water, the seed drinks, swells and the skin breaks down. At this stage we can also say that the seed is aware of where it can find water. I do not think that they have been studies done on the awareness of the high and low (orientation). On the edge of rivers and lakes the seed can also find favorable ground above itself.
The direction of the water determines an effort, which can also lead to the rotation of the seed in the right position to emit the radicle towards the water (and the earth). In this time the embryo "eats" the nutritional reserves contained in the seed.
Then precisely they decide which direction to go in. When the place and position are correct, the seed has open and the part to eat is almost eaten, then more light. The radicle grows to first, both in size and as the length. It hooks to the soil and establishes a firm basis. Starts to drink directly (and not by absorption of the tissues of the seed) and starts to push out the seedling, typically in the opposite direction.
The seedling "feel" the light energy and go to that.

If the plants have ability of decision or not, has not yet been established. But to me personally it seems that a functional DNA must be able to allow each subjet to handle each situation (consistent with its structure) in the best way to itself.
This seems to have been ascertained for the animals. A certain capacity of thought, namely to make decisions, is absolutely functional in a huge energy saving on the need for encoding and on the structure of DNA

I know little about the life of the colonies of ants. But I know all about bees. A swarm that is detached from the hive to found a new colony, it also stops two or three times. Sends forward scouts, followed by architects and, if the place is right, the architects have a network, and bees wax begin to build.
Your mention of the ants is not sufficient to me to find similarities.

so DNA encoding is allowed to "program in" "make a guess" "functions"? growing in every direction and only continuing to grow in directions the plant found suitable probably is very inefficient compared to making a guess based on a stimulus.

Yes, to me yes - that is more efficient and request less energy/structure than encoding each single decision. But, actually, you have you've piqued my curiosity about the lives of ants, that I know only superficially. But I figure that the marvelous discoveries, behavioral and chemical, which I did on bees, I can make too delving into my knowledge on the ants.


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Is lactic acid build up the cause of muscle fatigue or only a symptom?
If your body could magically instantly remove lactic acid as it is produced, would that make you immune to muscle fatigue, or is the lactic acid only a symptom of muscle fatigue and instead exists, at least partially, as a means for your body to measure the stress your muscles are under to keep you from overexerting and damaging yourself? Would your body still have other kinds of immediate and daily maintenance to do to deal with muscle fatigue even if lactic acid wasn't a limiting factor?

Always wondered this.

Accumulation of any biomolecules in any condition can't be a symptom. A symptom is defined as a physical or mental feeling that a person experiences, which can be an indication of disease. Symptoms can be headache, nausea, cough, running nose, change in body temperature and they never show up on the diagnostic tests. So, the accumulation of lactic acid can never be a symptom. However, lactic acid is one of the cause of muscle fatigue indirectly.

As a biochemist I know how lactic acid is normally handled in the body and how it might affect muscle function in circumstances that perhaps did not arise frequently in early man. What I do not know is the medical status of what you refer to as “muscle fatigue”. I doubt very much your ideas about it being a sensor, and wonder whether you are familiar with what is known as the Cori Cycle. However I do not know. Given the lack of response I wonder whether you would be better to migrate your question to SE Medical Sciences, where someone might know about muscle fatigue.

Couple of points:

Removal of lactic acid would only solve the lactic acidosis problem.
Conversion of glucose to lactic acid $\ce{(C6H12O6 \to 2 C3H6O3)}$ only produces two ATP per glucose molecule. You will still miss up to 34 ATP omitting the oxidative phosphorylation step.
Once the free glucose in your cell is exhausted, you will then have to rely on glycogenolysis which is rate-limited by glycogen phosphorylase.
As your glycogen gets depleted, you will have to import glucose (as well as fatty acids and certain amino acids) from the blood for sustained energy production.

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First genomic survey of human skin fungal diversity
"The researchers found that a single type of fungus, belonging to the genus Malassezia, is predominant on the head and trunk. Hands, which harbor a great diversity of bacteria, are home for relatively few types of fungi. In contrast, feet, including toenails, heels and toe webs contain tremendous diversity.
"Applying DNA sequencing to a study of the skin's fungi is the natural progression in understanding microbial life that co-exists on our bodies," said NHGRI Scientific Director Daniel Kastner, M.D., Ph.D. "Along with recent genome sequencing to define bacterial diversity, this analysis of fungal diversity provides a more complete human microbiome picture."
"Fungal communities occupy complex niches, even on the human body," said Heidi Kong, M.D., co-senior author and an investigator in the dermatology branch of NCI's Center for Cancer Research. "By gaining a more complete awareness of the fungal and bacterial ecosystems, we can better address associated skin diseases, including skin conditions which can be related to cancer treatments.""
Source
Is there another reference for this research please?

The link is given at bottom of the article that you linked to. It's a Nature paper so you need to have access rights.

Just a tip, links of the form http://dx.doi.org/whatever tend to link to academic articles.

@ChinmayKanchi I can't access that link.

The doi-based link looks like this: http://dx.doi.org/doi:10.1038/nature12171

Hi @AlanBoyd, how are you doing? thanks for your reference.


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Endophytic Xylariaceae: diversity and taxonomy inferred from rDNA sequence analyses
"Thailand is considered as one of the areas containing a high percentage of unknown taxa of Xylariaceae (Rogers 2000).  In Thailand, several studies on endophytic fungi have been documented, namely, from several bamboos (Luyong et al. 2000), banana (Musa acuminata) (Photita et al. 2001), monkeypod/rain tree (Samanea saman) (Chareprasert et al. 2006), and several xylariaceous endophytes were also reported from those plants."
Review quoted from Izumi okane, Prasert Srikitikulchai, Kyoko Toyama, Thomas Laessoe etc. Full Paper; Study of endophytic Xylariaceae in Thailand: diversity and taxonomy inferred from rDNA sequence analyses with saprobes forming fruit bodies in the field.
Have any of you known the similar cases (the high percentage of Xylariaceae) in the USA, France, or UK, proved by reference(s)?

Are you looking for areas that high a high percentage of Xylariaceae as compared with total fungi species richness? Or for areas that have a high percentage of unknown taxa of Xylariaceae compared with total Xylariaceae taxa?

@Oreotrephes: The high percentage of Xylariaceae in the USA, France, or UK, proved by reference(s), thanks.


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"Oblong to Allantoids" .... Is it valid?
I read on the text book:
The characteristic of Dinemasporium are: superficial, cupulate to Discoid conidiomata with brown satae, Phialid conidiogenous cells that give rise to hyaline, oblong to Allantoids, and Aseptate conidia with an appendage at each end.
My question:
the phrase "oblong to Allantoids"; Is the word oblong valid for this context? if not, what other word would associate?

Oblong is probably correct in this context, but "allantoids" should probably be "allantoid" to be the adjective form. It's describing translucent (hyaline), oval (oblong) to sausage-shaped (allantoid), undivided (aseptate) spore.

Thank you, I should have referred to this link.


