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Why has malaria only now started to develop resistance against artemisinin?
Why has malaria only now started to develop resistance against artemisinin, considering the compound has been in use for about two millennia in its herbal form in China?
The WHO has reported:

In recent years, parasite resistance to artemisinins has been detected in four countries of the Greater Mekong subregion: Cambodia, Myanmar, Thailand and Viet Nam.

However, the compound artemisinin has been used in its herbal form since at least around 400AD, when it was documented in the well known medical text 肘后方.
What are some reasons that malaria has only begun developing resistance now?
I would imagine that modern artemisinin would be more effective in completely eliminating malaria, as compared to use in its traditional herbal form. This means semi-resistant strains would more likely be killed before they are able to spread or develop resistance any further.

(archived WHO report)

The second source references a blog, which I would not consider a reliable source. However, I have read the actually text here, where the relevant page can be found in page 42 of the pdf. The book itself is quite well known, and its age is not disputed as far as I am aware. I had to post this link in the comments since I don't have enough internet points to include a third link in my post.

Selection pressure (1, 2). One way or the other, there were few enough people taking the drug that it didn't really "matter" to P. falciparum (the deadliest of the malaria-causing parasites) on a population level until recently.
According to the 2014 paper
Spread of Artemisinin Resistance in Plasmodium falciparum Malaria (3), the driver of Artemisinin resistance is a single point mutation (ie a change of a single DNA base pair) in a single gene. The thing to keep in mind is that these single nucleotide mutations happen all the time. You yourself most likely have 3 or 4 of them relative to your parent's genomes. Thus, this particular Artemisinin resistance mutation probably has occurred in the past.
However, as with most drug resistance mutations there is likely some fitness cost paid by the individual in which this mutation occurs. In environments without the drug, wild-type (ie non-mutant) parasites will outcompete the mutants, and the mutation will quickly disappear from the parasite population. It is only when the drug becomes commonplace that the mutant parasites gain the upper hand and the mutation spreads.

Thank you for the answer, it seems a very likely hypothesis. I've given this some thought since as well, would it also be possible that artemisia annua (the 'herbal' form) contains additional active ingredients which also combat the parasite, such that the development of artemisinin resistance provides it no survival/selective advantage? I should clarify that I am suggesting this not as fact but as hypothesis-to-be-tested, since it is starting to sound a little alternative-natural-remedy-ish.


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How does the Lgr5 receptor contribute to maintaining stemness in the intestine?
I don't understand the connection between Lgr5 receptor and Wnt between Paneth cells and stem cells. And how does this link to the EphB-EprinB inhibition between transit amplifying cells and differentiated cells?
My book "The molecular biology of the cell" 6th edition (Garland Science) only states that the Lgr5 receptor in the stem cells makes them able to create a mini-gut (organoid), but I am asked to present factors that makes the gut able to totally renew itself and maintain its structure.
I have already answered the Delta-Notch lateral inhibition pathway and its connection to Wnt signaling from the paneth cells in determinating differentiation and maintaining in ability to divide.

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sort: votes


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What's the mechanism for pain-induced swoon?
Is it true that people will pass out when subject to pain too much to bear, or there's no such threshold? What's the reason for passing out under acute pain, even if no physical injuries occur (e.g, loss of blood, etc.)?

Swooning, fainting otherwise termed Syncope or Primary shock (Triggered by pain or any unpleasant stimuli through the vaso vagal effect), is due to generalised vasodilation. The capillaries loose their tone and dilate resulting in an increase in volume capacity of the vascular system. This results in draining of blood to the dependent areas due to gravity thus hindering blood supply to the brain which shuts down and results in collapse (fainting) of the individual. This is a safety mechanism. Once the patient is in the lying down position the blood supply to the brain returns and the patient recovers. An individual who has fainted should not be propped up as this may result in seizures or worse.

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text:
How is bilateral asymmetry determined in embryonic development?
What are the mechanisms that ensure consistent left-right asymmetric placement of various internal organs (heart, liver, etc) or consistent left-right asymmetric development of paired organs (brain, etc.)? At what level, and how comprehensive is our current understanding about the underlying mechanisms?
(It seems to me a mirror image is just as good as the original one in terms of fitness and functionality. But why only one specific LR asymmetry prevails? Maybe this is a misguided way to think about the problem but that motivated to ask anyway.)

There are two morphogens called lefty and its antagonist nodal. Their signalling and interaction gives rise to the right-left asymmetry. However, to answer your question fully, one would have to look up on how exactly are lefty and nodal regulated.


text:
Exotic Cell Shapes
As far as I know, plant cell shapes are a difficult thing to pin down. However plant cells have cell walls and so can be very rigid. However the only plant cells I've seen have been either block shaped or tube shaped. Are there more exotic examples of cell shapes, particularly in plants? For instance have plants ever used honeycomb patterns or other forms of tesselation?

Pavement cells should content you:

From http://dev.biologists.org/content/131/21/5215.full


text:
What are the effects of muscle and fat mass on survivability?
If we have humans A, B and C who are different:

A is thin (skinny) without significant muscle or fat mass.
B is muscular
C is fat

Which one of them has the best body for survival in accidents like car crash, aircraft crash, fall from the ladder, fall down the stairs, being hit by a car, slip in the bathroom, etc?
What are the effects of muscle and fat mass on survivability?