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How does a plant cutting develop roots?
Please correct me if my understanding is incorrect; I understand branch/stem, and root are composed of different types of cells. Yet in some plants (e.g. rose, bougainvillea) a cutting from the stem is capable of developing and taking root.
How does this transformation from stem to root come about?
As an aside - I believe such root-generation happens only in plant cuttings, and not in a tree branch. Why? Is it a matter of the volume of nutrition required?

Plants grow only from regions at the tips of the roots and shoots called meristems.
Within the meristem areas there are stem cells ("blank" unspecialised cells).  Unlike animal stem cells, plant stem cells are totipotent - meaning that they can differentiate into any type of cell.  Therefore when the cutting is taken from the end of the shoot, the stem cells can differentiate into root cells or shoot cells depending on their conditions.
Because the meristems (therefore the unspecialised stem cells) are only located at the tips of shoots, you cant grow a cutting from the middle of a branch.

There are lateral meristems all along a plant - they are where branches grow from. Every node on a plant is, or was once, a meristem. That's why you cut just below a node to take a cutting. You could also create a meristem pretty much anywhere by applying auxin. That's why people use rooting/cutting powder, which is NAA, a synthetic auxin.


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Are there any multi-cellular organisms out there that do not sleep?
Looking around I see animals - ants, bees, birds, lizards, roaches all the way up to humans appear during a part of the day and not other parts. I would guess there is a sleep/recovery cycle involved.
Is there any multi-cellular organism with a nervous system, on record, that works without sleep/rest?

Well, you may want to re-state your question. There are numerous multi-cellular organisms without a nervous system. So you could say that they never sleep: sponges, plants, mushrooms.
This paper on the evolution of sleep concludes:

A phylogenetic evaluation of sleep demonstrates that all
  mammals, birds, and reptiles engage in sleep, and evidence
  for sleep in amphibians, ﬁshes, and invertebrates is strong if
  not certain.

So it seems that once you have a nervous system, you also have some rest periods. However, it may not be clear if the rest periods are dictated by the lifestyle (e.g. nocturnal foraging) or by a requirement to "recharge" the nervous system.

That paper does not exist there. Do you have another link or just title/author

Google is your friend :) John A. Lesku, Niels C. Rattenborg, and Charles J. Amlaner. "The Evolution of Sleep: A Phylogenetic Approach" Sleep: A Comprehensive Handbook. Ed. Teofilo L. Lee-Chiong. Hoboken, NJ: J. Wiley and Sons, 2006. 49-61.

Thanks. I can't find an accessible copy though.


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Can a person die instantaneously from internal damage to the brain?
Given the human heart is autonomous, can a person die instantly from internal damage to the head/brain? I would expect the heart to continue to pulse until it ran out of energy ...
My contention is whether brain-injury can cause death, albeit Memming raised a deeper question - What is the biological definition of death?

What do you mean by instantaneously? What do you mean by die? If one looses consciousness irreversibly in 10 ms, would you consider to be instantaneous?

Indeed, I would.

I did not downvote, but this question is not clear.  It sounds like there are two questions, a rather difficult philosophical question about the meaning of death in unspecified cases where it is difficult to tell if someone is dead and another question as to whether one can die quickly (again not sure how quickly) from brain injury, which seems a little to simple.  I mean why wouldn't someone die instantly of a brain injury?  What's the trick are you talking about nanoseconds?

Please consider this only as a starting point (although a lengthy one), and a race against an acute onset of  tl:dr ...
A person cannot die instantaneously from internal brain damage (under everyday circumstances). The reason is the non-centralized architecture of the brain and that consciousness is a global phenomenon which underlie the activity of many brain structures.
These brain structures are themselves comprised of a cellular hierarchy, with each cell being self-sufficient for at least a time regime in the order of minutes. As such the brain underlies to some extend the study of networks and robustness thereof. The brain also maintains a scale-free organization . Actual Scale free networks in nature are known to be robust.
Instantaneous in this context means a consciously discernible difference in time, which is on the order of tens of milliseconds (See: Inspection time, mental chronometry).
Also I narrow the medical cause of death down to a intracerebral haemorrhage, systemic shock or hypoxia. I definitely leave out all (rare) CNS-immunological phenomena (e.g. explosive brain death, Immune reconstitution inflammatory syndrome related,... )
But, effects that can mimmick instantaneous brain death are very plausible.
Notably, this question can be answered despite there being no rigorous consensus model of consciousness.

Consider the following just as pointers, but not as qualified, thoroughly sourced information, - contrary to a paper or review ( I will gladly include your resources, or turn this post into a community wiki if demand to do so exists):
**** Consciousness**:
The brain weighs only 2% of the human body mass, yet consumes 20% of the total energy at rest. Crucially the brain can deplete oxygen at a great rate, which is proportional to the brain activity in various regions, giving rise to indirect measurements of brain topology and images like these:

"Visualization of a DTI measurement of a human brain"-2006,
author: Thomas Schultz, DOR: 25/09/2012

Humans have different states of consciousness which show different overall patterns of brain activity. As such the result a scientist would witness through an high-resolution fMRI/PET scanner in a stroking-individual would differ during sleep, sleep/wake transition or various levels of awareness during the days. Stroking and the effects on the brain is studied quite extensively with rats(See: rat, fMRI, stroke).
Moreover the brain activity, fine-anatomy and orchestration of brain utilization differs from individual to individual. In short the brain is what neurologists call "plastic" Neuroplasticity is the change of entire brain structures, and the brain itself from experience and physical stress/trauma (on the brain).
We are biologial enetities which have evolved to be in-sync with the planetary rotation and solar energy influx. As such brain activity changes during the day, in accordance with our circadian rythm or biorhythm, and if it weren't for artificial lightning brain activity would change over the seasons as well.
Connecting all the dots: Describing brain death in a seconds-regime comes down to which areas in an individual brain consume the most oxygen and "shut down" first, and which processes steer brain activity till organic shutdown.
Since Stackexchange has a strong programmatic background, to put it in a somewhat programmatic analogy:
The output of a memory dump and its analytic result depend on the hardware, the software and the state of the application. Unfortunately the software is spread across processors, has multiple threads and applies a genetic algorithm with dynamic recompilation.
Death Definitions:
The notion of instant death is a cultural meme (which one can witness in child's play) and is further propagated in the media.  Additionally "death" is a highly political matter...
"Death" has numerous legal definitions (throughout various cultures) medical definitions and biological definitions depending on the context. Legal definitions depends on the culturally dependent legal corpus, medical definitions on the state of (pragmatic) technologies. The medical definition of human death is influenced by the legal definition. The legal definition in turn is influenced by politics.
The biological definition of death depends on the context and a threshold thereof, which in turn describes the level and and of hierarchical systems or one large system comprised out of systems such as organs. An organ is the collection of units in one structural one to serve a common purpose.
Finally to answer more accurately, a person cannot (under everyday circumstances) shutdown brain activity within the time-interval of one reaction time-unit or 'cycle', but may transition between discernible states of global brain-activity. Such states may only be measurable with functional Imaging techniques and classifiable using computer algorithms.

Interesting answer but please don't use random code formatting as it's not really suitable

I've replaced all instances with more appropriate highlighting, however I'm not sure they're all necessary so you might want to remove some of the emphasis.


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Is there a timeline for the frequency of evolution of any species?
Evolution is traditionally spoken of as an inherited change over generations.
Does evolution happen one change at a time - or are there multiple changes occurring between two successive generations? Is there a known timeline for the frequency of such changes in any species?
Something like ...
20 Million years ago - Species X showed A, B, C.. Z characteristics
19 Million years ago - Species X following characteristics changed A'
17 Million years ago - Species X following characteristics changed B', C', Q', M'
16 Million years ago - Species X following characteristics changed A''

Your question presumes that species X is recognizable as species X for 4 billion years. And, the universe is only ~13.75 billion years old.

If not X, then it's most probable derivative. Homo Habilis, Homo Rudolfensis ... so on.

I think you want some kind of character mapping. e.g., http://mesquiteproject.org/mesquite_folder/docs/mesquite/CharacterEvolution/AncestralStates.html

It's unlikely that multiple independent, fitness-relevant changes would occur at exactly the same time. I mean, if getting a beneficial random mutation is like rolling a 1 on a 1000-sided die, then getting two of them is like rolling 1s on two dice simultaneously. However, you could have multiple changes in phenotype if they both trace to the same genetic change (e.g., an increase in metabolic efficiency leads to increased size and also changes in foraging behavior).

There can be multiple changes at the DNA level generation after generation, however most of these changes are insignificant (doesn't contribute for any specific character). But rarely, there can be a significant trait/change gained by an individual because of such changes in DNA level. Unfortunately such changes gets 'lost', unless it is fixed in the population (i.e., the gained individual should be successful in breeding and passing the trait/change to large number of progenies. Those progenies should further continue to pass on the trait till about every one (or most of them) in the population has those trait/change). Only such changes contribute for the species development (continuous accumulation of such changes, over time will result in the novel population that is very different from the original population).
Most of the timelines that we know are reconstructed from the DNA/protein sequences. Usually, DNA or protein sequences from the closely related species will be compared and looking at the differences they have, using suitable models, ancestral state of those sequences are determined. Once the sequence for the last common ancestor is known, mutational rate per unit time can be used to estimate the evolutionary time for those species.
A simple example would be the blue eye color in humans: it occurred about 10,000 years ago and it is still not fixed in the population.

Blount ZD, Barrick JE, Davidson CJ, Lenski RE. (2012) Genomic analysis of a key innovation in an experimental Escherichia coli population. Nature 489:513-8. doi: 10.1038/nature11514

Richard Lenski is conducting an experiment called the long-term evolution experiment (LTEE) in which twelve populations of E. coli are grown in a glucose-limited minimal medium. This experiment has now been running for over 40,000 generations (>20 years). If we take a human generation as being 25 years, this is equivalent to one million years of Homo evolution.
One of the diagnostic traits of the species E. coli is the inability to grow aerobically on citrate. The medium that is used in the LTEE does however contain citrate as a chelating agent (probably to solubilise ferric ions, although I haven't been able to confirm this). The Lenski group have recently reported on the appearance of a novel citrate-utilising mutant in one of the populations. The Cit+ variant appeared at around 31000 generations, and became dominant after 33000 generations. Because the LTEE involves storing samples of each population every 500 generations it has been possible to analyse in detail the emergence of this new phenotypic trait, and indeed to replay it.
The process that they describe has three phases:
1) Potentiation. This stage involved the appearance of mutations that were a necessary prerequisite for subsequent events. In this case it is thought that there were at least two potentiating mutations. These are as yet unidentified but their existence is inferred from replay experiments.
2) Actualization. This is the emergence of the new trait, and in this case is the event that took place at 31,000 generations. This involved a tandem duplication event at the citT locus, bringing citT under control of a new promoter, belonging to the rnk gene. The citT protein is a citrate transporter that is only expressed under anaerobic conditions in wild-type E. coli. The gene duplication event led to the expression of the transporter under standard aerobic conditions, opening up the possibility of taking up citrate and metabolising it. Replay experiments indicate that this event originally conferred a very weak Cit+ phenotype.
3) Refinement. This involves changes that strengthen the Cit+ phenotype. In this case these seem to have been further gene duplications of the rnk-citT module (with up to eight copies in one replay experiment). This eventually stabilised with the presence of four copies.
This may be the nearest that we can hope to get to defining a timeline of evolution of a new characteristic.


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Why does the butterfly have a cocoon stage in its life cycle?
Why does the butterfly have a cocoon stage in its life cycle? It could have simply grown up within the egg/cocoon, and emerged as a butterfly. Instead it is first an egg, then a worm, then a chrysalis, and finally after some time a butterfly.

It's not just butterflies; many insects (e.g. bees, wasps, fleas, ants) go through a similar complete metamorphosis during their life cycle.

@BruceAlderman: Agreed. What could have been the motivation for such a life-cycle?

Fyi, if one wanted to be technical, the  pupal stage of butterflies is called a chrysalis not a cocoon.

In addition to the list provided by @BruceAlderman, beetles also undergo complete metamorphosis.

Holometaboly is believed to have evolved only once (Labandeira, 2011), but is arguably the most successful mode of development we know of in terms of species richness (Kristensen, 1999 - PDF link). Insects which have adopted this method are far more diverse than their hemimetabolous counterparts. A conservative estimate by Hammond (1992) is that holometabolous insects comprise more than 60% of all living organisms.
The subclass Pterygota (winged insects) is divided into (super orders) endopterygota (wings develop interiorly) which are holometabolous, and the exopterygota (external wing development) which are hemimetabolous.
Hemimetabolous insects (usually) develop from an egg to an adult through a series of immature forms (known as nymphs or instars) which are slightly modified (and usually slightly larger) forms of the preceding form. There are exceptions to this mode within the exopterygota including asexual parthenogenesis which is common in aphids. The general life cycle is well illustrated in the Dermaptera (earwigs). All stages inhabit the same ecological niche and so maintain the same general body plan.