Is this question specifically about resilience to falls/impacts? Or does this question also include disease risk? A major factor would be the age of the people in question... for instance, a high BMI is predictive of increased cardiovascular risk when younger, but in aged individuals (>65) a high BMI is actually protective, which may be due to an inverse correlation with frailty, or other complicating factor. Also, if you down-vote, provide a constructive comment for the poster.

The question is about resilience to falls/impacts. For example, can stronger neck muscles prevent my neck from breaking if I fall?

Depends, if C falls on their but, they'll be better off, if they fall on their heads the fat will make no difference. This is really way too broad, the details of how the fall occurs will always decide the outcome, voting to close.

I'll be happy with a broad answer. There is no need to go into extreme details nor close the question, that would just be a cop-out.

For car crashes, it's a mixed bag:

Better
Better
Worse
Worse

Basically, it looks like, if wearing a seat belt, slightly overweight is more likely to survive a car crash, but if no seat belts are worn they are at a disadvantage; the very obese are always more likely to die, however.  Also, some of this was found only for males, not females.

Interesting. What about muscles? Do they have the same effect as fat?

That's harder to test, as you can't measure "muscles" from old data but you can estimate BMI from height and weight.  That being said, muscles might help a bit, but only because people are muscular tend to be "harder," that is, they have stronger bones and joints and have stronger muscular walls protecting their organs.  Conjecture, of course.

@Amory, the studies you referred to look at BMI, but it doesn't specify whether the BMI increase was due to muscle or due to fat.  After all, muscle is heavier than fat.

Correct, but most people aren't Arnold Schwarzenegger.


text:
Just how dangerous is ethidium bromide?
A common precaution for preparing EtBr-agarose gels is to add EtBr only after the gel solution has cooled somewhat, because EtBr is a dangerous mutagen. Supposedly, adding it to a hot liquid allows EtBr vapors to get into the air and everyone's lungs, where it can act as a carcinogen.
In addition to this are commonly seen special procedures for handling EtBr vials and gels (fresh nitrile gloves, avoid contaminating other work areas, special waste disposal rules).
However, there's also some saying that EtBr isn't all that mutagenic and all this care is over the top.
What's the reality? Just how dangerous is EtBr, especially in amounts used at a typical biological lab? How long does the danger persist? Are even trace amounts hazardous (for instance, touching a "clean" pipette without changing gloves after working with EtBr)?

I've heard that you shouldn't put EtBr in hot agarose to prevent degrading the dye in the heat.

I also believe you loose intercalate abilities if you break it down with heat.  Thus I don't think the risk is vaporized EtBr in the steam.  It might be a carcinogen/mutagen given that it intercalates DNA so well, but I think it's toxic effects are more substantiated.  With proper PPE you are at little risk.  I certainly wouldn't bathe in it.

Cows are injected with the stuff in quantities thousands of times higher than are used in a lab without any ill effects.  That said, you're probably not a cow, so you might as well wear gloves.  Being overly cautious isn't going to hurt anyone, and contaminating someone else in the lab because you're not concerned about what is probably a very low level risk is inappropriate.

Oh it is not that dangerous as its current image. Pouring hot gel has another problem too; it damages your gel tray and combs. I guess EtBr is not that volatile (MP=260 deg C) that it will fume in a hot gel @ 70deg C.

I usually find the treatment of Ethidium bromide in the lab widely exaggerates the true dangers of this chemical.
It is not really toxic (the LD50 is 1.5 g/kg bodyweight, as a comparision NaCl has a LD50 of 3 g/kg). It has also only been shown to exhibit mutagenic potential to bacteria after it had been treated with liver extracts. This means that some of the metabolized products of EtBr in the liver are mutagenic, but EtBr itself not. See reference 1 for details here. It is also not classified as a cancerogenic substance by the regulation bodies (for example see the National Toxicology Program of the US on Ethidium bromide).
As already mentioned, it is used to cure Trypanosoma infections in cattle (reference 2). Here up to 1 mg/kg bodyweight are given, with no signs of toxic or other adverse effects. The typical concentration used in the lab to prepare gels is 1 μg/ml. It works as a drug by interfering with the mitochondrial DNA (changing it to the Z-form, which is not available for replication). See reference 3 for details. Ethidium bromide also acts as a Topoisomerase I inhibitor as other chemotherapeutic drugs. See reference 4 for more details.
Additionally, EtBr is negatively charged and cannot enter cells or the nucleus, since cannot pass the membranes. I would wear gloves and also apply the usual safety rules when working with gloves (do not touch anything you don't need to touch, especially things like door knobs, keyboards or phones as you might spread contamination) dispose your gloves when not needed anymore and you should be fine.