Image file from Wikimedia Commons here
Although hemimetaboly is a more gradual process than holometaboly, it happens in a small number (often four or five nymphal instars) of discrete steps rather than the more continuous development of other animals such as mammals. Although all insects fall into either the exopterygote or endopterygote categories (i.e. wings either develop externally or internally), there are examples of intermediate processes which lie somewhere between hemi- and holometaboly. A notable example are the Cicadas. Cicadas are Hemiperans (true bugs) which lie in the exopterygota and so are, by default hemimetabolous. However there is a considerable difference between their immature and mature stages:

Illustration by Debbie Hadley, using drawings from Insects - Their Ways and Means of Living by Robert Evans Snodgrass, U.S. Bureau of Entomology. These drawings are in the public domain. From here.
During the immature stages, the larva (or nymph) will burrow underground, sometimes for many years. This requires strong front appendages, which they also use when they surface to grip onto a surface whilst they shed their final skin to become an adult. This differential niche exploitation is likely to have given rise to the morphological differences between immature and mature life stages.
Exploiting different niches during different developmental stages not only reduces intra-specific competition between young and adult, it also enables the insect to be more specialised to fulfill their specific role, which changes as they develop. The role of the immature is to grow, they do not yet need to be able to reproduce or disperse; whereas the role of the adult is to find a mate and reproduce. Young often develop below ground where there are fewer predators, adults often fly to enhance dispersal (further reducing competition and also decreasing inbreeding). These two activities call for vastly different body designs.
Some other common holometabolous insect orders are Coleoptera (beetles), Hymenoptera (bees, wasps, and ants), and Diptera (true flies), whereas hemimetabolous groups include Orthoptera (grasshoppers, crickets etc.), Mantodea (praying mantids), and Blattaria (cockroaches).
As for the chrysalis which Lepidoptera (butterflies and moths) have evolved to surround their pupal stage, the main role is likely to be protection. Larvae (caterpillars) are a highly nutritious and energetic food source and thus have adapted defensive mechanisms such as mimicry, warning colours, and dropping to the ground when disturbed. This drop would damage the metamorphosing pupa (the most vulnerable stage as it is usually relatively immobile), as the cuticle softens to allow for cell-rearrangement.
The process of insect development is regulated by juvenile hormone (JH), see Konopova et al, (2011) for more on this.
References

Hammond, P. (1992) Species Inventory. Global Biodiversity (ed B. Groombridge), pp. 17–39. Chapman and Hall, London.
Konopova, B., Smykal, V. & Jindra, M. (2011) Common and Distinct Roles of Juvenile Hormone Signaling Genes in Metamorphosis of Holometabolous and Hemimetabolous Insects. PLoS ONE, 6, e28728.
Kristensen, N.P. (1999) Phylogeny of endopterygote insects, the most successful lineage of living organisms. European Journal of Entomology, 96, 237–253.
Labandeira, C.C. (2011) Evidence for an Earliest Late Carboniferous Divergence Time and the Early Larval Ecology and Diversification of Major Holometabola Lineages. Entomologica Americana, 117, 9–21.

The cocoon phase allows lepidopterans (and other holometabolous insects) to reorganize their body and undertake the dramatic metamorphosis from larvae to adult in a safe environment. Cocoons and pupae are typically attached to branches by silk (oftentimes after climbing high into the canopy), thereby removing them from many predatory interactions and providing a protected environment to breakdown the larval body and develop into the adult phase.
In my mind, the main adaptive significance of the cocoon/pupal phase is to provide an environment within which the animal can metamorphose while reducing exposure to both predators and any harsh elements.

The butterfly is the reproductive stage while the larvae all it does is eat an accumulates energy to be succesfull during the reproductive phase.
In terms of adaptation this life cycle would be much more efficent.

I’m not convinced – it certainly requires a much more complex regulation and gene setup. I’m not sure that this optimises the adaptation of the organism.

I agree it requires complex genetics, but that does not imply higher energy cost or low efficiency.

Could you expand on why it would be more efficient, or toss a link? I'm inclined to concur with Konrad's comment.

I talk about efficiency as in survival fitness. What I meant is that maybe the metabolic expense of such life-cycle it's compensated by the adaptation capabilities provided. I have no proof of this, I's just a though.


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Is sperm contagious?
A person may have a cold or any other disease that is an airborne-infection.
Is their sperm also contagious? Should the person take any precautions?

Most airborne infectious pathogens (including flu and common cold) will not be sexually transmissible.

Had to laugh at the title. Yes, sperm may indeed be confer other sperm-bearing life-forms so I’d say that it’s contagious.

Why would a pathogen NEED to be airborne to be contagious?

I don't think it need to be airborne, but I'm interested in airborne diseases.

@KonradRudolph: Also, sperm can't reproduce without invading, and interfering with the genomes of other human cells. So perhaps they could be classified as some kind of ultra complex virus?

Spiderman killed Mary Jane with his radioactive sperm so yes :P

I'm unsure about the use of the word "contagious" here. If you would describe it as an organism "catching something" from another only once, this answer applies (vaguely perhaps).
One example of "contagious" sperm: sea urchins spray their sperm (called milt) into the surrounding water, so that it can hopefully fertilize roe, which are fish eggs. The eggs are also expulsed for some species, but for others they stay on the surface of the female sea urchin, as this Wikipedia article explains.

The gonads are lined with muscles underneath the peritoneum, and these allow the animal to squeeze its gametes through the duct and into the surrounding sea water where fertilization takes place.
  ...
In most cases, the eggs float freely in the sea, but some species hold onto them with their spines, affording them a greater degree of protection.

Thus, it's entirely possible for a female sea urchin to be bombarded by free-floating sperm, to ultimately fertilize the eggs on its surface. I don't know if one would strictly consider this a contagion, but it's what I initially thought of after reading the question.

When referring to sexually transmitted disease however, sperm in itself is not contagious, as it would require the pathogen to "tag along with it" in whichever environment (whether it be airborne or aquatic). Also, if considering impregnation as "contagious", physical contact would certainly be required.
In short: For humans, no. For sea urchins (and likely other aquatic animals), sort of.


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What nutritious insects exist to farm that require the least attention?
What nutritious insects exist to farm that require the least attention? I'm looking to automate simply, in a self regulating way.
Edit: To add detail, I imagine the insects would live densely in a large tank and be isolated from the outside. They would be able to breed and would co-exist with a plant that is also able to propagate, that could if needs be even be an air plant, that is eaten by the insects, dead insects either return to nourish the plant, or leave through a funnel, water also evaporates and falls as rain inside the tank.
The idea is to produce food without human effort. This could be in the form of a very cheap to use coin operated vending machine. The insects could be compressed and dry fried into a block to be dispensed, maybe like a bar, the machine could be solar powered.

Nutritional? To whom or what are you planning on feeding these to?

@rg22: insects are part of the human diet in many countries and they have been suggested as an alternative sustainable source of proteins (see refs 9-12 of the entomophagy Wikipedia article).

I suppose it would depend in part as to which part of the world you live in, and what is native/endemic to that region. Also, what is the scale you're looking at - an occasional snack, a major part of your diet, a family, a commercial enterprise?

I've updated the question.

might be worth asking over on [sustainability.se] in a few days, if you don't get the answer(s) you're after, here

@nico I know, I was just wanting to clarify if they were looking for themselves or a pet lizard - the requirements would be different

The leaf cutter ant Atta laevigata is a popular delicacy in Colombia where it is known as hormiga culona (big-ass ant). The ants are usually salted and fried and play a similar culinary role (I am told) as pop corn (image source):

I can't testify as to how hard it is to cultivate them, but one difficulty will be chosing the edible ones. Apparently, only the queens are edible.

"Analyses conducted at the Industrial University of Santander about the nutritional value of the ants show high level of protein, very low levels of saturated fat, and an overall high nutritional value.", looks good.