References:

Detection of carcinogens as mutagens in the Salmonella/microsome
test: assay of 300 chemicals.
Comparison of isometamidium chloride and homidium bromide as
prophylactic drugs for trypanosomiasis in cattle at Nguruman, Kenya.
A low dose of ethidium bromide leads to an increase of total
mitochondrial DNA while higher concentrations induce the mtDNA 4997
deletion in a human neuronal cell line.
The geometry of DNA supercoils modulates the DNA cleavage activity
of human topoisomerase I

The dangers of this compound are wildly exaggerated but like @chris said, the dangers aren't completely known. I wouldn't recommend shaving with it. I think the deep red color actually is what  heightens people's curiosities and fears most.

I wouldn't recommend this either - and I recommend wearing gloves when handling it. But besides that, irrational fears and actions are really not necessary.

Inspired by Jason Patterson's comment, I looked up "ethidium bromide cattle" and found a blog post about ethidium bromide toxicity. Apparently ethidium is routinely used to treat sleeping sickness in african cattle at 1mg/kg without ill effects. All data concerning ethidium toxicity comes from in vitro tests that may not apply to in vivo use. You should still wear gloves, but don't freak out over it.
The blog post had some references, but most are dead links now. Here is the only working link left. Here's a review article on dye therapy for parasites.


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How does air-liquid interface (ALI) culture work?
For studying diseases, such as chronic obstructive pulmonary disease (COPD), cells are often grown in air liquid interface.
I understand that the common way of establishing this these days is to grow cells in culture well inserts with a permeable bottom, then put medium only in the well and not the insert.
Here is an image from Stemcell Technologies:

The last images implies that the level of the medium is just high enough to cover only the basal side of cells. Is this realistic? Given that the monolayer is a few microns thick, is it really just a matter of carefully pipetting just enough medium? It seems like the error of a pipette is too high for this.
In practice, I am getting the impression that the level of liquid is actually higher than the apical surface of the cells, but it is somehow prevented from seeping out of the well and into the insert. If so, how? The bottom of the insert is permeable; even if you grow cells to confluence, surely there will be a small hole or two somewhere which causes a leak?


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CDK3 1 simple coding mutation/missense mutations (S106N) glioma
I found the below quotation in (Peyressatre, 2015)

CDK3   1 simple coding mutation/missense mutations (S106N)   glioma
  [135]

The author has cited a database but not a paper. I want to find the paper that talks about the above mentioned type of mutation in CDK3

Welcome to SE Biology. Two points about your question. 1 "Peyressatre, 2015" does not allow anyone who doesn't already know to find the paper your quotation comes from. Please include a proper journal reference, perferably with a link. (Also to the database). 2. What effort have you made to search for this yourself and with what results? This sounds a very specialized question for this list. You must help anyone who is interested in the area to help you.


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Why are IMAC and gel filtration combined?
In a practical course I used an Biorad Profina system to purify a protein with a histidine tag.
The device uses a column for IMAC and one for gel filtration. Why are these two devices combined in one? Why is there a need for gel filtration?
I missed my chance to ask this in the practical training, thats why I ask here!
Thanks for your help!

What is IMAC? Please do not use non-standard abbreviations in questions or include thanks.

Immobilized metal chelat affinity chromatography

Then spell it out! (And get chelat spelt properly when you edit your question.)  And do some research and provide some detail if you post here.

Without knowing your specific protocol, it is common to use more than one purification method for a single protein. Given the broad similarities that all proteins and even most biomolecules share, it is impossible to completely purify a protein in a single step. The strategy therefore must be to purify via as many properties unique to the target protein as possible until the purity of the sample is sufficient for the desired application. These properties can include most commonly affinity (eg immobilized metal), charge (ion exchange), hydrophobicity (reverse phase) and size (gel filtration).
In a perfect world, a protein could be purified in a single step affinity-based protocol. In the real world, however, non-target proteins can bind the column nonspecifically (for example, binding to the positively charged nickel column or to the agarose matrix itself). Nucleic acids may elute with your target protein or your target may form large, undesirable aggregates. The list of potential problems is long and this is why multiple different rounds a purification can more effectively discriminate between the target protein and other contaminants in the mixture. As an example, let’s say there there is a contaminant binding the Ni-NTA matrix by charge. Using gel filtration afterwards, which separates by size and not charge, allows removal of the contaminant from the target protein.
A major benefit of gel filtration as a final polishing step is that it can also be used as a desalting column. Besides further purifying contaminants from your target protein, gel filtration allows removal of unwanted small molecules (eg imidazole from IMAC) and elution in a buffer desired for downstream applications.
I looked for some further reading in case your interested and found this protein purification handbook which talks about developing purification strategies.

thanks a lot! Not all heros wear capes, some wear lab coats!

@Mourinho_1 Haha you’re welcome.

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Correct term for initially neutral mutations that subsequently cannot be reversed
Can anyone tell me what the correct name is for a neutral mutation to a protein that occurs when that mutation becomes "locked in" due to a subsequent mutation?
For example: mutation A is neutral initially and can be reversed with no deleterious effects, but after mutation B, the reversal of mutation A would now become deleterious. What is the correct terminology for a mutation of A's type?

Silent mutations are mutations in DNA that do not significantly alter the phenotype of the organism in which they occur. Silent mutations can occur in non-coding regions (outside of genes or within introns), or they may occur within exons.