Only the queens being edible might be a problem, it's not impossible to create an automatic filter, but does seem to add complexity, particularly if needs vary between types.

@alan2here Why do you want insects anyway? Why not algae or fungi? Perhaps even bacteria? Any kind of multicellular animal life form will be harder to grow than simple mushrooms.

Plants will be needed anyway, so an option could be not to include the insects. I suspect that the plants grow too slowly and then require a more complex process of cutting and removing from the isolated environment, particularly if they require soil, additionally insects are meat, although this needn't matter a great deal. At the risk of going off topic, do you have any ideas on this front? Simpler lifeforms also seem interesting although might be difficult to make palatable.

@alan2here there is nothing unpalatable about mushrooms, some of which are considered great delicacies. Some mushrooms grow very fast and need no care to speak of. Insects are complex and they move around. I don't see why you think they will be easier to deal with than plants.

You make good points.

http://community.theurbanfarmingguys.com might be a good place to start more of a discussion.

The silkworm Bombyx mori is farmed for silk, but the pupae are also eaten across the Far East. Since these insects (larvae) have been domesticated for centuries there are well-established procedures for growing them.

Sorry to go updating the question like this, does it affect your answer?


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Is "aggregate percentage" still a valid term in ecology?
Martin et al. 1946 define "aggregate percentage" as a metric that describes the mean percentage contribution of a group to the total mass/abundance of all samples. The metric is useful in datasets that are plagued by outliers and non-normality, something that is a commonplace with most ecological community and diet studies in my experience. Aggregate percentage is calculated as follows:
$AP_i = \frac{100\%}{N_y} \times \sum\limits_{j = 1}^{N}(\frac{a_{ij}}{\sum a_j})$
Where i is the i$^{th}$ taxon, j the j$^{th}$ sample, N total number of samples, a$_{ij}$ the abundance or mass of i$^{th}$ taxon in j$^{th}$ sample, and $\sum a_j$ the summed abundance or mass of all taxa in j$^{th}$ sample.
Martin et al. 1946 illustrate this as follows:

I am sure that "aggregate percentage" is a standard method in ecology, but I cannot find many studies using this term by googling. Probably the method has synonyms and there might be a more accepted term for the method nowadays. My question is what is the valid term to use for the method?

The formula of "aggregate percentage" that you show is just the arithmetic mean of percentages, and I suspect that no special term is used in most studies that use mean percentages as a measure of e.g. prey composition in a certain predator (as seems to be the case in your example).
When searching for studies I think you will have more luck with using "mean prey percentages", "prey percentages" or "mean percentage composition". For instance, see Shoup & Lane (2015) which includes the text (with my emphasis):

Results of regressions correlating Secchi depth (mm) with prey percentages by weight in the stomach contents of Largemouth Bass sampled from Boomer.

Also (Ahlbeck et al, 2012):

For each of the 25 individuals in each size class, the diet composition was calculated as the mass percentages of different prey, and then the average mass percentages were calculated for the size class.
  [...]
prey percentages were first calculated for each fish separately and then averaged over all individuals in the sample (Hyslop 1980).

Finally, Ledger & Hildrew (2008):

Mean percentage composition (food category area as percentage total particle area) of faecal pellets of N. pictetii nymphs fed biofilm from four acid streams and four circumneutral streams.

Thanks for clarification. It certainly seems that there is no standardized name for this method (which is just a mean of percentages, as you say). I suppose I was thinking about "frequency of occurrence", also a simple method that had several names until people settled to that term. I'll wait for some days and accept this answer unless someone comes up with a better one.

@Mikko I agree that it's not entirely obvious, and people come up with all sorts of terms for basically the same thing (which can be a big problem). Personally, I hadn't heard of "aggregate percentage" before, and my main point is that most that use it as a statistic are probably not calling it that (or any other specific term necessarily).


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Plotting metabolic networks?
I need to draw a map of the core metabolism of E.coli. Associated with each reaction in the map I have a number that indicates the flux through this reaction. I want the map to reflect these fluxes through the color of each reaction in the map.
I have tried using tools like Mathematica and Cytoscape, but it is very hard to get a nice layout of the metabolic network. I have seen maps of E.coli metabolism which look very nice on paper. What I need is a map like these, but where I can define the colors of the reactions.
For example, see the image below for an example. Forget about the yellow bounding boxes delimiting compartments. I can spare those.

Can you provide a link or two to the type of metabolic map design / layout you prefer?

@MikeTaylor Added a picture to the question.

Have you looked into papers from systems biology groups which publish these networks reconstructions? They should state there what software was used.

@Chris I haven't found any. There are some tools available, for example, http://www.metdraw.com/. But when I upload my E.coli SBML model, the plot layout is a disaster. There used to be a web IPython notebook that one could use for some prebuilt models, where you just had to input the reaction fluxes. But now it's gone: http://nbviewer.ipython.org/github/opencobra/cobrapy/blob/master/documentation_builder/visbio.ipynb

There is a package called igraph in R but I am not sure that will be very convenient. If you don't get a satisfying answer here you may want to try asking on stackOverflow.

I echo @Remi.b and asking on StackOverflow.

Afaik. there is no good automated layout for graphs. I tried everything (even d3 force layout) with much smaller graphs (not in biology topic) and nothing worked... I am afraid you have to do it manually. I usually order the nodes manually with yed and after that it can draw the links automatically.

I would check out the intelligent diagram drawing software, like Graphviz which can really assist in making good layouts (requires some computer and maybe programming affinity) which can be made beautiful later with Photoshop or like. Or Yed, which could work for more manual style of work. And, if you are capable of writing computer programs, then tools like https://processing.org/ are a nice choice. All in all what you need is on the border of diagramms and infographics, so it's not just diagramming. And of course you must understand what you draw and what is the hierarchy in the diagram.

This is an old question, but Escher is a web app that has been developed that now enables the drawing of these maps using a web tool. Further customization (like reaction colors) could be manually manipulated in the downloadable SVG file.
From the main page linked above, you can load in the E. coli core model and look at (and manipulate) the map:

Escher is described in this publication in PLOS Computational Biology.

A very useful contribution to SE Biology. The fact that the question is old is irrelevant, as you have realized. I imagine there will be others like me that were unaware of this.

@David if you are interested in exploring further, Escher now has add-ons for simulating and visualizing model output overlaid on the map using Escher-FBA described in a very recent publication. You can knock out reactions, change reaction bounds, and all sorts of things (simulates using glpk on the front-end).

I'm not sure if they will be useful for your application, but you should look into software used to visualize ecological networks (and maybe also software used for drawing electrical charts). The type of data used there is very similar to what you want to plot, with nodes and links along with metadata for links on e.g. rates or connection strenghts.
I can point you to mangal by ecologist Tim Poisot (blogpost on mangal here), SBGN (Systems Biology Graphical Notation), and there is also the R-package diagram. However, I haven't used them much so I cannot say how useful they will be.