Well, what will happen is proceeding to fixation if A does, but I don't think that really answers your question. The answer could be here.

Mutation A is a suppressor of Mutation B. The Wikipedia article on the topic (https://en.wikipedia.org/wiki/Suppressor_mutation) mostly describes situations where Mutation A occurs after B and reverses B's deleterious effects, but the principle is the same.


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Can low temperatures induce a withdrawal reflex?
I read in "Essentials of Pathophysiology: Concepts of Altered Health States
By Carol Porth" that

"The thermal pain receptors are stimulated only by extremes of temperature such as "freezing cold" below 5°C and "burning hot" above 45°C."

Also in "The Journal of Neuroscience, April 7, 2010 • 30(14):4933– 4942 • 4933" it states:

"In lightly anesthetized rats, hindpaw cooling with ethyl chloride, but not acetone, was sufficiently noxious to evoke withdrawal reflexes"

We know, 'burning-hot'-receptors induce a withdrawal reflex when we touch a very hot object, say hot frying pan.
But does this mean if we touch a very cold object (temperatures below 5°C), the 'freezing-cold'-receptors would induce a withdrawal reflex in humans?

The withdrawal reflex is a nociceptive flexor reflex and is a spinal reflex intended to protect the body from damaging stimuli.
In other words, activation of heat receptors is not the trigger of the withdrawal reflex, it is the activation of pain receptors at high, tissue-damaging temperatures.
Extreme cold is also damaging and causes skin lesions akin to heat-induced burn wounds. Again, at a certain tipping point extremeley low temperatures become damaging, and cause frost bites (Sachs et al., 2015). At this point tissue damage will activate pain receptors and these cause the withdrawal reflex to be initiated.
Reference
- Sachs et al., Dtsch Arztebl Intv; 112(44): 741–7

How cold does it have to be to cause harm? to cause withdrawal?

@DisplayName - I deliberately left that out as it depends on the duration of the exposure. It's hard to say.


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Is dietary fat directly stored in adipose tissue or is it immediately metabolized?
I know that fat goes to adipose tissue and even sugar gets converted to fat and goes to adipose tissue, but what happens to fat (unsalted cow milk butter) I just ate? Will it give me energy now, or does it automatically goes to adipose tissues for future energy storage?

first come, first server mechanism: for example, if you have not eaten a single thing in 2 days, the first thing you put in your mouth will be used for energy immediately and you will feel satiated. note that since you did not die in those 2 days your body is using the energy in your adipose stores (from your physical body fat) first and only then from outside sources.

What research have you done before asking it here?


text:
Why does increased humidity decrease coronavirus "survival"?
All news I can see scientist telling that the SARS-CoV-2 virus survive more in cold and dry weather. I can understand cold as hot weather will desiccate virus, but why dry  weather.
Would not dry weather dry droplets of saliva sooner also desiccate virus, would not humid weather support virus?

So I found this information regarding humidity from an article by MIT on corona:
1) High humidity leads to condensation of sneezing cough saliva particles sooner, so it does not spread to farther distance
2) Low humidity leads to less condensation and higher range of movement of saliva particle, hence more spread area.
Apparently it has to do with physics and range of infection not on survivability.

The statements about humidity are based on cultures from surfaces, see for example http://downloads.hindawi.com/journals/av/2011/734690.pdf (this paper is about a previous coronavirus, not the current strain, but still likely applies for qualitative data). These are specifically measures of survivability, and not infection.

I found an answer to this mystery in the literature, but it is a somewhat tentative explanation from a relatively recent (2012) paper by Yang et al. In a nutshell, [respiratory] viruses do worse in small droplets compared to large/unconstrained ones. Even being "totally" dry is apparently somewhat better for them than being trapped in a small droplet. So you get a V (or U)-shaped survival curve as a function of relative humidity.

There appear to be three regimes of IAV [influenza A virus] viability in droplets, defined by humidity: physiological conditions (∼100% RH) with high viability, concentrated conditions (50% to near 100% RH) with lower viability depending on the composition of media, and dry conditions (<50% RH) with high viability. This paradigm could help resolve conflicting findings in the literature on the relationship between IAV viability in aerosols and humidity, and results in human mucus could help explain influenza’s seasonality in different regions.
[...]
After release from the respiratory tract, where RH is ∼100%, a respiratory droplet shrinks by 40–50% in diameter at RH below 90% due to evaporation [16]–[18]. As a result, concentrations of solutes in the droplet increase by up to 15 times, and solutes such as salts (e.g., sodium chloride (NaCl)) that are harmless at physiological levels may become harmful to the virus. For example, avian IAV has been reported to be less stable at salinities greater than 25 g L−1 [19]. Evaporation induces changes to IAV’s microenvironment inside droplets that may affect the virus’ viability, and the toxic effect of solutes may be enhanced at lower RH due to higher concentrations that result from greater loss of water.

Yang et al.'s paper has been positively cited in a couple of subsequent reviews  Lowen and Steel (2014) and Paynter (2014)
So it seems to be a fairly credible explanation as far as influenza is concerned. Paynter's review also discusses similar observations on RSV:

One study examined the effect of humidity on RSV survival in 1 μl droplets of tissue culture medium on polythene at room temperature. Over the first 5 h, RSV survival was highest at the highest humidity, while over the next 67 h, RSV survival was highest at the lowest humidity. The explanation of these findings may lie in the droplet drying time in this study. Droplets exposed to 77% RH were still wet at 18 h (no data were given for drying times at 32% or 52% RH). The relatively high survival at higher humidity over the first 5 h was probably due to the fact that the droplets remained wet in these conditions. The survival over the final 48 h (when all droplets were dry) was progressively reduced with increasing humidity. Consistent with this explanation, only 1% of RSV was lost over the 72 h when stored in liquid culture medium, and in addition, the authors noted that RSV survival was increased with increased droplet size. Similarly, in another study the survival of RSV on countertops was reduced if the virus was in droplets that were dried quickly. These results are consistent with the studies examining influenza survival on surfaces, suggesting that while the virus remains ‘wet’ in droplets, high humidity prolongs its survival, by reducing evaporation.

There might be more recent advances in this area though, especially regarding mechanisms of the "middle regime".

Great answer.There's much to be discovered in how viruses spread through droplets, and these studies probably involve physics too.

Increased temperatures and  humidity slows down the spread of virus, as warmer air holds more moisture it prevents viruses from traveling through air in comparison to the dry air conditions. As humidity increases, the size of water droplet is larger which settles out of the air quickly. This the reason why influenza-like viruses spread more in winter season.
The SARS CoV2 (strain of coronavirus presently causing COVID 19 disease) has the basic reproduction number (R0) approximately 3, which means each infected person can pass virus to about 3 other people. And researchers have found by increasing temperature by one degree Celsius and one percent increase in relative humidity decreases this R0 value by 0.0383 and 0.0224, respectively. This means less number of people are infected further by single infected person.
Checkout this review: https://www.ncbi.nlm.nih.gov/pubmed/32196426

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Crossover Equivalence - Does AB/ab X AB/ab result in no effect in crossover 50% of the time when crossover occurs?
I might be using symbols wrong, so my symbol definitions for this post:

DEFINITIONS:
AB / ab : gene alignment on chromatids.

Another way of looking at the above is
a   b
----- chromatid 1
----- chromatid 2
A   B

or
a||A
b||B

AB/ab || ab/AB : alignment of sister chromosomes during metaphase I when alignment occurs. So in this case, crossing over of ab and ab would result in no effect on the gametes
AB/ab X AB/ab: Crossing two parents

If you were crossing AB/ab X AB/ab with a mu of 20 between a and b, that would imply crossing over occurs 20% of the time. When crossing over, the chromosomes could be aligned either:
AB/ab || ab/AB,
AB/ab || AB/ab,
ab/AB || ab/AB,
ab/AB || AB/ab.
This implies to me that 50% of the time during crossing over events with AB/ab, there would be no effect of the cross-over for the genes a and b.
This would then imply to me that the gamete distribution would be:
AB: 45% (40% from no crossover, 5% from crossover)
ab: 45% (same reasoning)
Ab: 5%
aB: 5%
Which if you then did the test cross, would mean if you were asked what is the frequency of AB/AB in the cross progeny, that the resulting progeny would be 45%*45% = 20.25% AB/AB, and not 16% AB/AB if crossing over always resulted in unique gametes.
Is the above reasoning correct?

I also don't see any reference to this either, what I assume to either be a misattribution or misunderstanding of how the process works, or that it's already baked into the understanding of MU and that crossing over would always result in effective cross-over and not just a 'null' cross-over

I am thinking that mu already bakes this assumption of recombination of two genes by definition, as recombination is looked at wrt two genes.


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Have elephants (or any species other than humans) been known to cover their dead?
I was just reading this blog on HarperCollins website about 5 animals that grieve. Of elephants, the following claim is made:

They bury their dead and pay tribute to the bodies and to the bones. [my emphasis]

Now, I don't doubt that elephants "pay tribute to the bodies", which I take as mourning, as THIS VIDEO (WARNING: if you are an animal-lover, these two videos may be disturbing to you and THIS VIDEO appear to show some sort of concern over the dead. I am aware of the complex emotional lives of many animals, such as cows experiencing PTSD-like symptoms from wolf attacks, or any number of animals that experience PTSD-esque symptoms. Or, how a mother orca carried around her dead calf for 17 days, and I could go on for awhile here.
My point is that I am not doubting that elephants experience a complex inner-world. What I am questioning is elephants' (or ANY creature's) propensity to cover their dead. I find the suggestion that they "bury" their dead, as doubtful almost to the point of disregarding it entirely (for an elephant to dig a grave large enough for another elephant, or to dig up enough material to cover another elephant to effectively "bury" it would be a tremendous amount of work and truly astounding, indeed). However, it would not be too terribly surprising to find them covering their dead. The question would be, to what extent? For example, is it a single branch or a single scooping of dirt with the trunk by a single member of the herd, or is it a concerted effort by the group to cover the deceased with a good amount of material?
The only place I can find with an apparent expert mentioning this behavior is in a Daily Mail article from 2013. It is a passing mention of the behavior:

According to Charlie Mayhew, of the Tusk Trust, elephants will ‘bury’ their dead, covering carcasses with branches and even taking the tusks to be placed at a different spot.