The basic problem is one of prior knowledge. The information you have about E. coli metabolism is in the form of a simple network, i.e. a list of nodes and the edges (along with their weights) that connect them. From this information alone it's impossible to know, for example, that the reactions in the TCA cycle should be plotted as a perfect circle (that's the circle in the middle of your example graph).
The only source for that information that's likely to be compatible with all of the metabolite/reaction names in your SBML file is the BiGG database. You can download maps that contain, among other things, x-y coordinates for all of the nodes in a metabolic network so that when you plot them they're not arranged in a big sloppy mess. You can then use a tool like COBRA to make the actual plots (look up the documentation for readCbMap and drawFlux).
Even this won't be as pretty as you'd like. The best answer, unfortunately, is a piece of software called Simpheny, which is commercial software that costs about a zillion dollars and is not freely available.

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


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Was the recent "conservation hunt" of a black rhino supported by science?
CNN recently covered a sanctioned black rhino hunt in Namibia by Texan Corey Knowlton, who bid US$350,000 for the license. In the story, he claims that the hunt was actually supporting conservation of the critically endangered species, as they were looking to kill an older, non-reproducing male that was consuming resources and potentially threatening younger, breeding males. The Namibian government has a list of 18 rhinos in the country (out of a total population of about 2,000) that meet the criteria.

Knowlton is targeting one of four black rhinos at the top of the government list, the ones considered "high priority threats to the herd."

Knowlton eventually caught up to and killed the animal he was targeting, and donated the meat to a local village.
CNN.com later published two opinion pieces, one in support of the hunt by Dr. Mike Knight, the Chairman of the International Union for Conservation of Nature (IUCN) Species Survival Commission's African Rhino Specialist Group (AfRSG) and the South African Development Community Rhino Management Group (SADC RMG), and one opposed to it by Jeffrey Flocken, the North America Regional Director of the International Fund for Animal Welfare (IFAW). Knight cites black rhino-specific data in his piece, arguing that in the case of this particular species, limited hunting is actually beneficial. Flocken instead uses a wider argument, citing hunting of polar bears, elephants, and lions, among other species, and claiming that the idea of "conservation hunting" as a whole is flawed. He does not, however, directly address the situation of black rhinos.
I have evaluated each side's argument, but have not yet formed a solid opinion, which is why I'm asking here. In the specific case of the black rhino, does the science support the notion of limited elimination of older males? Are there studies that show this has led to an increase in other types of conservation efforts? Does the money spent for licenses actually go towards conservation and assistance for locals?
As a second, optional question: Are the arguments posed by Flocken against "conservation hunting" in general supported by independent research? Just thinking logically I can imagine they are, as a lot of what he says makes sense in a broader context, if not necessarily in the case of the black rhino. Is there a scientific case for limited, situation-specific hunting, or should all forms of it be discouraged?
Note: I'm asking this here instead of Skeptics because I'm looking for a scientifically-supported answer. If you think it's better suited there, let me know and I'll move it.

"Support" how? For instance, I think that there are different answers to different questions depending on whether you're looking at it from the perspectives of population biology ('can we remove some individuals without affecting the long-term population growth rate?'), conservation biology as a coupled human-natural system ('where does the money go?', 'what effect does this example have on poaching?'), ethics ('does this harm animal welfare?'), or aesthetics ('is this distasteful?'). Part of the issue with those two editorials seems to be that they addressing different questions.

I see no reason why you can't post it on both sites, I have crossposted to Skeptics on occasion.

There are a bunch of meta posts about cross posting and it seems that the community still disagree on the question. I think however that most people think that cross posting is bad (see this meta post)

This question is still unanswered, partly because as @Oreotrephes points out, the question isn't actually clear on what its asking. Otherwise this is a nice question on a stimulating and interesting topic.

Looking at the question again, I think that someone could very easily put together a well-cited answer to the final sentence: "Is there a scientific case for limited, situation-specific hunting, or should all forms of it be discouraged?"

Not supported by "science," but supported by logic.  The bottom line is this:  the rangers were GOING TO KILLER THE RHINO ANYWAY.  The older male rhino was aggressive and actually killing other rhinos.  So, we have three scenarios:

Leave the rhino, letting it kill several more rhinos.
Have a park ranger kill the aggressive rhino (so that one rhino dies instead of many), which costs money.
Kill the aggressive rhino (so that one rhino dies instead of many), but auction away the rights to someone willing to spend big money, which will go toward paying the park staff to protect the young rhinos that remain.

There are economic arguments in favor of this practice [1].  The idea of culling individuals to either maintain or increase a population is also derived from the idea of "Compensatory Mortality" and has been demonstrated for a variety of ungulates [2][3][4][5][6].
I think the major flaw of any argument against this practice is the assumption that the rhino would not have been killed if there hadn't been an auction... The rhino was already on death row.  They marked it for culling because they wanted to preserve the maximum number of living, breedable rhinos...  It was only a matter of how to go about doing it, and I think they made the right choice by raising funds.
P.S.  I don't hunt, and I love animals.  In fact, I was a little bummed about this story when I heard about it, but once I learned that the rhino was going to be killed anyway, I realized it's the best, most logical answer available.
P.P.S.  Check out the Radio-Lab about this story [7].  They site that rhino populations rebounded following the creation of hunting ranches, because it gave a monetary value to the animals on ranchers' land, and they wanted to maintain that resource (by creating a breeding population).

[1] Lindsey, P.A., Rouletb,P.A.,  Romañach,S.S. 2007. Economic and conservation significance of the trophy hunting industry in sub-Saharan Africa.  Biological Conservation.  Volume 134, Issue 4.  Pages 455–469
[2] Staines, B. W. 1978. The dynamics and performance of a
declining population of red deer (Cervus elaphus). Journal of
Zoology 184:403–419.
[3] Burnham, K. P., and D. R. Anderson. 1984. Tests of
compensatory vs. additive hypothesis of mortality in
mallards. Ecology 65:105–112.
[4] Peek, J. M. 1986. A review of wildlife management. PrenticeHall,
Englewood Cliffs, New Jersey, USA.
[5] Bartmann, R. M., G. C. White, and L. H. Carpenter. 1992.
Compensatory mortality in a Colorado mule deer population.
Wildlife Monographs 121:1–39.
[6] White, G. C., and R. M. Bartmann. 1998. Effect of density
reduction on overwinter survival of free-ranging mule deer
fawns. Journal of Wildlife Management 62:214–225.
[7] Radiolab. (2015, September  07). The Rhino Hunter [Sound recording]. Retrieved from WNYC Radio website: https://www.wnyc.org/widgets/ondemand_player/radiolab/#file=%2Faudio%2Fxspf%2F529748%2F

This kind of hunting for conservational reasons is practiced in several countries in Europe where big predators numbers are kept at level where damage to farmers are acceptable. This way pouching by farmers is avoided or kept low resulting relatively stable population size of species. Good example is Finland where was too numerous wolf population which eventually was wiped out by farmers/reindeer herders as retaliation.

Yes it is.  Besides Dr. Knights article which is very focused on the issue and describes numerous benefits, there are other sources of research that show this can be good not only for the animals but also the community.  And specifically that this has worked in Namibia (where the black rhino was hunted) extremely well.
Namibia has encouraged communities to see their local animals as resources to be protected and that they can profit from.  In cases of endangered species, the federal goverment abides by CITES and only allows so many to be killed. Other than that limitation communities are allowed to profit from their local animals both from trophy hunts but also tourism.  This has led to a reintroduction of many of these animals (endangered and not) onto private lands.  The survival and thrival of these animals is now an economic concern to the communities and land holders, and are protected as such.  This has worked for the recovery of many animals in Namibia.  In summary, the selling of a license to hunt one black rhino brings big profits to the community and therefore encourage the people to protect these resources.
The CITES articles are also a good resource when looking at this.  It's very clear in the resolutions to allow quotas for endangered animals that it is not harming the population.
And one other paper, though it's behind a paywall, describes how South Africa's white rhino population went from fewer than 100 to over 11,000 as privatization and legal hunting were legalized.
As a side note, the wildlife conservation department where I live receives almost half its funding from hunting licenses.  Since it has been in operation the deer population has gone from nearly wiped out in the state to over half a million animals.
Flocken's arguments are based on fact but are really targeted at examples of bad wildlife management rather than against the practice of conservation hunting.  There is some concern that allowing the legal killing of any endangered animals will lead to more poaching, but I haven't seen any evidence in the literature of that.


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How do polygyne Carebara affinis or C. diversus (a.k.a. Pheidologeton affinis and P. diversus) colonies work?
I live in Hong Kong. Typhoon Hato hit yesterday and a whole bunch of Carebara queens decided to take their nuptial flight. I caught close to 20 of them within 15 minutes.
I'm pretty sure they are Carebara affinis, though they can also be Carebara diversa. They are also known by their old names Pheidologeton affinis and P. diversus, respectively.
In any case, I have read from multiple places that both Carebara affinis and Carebara diversa are polygyne, which means they can found a large colony with multiple egg-laying queens.
So I decided to temporarily put them into the same lunch-box-sized plastic container.
However, soon after I put them into the same container, I discover that some of them would get their legs and even their antennae bitten off. I thought maybe it's because they found the container too crowded and wanted to eliminate some competitors, so I added two layers of toilet paper to give them more surface to crawl around. That didn't really help. Tonight, after coming home from work, I found most of them have been completely amputated. They aren't dead yet though; they are just left there wiggling around without legs. A few of the queens come out intact so I suppose they are somehow dominant. The ones who get amputated tend to end up in a pile. I'm not sure if the "dominant" queens decided to drag them and pile them together.
Is that at all normal? Is that how Carebara ants start a polygyne colony? Basically one or a few dominant queens amputating their sisters to turn them into egg-laying slaves of some sort? If the dominant queens wanted to kill the weaker ones, why not bite their heads off? I'm pretty sure they had the jaw strength if they wanted to. So, supposing that the amputated queens do survive, I'm not sure I see how that helps in the evolutionary sense. Unless that's actually how it works: one or a few dominant ones amputating weaker ones to force them to lay eggs together?
Does anybody know how to properly start a polygyne Carebara diversa or affinis colony from scratch?

I don't know about their polygyne nature, but carebara diversa queens are between 20-25mm and carebara affinis queens are between 14-16mm and are slightly lighter in colour. Hopefully that should help you identify them.

They are not polygynous, they just participate in pleometrosis. This means a colony is founded by multiple queens. The workers select a "dominant" queen and execute the others, so after a short time the colony has only one queen.

Welcome to Biology.SE! Without supporting references only an expert in this area could evaluate your answer. Consequently, your answer is much more likely to receive a favorable response if you include supporting references (primary literature is best). ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively. Thanks!


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How can sex ratios remain Fisherian (1:1) in species where only the dominant male gets to mate
In certain species only the dominant male gets to mate (or given strong preference), and yet the sex ratio remains 1:1. (I'm thinking in particular of gorillas). How does this happen? It doesn't seem like Fisher's argument should apply in this case.

The average reproductive success of males is what counts, when a parent is 'deciding' whether to make a son. A low probability of your son getting to reproduce, can be balanced by his high output if he does reproduce. It's like a lottery (and at equilibrium, it's a fair lottery).

Fisher's principle applies to such cases as much as it does to species where only pairs mate.  Consider a species where a successful male has exclusive mating with a harem of 20 females, and for each such male, 19 other males are not able to mate.  A female has 100% chance of mating, and a male has a 5% (1 in 20) chance of mating. Assume a female has two offspring.
In this scenario, an equal sex ratio would mean having a female offspring would lead to an expected number of grand-offspring of 2 (100% chance of 2 offspring from that female).  Having a male offspring would also lead to an expected number of 2 grand-offspring (95% times 0 offspring plus 5% times 20 harem females each having 2 offspring).
What would happen if the ratio of births was off from 1 to 1, say 5 females were born for each male? Then expected number of grand offspring would be for a female is still 2, but for a male it is 25% (chance of taking a harem of 20 females against the 3 other males born alongside those 20 females) x 40 (20 harem matings x 2 offspring) = 10. Hence with a lopsided sex ratio in this situation, having a male is much more valuable genetically than having a female.  If a mutant arose which produced more male offspring in this imbalanced situation, it would have success until the population sex ratio became close to 1:1.

as a very belated comment on something I stumbled upon this assumes all children are equally fit.  If, for some reason, you are less likely to raise a fit child, capable of competing and besting other males for mating rights, you would be better off having a female with a far more likely chance of reproductive success despite her overall lower level of fitness.  In deed I believe studies have confirmed that there are slight variances such as this in many species.

mgkrebbs has already covered the maths that leads to the preservation of ratio, so I'll not recap.
You might have noticed that the argument only remains true if you don't know whether the particular male you produce is likely to be the dominant male or not. If you could "know" in advance that your particular son was more likely to be dominant it would make sense to skew their sex ratio towards male and vice versa. It may interest you to know that this actually happens.
Males born to high ranking females are more likely to succeed than males born to low ranking females. This makes intuitive sense as they'll get better access to food and the same genetic traits that help a female become dominant may help the male become dominant too. What's fascinating is that this actually leads to top ranking females having a male-skewed sex ratio among their offspring, and low ranking females having a female-skewed sex ratio.
See Great expectations: dominance, breeding success and offspring sex ratios in red deer for the original paper. I do not know what the mechanism behind the sex selection is.


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What kind of mushroom(?) is this?
I found groups of these growing in the Lassen National Forest (Susanville, CA, USA). It looks like some sort of mushroom. I have Googled extensively, but can't seem to find a match.