I can find no other mentions of this behavior, outside similar briefly passing mentions in places such as Quora or Facebook.
So, the PRIMARY question is do any animals bury their dead? The reason I have focused primarily on elephants here is because they are the only species mentioned by my Google searches that exhibit this behavior. SECONDARILY, I would like to know what form these "burials" take; i.e., like I mentioned earlier, how much covering of the deceased is performed, and by how many individuals. ULTIMATELY, someone will find a YouTube video or (even more preferentially, multiple) videos showing the act. Thanks for any help you can give.

Elephants are very intelligent and they do so.

Yes.
I was able to find a book1 (see p. 237-239) and a paper2 (I couldn't access this one) suggesting elephants bury their dead and other animals in African elephants (Loxodonta africana). I also found references to a paper/article in the American Psycologist3 that apparently catalogued some reports of these event in the 1980's (see reference 22 in Pinel et al. referenced below, this ref may be the same as ref 2.).
I believe the elephant burying behaviours are simply covering the animal with dirt or other items (leaves etc). How extensively they get covered, I don't know.
However, there are apparently two mammalian species (besides humans) that physically bury their dead. These are the rat4 (Rattus norvegicus) and the mole rat (see pay-walled NY Times link in 5, if you can access either of them) (Heterocephalus glauber). It seems that both species bury their dead in response to release of chemicals related to decomposition.
In the case of the common rat, dead rats of the same species are buried only between 5 and 40 hours post-mortem. In naked mole rats, it seems that the dead are dragged to the latrine/toilet area, which is then subsequently filled in and a new one dug.
Refs:

Douglas-Hamilton, I., Douglas-Hamilton, O. (1977). Among the Elephants. United Kingdom: Collins. (read for free at Archive.org)

Siegel, R. K. (1977). Religious behavior in animals and man: Drug-induced effects. Journal of Drug Issues, 7(3), 219–236. https://doi.org/10.1177/002204267700700302

Siegel RK. The psychology of life after death. Am Psychol. 1980 Oct;35(10):911-31. doi: 10.1037//0003-066x.35.10.911. PMID: 7436117.

Pinel JP, Gorzalka BB, Ladak F. Cadaverine and putrescine initiate the burial of dead conspecifics by rats. Physiol Behav. 1981 Nov;27(5):819-24. doi: 10.1016/0031-9384(81)90048-2. PMID: 7323189.
Format:

Piel, A., & Stewart, F. (2015). Non-Human Animal Responses towards the Dead and Death: A Comparative Approach to Understanding the Evolution of Human Mortuary Practices. In C. Renfrew, M. Boyd, & I. Morley (Eds.), Death Rituals, Social Order and the Archaeology of Immortality in the Ancient World: 'Death Shall Have No Dominion' (pp. 15-26). Cambridge: Cambridge University Press. doi:10.1017/CBO9781316014509.003 (you can see this chapter through google books - do a title search)

note the mole rats likely evolved the behavior for the same reason ants bury their dead.

Those pages are missing from the first source on Archive. Are you somehow able to see them, or did you read that from a book you actually have?

Also, where did you read that about the naked mole rats dragging their dead to their latrine? I could not find that on the page you listed, or under the "Behavior" tab on that website. It would be interesting considering it says that they get their sent from their latrines, so maybe they stop using a latrine once they dump one in?

@JimmyG. Here;s the quote from ref 5 on naked mole rats: Mole rats (Heterocephalus glaber) show a comparable behaviour, quickly detecting a corpse in their den, before dragging, kicking, or carrying it to the communal latrine. ‘When the latrine is filled they seal it off with an earthen plug, presumably for hygienic reasons, and dig a new one.’1 What the 1 is, I have been unable to determine, can't see any footnotes, doesn't fit ref style in article; may refer to table 2.1 in article but also doesn't fit other table refs.

@JimmyG. I see page 237 in the book linked; I read it on Archive. The linked book does have some problems with the colour plates and the scroll bar, but gets past that once you are past the plates. Exact page link: here

@JimmyG. sorry for the mixed comments - Presumably the mole rats make a new one, as it seems they seal off the old one. My local library has allowed me access to the NY Times article, so quote: For some animals, the death of a conspecific is a little tinkle of the dinner bell. A lion will approach another lion's corpse, give it a sniff and a lick, and if the corpse is fresh enough, will start to eat it....

@JimmyG. ...For others, a corpse is considered dangerous and must be properly disposed of. Among naked mole rats, for example, which are elaborately social mammals that spend their entire lives in a system of underground tunnels, a corpse is detected quickly and then dragged, kicked or carried to the communal latrine. And when the latrine is filled, said Paul Sherman of Cornell University, "they seal it off with an earthen plug, presumably for hygienic reasons, and dig a new one."