Found it. It's a Sarcodes or snow plant:
http://en.wikipedia.org/wiki/Sarcodes

not a mushroom after all! How did you find it?


text:
How do I compare the variance of a distribution of species in one area versus another?
It's possible that this question is better suited for stack overflow, but I think the ecologists on this site might be better equipped to answer it.
I'm trying to study two geographically-isolated populations of the same species. Inspecting the distributions, I see that both are bimodal (there's some seasonality to their occurrence), but the peaks in one population are much higher and much narrower (i.e., the variance of the local peaks is smaller).
What sort of statistical test would be appropriate to determine whether these differences are significant?

There's now way that I could ever answer this, but it seems a little cryptic. What is the parameter that is being measured in these distributions?

Number of individuals caught in a trap on the y-axis, julian day on the x.

While I am sure someone on this site could help you, this is really better suited to [stats.se] since the fact that you are looking at biological data is completely irrelevant to the actual question. I suggest you flag your post for moderator attention and ask them to migrate it.

I think that the question is useful here as well - this type of problems are common in ecology and there also exists a number of relatively ecology-specific software for studying this. @terdon

@fileunderwater I agree which is why I did not vote to close. I just think the OP is likelier to get an answer on the stats site. There are more users and all of them are stats people. Here we have both fewer users and a smaller percentage of statsheads.

@terdon I agree that some aspects are probably better answered there. Maybe a split Q, with one part focusing of the statistical/test aspects and one on the biological process that is being modelled would be a good idea.

Question now cross-posted: http://stats.stackexchange.com/questions/76962/how-to-test-whether-the-variance-of-two-distributions-is-different-if-the-distri

These are just some preliminary ideas...
I think you should look at the seasonal distributions separately, since the bimodal distribution is the outcome of two fairly separate processes. The two distributions might also be controlled by different mechanisms, so that e.g. winter distributions might be more sensitive to yearly climate. If you want to look at population differences and reasons for these I think it is therefore more useful to study seasonal distributions separately. An exploratory analysis could be to compare distribution percentiles (north/south and east/west coordinates) to look at range edges, or to use a fixed number of edge observations to establish borders. The weighted centre-point of population distributions can be used to look for differences in overall position. If you have grid occurences, percentage overlap between species/populations could maybe also be useful.
If you haven't already, you look also look at Maxent, which is a widely used software for modelling species distributions and habitats. Look at Elith et al. (2011) for an overview. If you want to look at changes over time (even if this doesn't seem to be your main point) you should also check out dynamic occupancy models that use occurrence records to model species distribution while taking detectability into account, e.g. MacKenzie et al. (2009).
As for a simple test for differences in variance (basically a test of homoscedasticity), there is Levine's test, which is used to compare variances of distributions between groups. Bartlett's test is an alternative, but Levene's test is supposed to be more robust to non-normality. In R the Levene's and Bartlett's tests are found in library(car). However, these are only suitable for unimodal distributions so, again, you should look at seasons independently.


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Are there any types of cancer that cause neurons to divide?
After birth neurons generally do not divide. But is there any specific type of rare cancer or tumour where neurons divide? And if there is such a cancer, then how is it possible for a neuron to regain the division power?

Related: http://biology.stackexchange.com/questions/10809/extremely-rare-occurence-of-heart-cancer

You mean brain tumors? Those are actually not that rare...

@nico I think brain tumours are caused by uncontrolled division of glia that surrounds the neurons not of neurons themselves.

@biogirl: actually you are right, most brain tumours are glial. However, gangliocytomas have neuronal components and neurocytomas are strictly neuronal, although rare.

@nico Then I think the author is specifically asking about neurocytomas. Hmmm Interesting !

@nico pinging you cause you seem to be our resident neuro person. Surely it's not true that neurons don't divide after birth! They don't divide after a certain age but that's a good few years after birth isn't it? I thought it was after adolescence.

@terdon: new neurons can be born in the adult brain. The phenomenon is less important (in terms of numbers) compared to other cell types, but still it exists. Adult neurogenesis has been reported in pretty much all mammals (see for instance: http://www.ncbi.nlm.nih.gov/pubmed/16022595 ). To be honest, I do not know until what age this happens. Surely in the mouse adult neurogenesis is seen also even well after adolescence.

I think that most mature cells do not divide in all tissues. If an organism needs to repair tissues, it uses tissue cell precursors -- stem cells.
In case of neurons, these are neuroblasts. Neuroblasts can divide and can repair brains under some circumstances (I don't know under which).
There is a cancer grown from neuroblasts, called neuroblastoma.
I think it is very improbable to have tumor from neurons, because division genes are turned off in mature cells. Can't state it is not occurring in practice.


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What's the Evolutionary Purpose of Religion?
I would imagine the answer to this question would be that religion tends to cause greater compliance of individuals within society, so it is pro-society. Plus these religions tend to incorporate some knowledge obtained by trial and error, an example of this is the fact that in Judaism the consumption of swine is forbidden which would be an evolutionary advantage seeing how swine is notorious for its parasitic constituents. Additionally religion offers an explanation for some of the phenomena that were once and still are poorly understood. Such things include near-death experiences. It also adds to motivation and tends to confer some other advantages such as a decreased rate of suicide due to the condemnation of suicide by the majority of religions.

This sounds to me as social advantages, not evolutionary ones. Not everything needs to have an evolutionary advantage.

In my opinion, social evolution is a continuation of biological evolution. In that sense, the question might be considered legitimate here.

In terms of genetic evolution, religion itself cannot really be considered to have an evolutionary advantage or disadvantage, as it is not anchored in any genes. This means that it is not an evolutionary trait and hence the principles of evolution do not apply to it. However, religion is a product of underlying capabilities of the brain (for example imaginative capacity?), and these are genetic and evolutionarily advantageous. Aside from this, asking for the 'evolutionary purpose' of anything is the wrong way to approach the topic, as things do not evolve to have a purpose but they simply evolve and stick around unless they produce a net disadvantage compared to a competing version of the same trait.
You could look at religion from a memetic point of view however, i.e. as an idea which competes with other ideas. The idea of religion has many aspects to it that would help it to 'survive', i.e. not be forgotten. These include the drive to tell other people about it, ease of understanding, the claim of exclusivity, addressing many social cravings, and filling in gaps of knowledge for which explanations are desired.


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What's the mechanism of action of Levomepromazine's analgesic effects?
I have absolutely no idea as to how Levomepromazine elicits its analgesic effects so please do direct me to journal articles and other credible sources with you, the answerer, making a summary of Levomepromazine's mechanism of action in your answer.

According to Drugbank and the articles cited below, Levomepromazine is an antagonist of several different receptors: These include dopaminergic 2, dopaminergic 4, alpha-1 adrenoceptor, 5HT-2, histamine type 1 and muscarinic-cholinergic receptors.
References:

Evidence for the use of Levomepromazine for symptom control in the
palliative care setting: a systematic review
Muscarinic cholinergic and histamine H1 receptor binding of
phenothiazine drug metabolites
Levomepromazine receptor binding profile in human brain—implications
for treatment—resistant schizophrenia
Phenothiazine drug metabolites: Dopamine D2 receptor, α1-and
α2-adrenoceptor binding