The quoted (Professor) Paul Sherman is at Cornell and does work on behaviours of animals, including naked mole rats; so entirely plausible that he would know. You can look at his Cornell page here and look through some of his books/articles.


text:
What are Codominant vs Dominant Genetic Markers?
When talking about types of genetic markers, the adjective "dominant" and "codominant" are often used. I don't fully understand their definitions and found contradicting definitions.
Foll and Gagiotti (2008)
Typically reading from  Foll and Gagiotti (2008), they list give two examples of markers of each type

Codominant markers

SNP
microsatellite

Dominant markers

RFLP
AFLP

reddit
This reddit post indicates that RFLP are codominant markers (unlike stated in  Foll and Gagiotti (2008)).
wageningenur
On wageningenur.nl (random website I never heard of before), they define dominant and codominant markers based on gene expression suggesting that the terms dominant and codominant used for markers have the same definition than those used for allelic effects on the phenotype (dominance, recessivity, overdominance, etc..).
Questions

What are the definitions of dominant and co-dominant genetic markers?
Can you please offer examples for each type and explain why they fit in one or another category?
Do the terms dominant and codominant have the same definition when used to describe a marker and when used to describe allelic effects on the phenotype (dominance, recessivity, overdominance, etc..)?

So does it make any sense to say that SNPs are codominant while RFLP are dominant (or vice-versa)? Thanks

I don't think that would be right. RFLP is a technique which may in certain circumstances differentiate SNPs as well. It is a low resolution technique. Now SNP is just a physical feature on the DNA: it is not a phenotypic marker; more of a genotype you can say. However SNPs may be in a non-geneic region and affect the phenotype. SNPs create allelic variants (let's also consider any region that affects the phenotype as a part of the allele i.e. include the promoter/enhancer etc). These alleles can be dominant, co-dominant or recessive. It does not make sense to say SNPs are codominant.

I would agree but these terms I used over and over. See a search on Google Scholar with the terms "codominant dominant marker".

From wikipedia

If the genetic pattern of homozygotes can be distinguished from that
  of heterozygotes, then a marker is said to be co-dominant.

This definition seems to be different from the one used to explain allelic effects. For example, as you would know a SNP is basically a feature of the DNA sequence. It is more of a genotype rather than a phenotype. Markers are supposed to be phenotypes (can be a molecular phenotype too for example a marker for stem cells etc). SNPs do create allelic variants but they may or may not contribute to different phenotypes. Consequently, the allelic variants may exhibit dominance or co-dominance with respect to each other. So, going by the definition used in classical genetics, you cannot call SNP as a "dominant"/"co-dominant" marker.
That is a weird usage of the terminology but people have done it so the deed cannot be undone. I would avoid future usage of such misleading terms. Having said that SNP would fit the definition of a "co-dominant marker" if it is observed by DNA sequencing .
Personally, I would consider RFLP a technique and not a marker per se. RFLP can be used to differentiate SNPs but sometimes it may not even resolve different strongly visible phenotypes (its efficacy basically depends on the polymorphism at restriction sites). Heterozygotes however, would have a different band pattern compared to homozygotes. So it should be a "co-dominant" marker.
AFLP, as far as I know is simply PCR amplification of restriction fragments. It would be "co-dominant" for the same reasons. However, just a PCR based screen would not differentiate between homozygotes and heterozygotes and would thus be a "dominant" marker. Now again, these are techniques and not, in a true sense, "markers" whereas SNPs and microsatellites are actual DNA features. So these cannot be even compared. A technique, depending on its resolution, can be "dominant" or "co-dominant" as per these definitions.

For general interest
I would want to reiterate that these definitions, for some reasons mentioned above, are quite flawed and are therefore misleading (they may have been okay at certain point of time but are obsolete now). Please avoid their usage in your papers and reports and if possible point these flaws out, so that they do not propagate.


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How to define "evolution"?
The standard answer found in intro course to evolutionary biology to the question:

what is evolution?

is:

It is a change in allele frequency over time!

I believe a complete definition should encompass the following concepts:

mutations
copy number variation (CNV)
codon usage
chromosome numbers
phenotypic change (whether heritable or not)
Complex phenotypic trait such as plasticity and developmental noise
maybe some other things...

My questions are:

Would it be worth it to talk about phenotype in a definition of evolution?
What are the alternative definitions that have been proposed?
What is your definition?

Note: I would rather talk about genetic evolution, but if you think it is worth making one definition for genetic and cultural (and some other stuff maybe) evolution, you're free to suggest it!

@Sancho I think a definition is never objective. It is totally arbitrary to decide what is hidden behind the word "evolution". Therefore, I would have expected several suggestions of definition. I guess a good definition is a definition that fits quite well the everybody sense of what is the boarder of a concept. "Worth" to any individual person willing to answer this question.

@Sancho Explanation? Explanation of what? I don't think I'm expecting any explanation about the science of evolutionary biology. I guess my question is close to a question of philosophy but I expected better answer by posting here than on philosophy beta.

@Sancho "It is a change in allele frequency over time" does not encompass some concepts that I listed in my question. No, there might have no True answers but rather useful answers. That makes my question rather a philosophical question but I guess evolutionary biologists are better than philosopher to define "evolution".

I think you are confusing a definition of evolution with a complete description of evolution. the first should be a sentence the second should be  several books worth of information.

What is evolution?
In a non-biological sense, evolution means change:

"a process of [...] change"

Biological evolution (seeing as this is Biology stack exchange) then needs to be tweaked to give a biologically specific context. Many textbooks etc. give definitions of evolution and here are a few good ones from across the history of evolutionary biology:
Charles Darwin:

"Descent with modification".

Mark Ridley1:

"Evolution means change, change in the form and behaviour of organisms between generations. ... When members of a population breed and produce the next generation we can imagine a lineage of populations, made up of a series of populations through time. Each population is ancestral to the descendant population in the next generation: a lineage is an ancestor-descendent series of populations. Evolution is then change between generations within a population lineage."

Brian and Deborah Charlesworth2:

"Evolution means cumulative change over time in the characteristics of a population of living organisms. ... All evolutionary changes require initially rare genetic variants to spread among the members of a population, rising to high frequency..."

All of these have a common theme. Biological information is moving through time, descending with a degree of directionality (e.g. parent $\rightarrow$ offspring), and the information is modified with time.
Personally I would define evolution as:

Evolution is a change in gene frequencies, resulting from four mechanisms (mutation, migration, drift, and selection) which can all affect the transmission of heritable genetic information within populations. Evolution has the potential to cause phenotypic change (when genotype affects phenotype) and has the potential to cause both adaptation (microevolution) and divergence (macroevolution).

This definition captures that biological evolution occurs through changes in heritable genetic information, the prerequisites of evolution, the mechanisms of evolution, and what the consequences of those changes can be.
I think it is important to include mutation (and drift, selection, and migration) because these explicitly state how evolution occurs. I don't think it is necessary to include copy number variation, chromosome numbers, or codon usage as they are not central to the process of evolution (though they can be important).
Whilst only the first sentence of my definition is critical, I think it useful to include the latter part (or something of a similar effect) whenever possible as it helps to clarify evolution and it's relevance.

ISBN: 978-1-4051-0345-9
ISBN: 978-0-9815-1942-5

Nice +1. It is good to have this short review of definitions. I like your definition, I would just note that often when talking about divergence, people are talking about neutral molecular divergence and not phenotypic divergence. Thanks

The problem with defining it as only change from these four sources is when we find other sources of change, like recombination, engineering, or possibly extinction. The entire second sentence of your definition does not belong in a definition, it is accessory information. It is like a inserting a specific reference to kin selection in the definition it does not need ot be there. Worse it tires to define other terms as well, many will disagree that divergence=macroevolution.

@John recombination doesn't change gene frequencies, extinction will either occur through selection or drift, and one could argue that mutation also includes engineering (if you mean changing the genes). The second sentence is there to clarify that phenotypic change and evolution are not synonymous terns.

Also why do you not think that divergence is macroevolution?

Depends on the organisms, in unicellular organisms it can lead to speciation by creating a novel combination of existing genes. divergence does not have to result in speciation speciation while macro evolution is defined by occurring at or above the species level. More importantly not all macroevolution is a result of divergence. Wiping out part of a ring species for instance would create speciation while not creating any new genes or structures. They are closely related but not identical. but more importantly you should not be defining one term in the definition of another.

I'd argue that wiping out the middle of a ring species is not divergence or speciation either, the species remaining at the ends are already diverged from one another prior to removing the connection @John

they had already diverged but they were not separate species until the middle were wiped out,  It is most definitely a speciation event directly caused by the death, without it it is not speciation. But this debate itself shows another problem with the definition by adding unnecessary terms it makes the definition evern more open to interpretation and confusion. The accessory information should not be part of a definition,  A definition is for defining something not listing all the possible outcomes of it.

I really don't understand why you have such a big issue with the answer. I even addressed that the second part is not necessary in the original answer (see the last paragraph). The fact is that the answer defines evolution as it is understood within the field, genetic change by any of the four mechanisms - there are no other mechanisms. Removing the middle of a ring species may be a speciation event, but it's not evolution. @john

debatable, it is essentially an extreme form of genetic drift, but the argument itself is why all the extra stuff should not be part of a definition. The first seven words of your defintion all all that are needed for a definition, the rest of it really adds nothing to it as a  definition. There is no benefit in defining it as only those four mechanisms becasue there could be others, but those new mechanisms would still be evolution.

Well that's is your opinion. Personally I think the extra detail in the answer add to the definition to help make cleat what evolution is not. Perhaps we can just accept that we have different opinions on that. Something that you should note, however, is that it is well accepted in the research community that these are the four possible mechanisms of evolution, there's not much else that could occur - they kind of cover all the bases @John

Theoretical biology spans multiple disciplines and the unaccompanied term evolution is defined differently in each:
As such chemical evolution is different from time evolution in physics and many other systems in theoretical biology that "evolve". These do play a role in theoretical biology.
Also, what standard answer to evolution in the field of theoretical biology are you referring to?
I recall learning that an allele as a special[:species:] gene variant, is defined as such as being present in at least one percent of the population. That definition has broadened meanwhile. A definition that has broadened.
Point in case, I don't believe there to be an evolutionary master-framework to (yet) exist, along the lines of desires for a Theory of Everything in physics.
On the other hand, as soon as you cross the boundaries of biological evolution, like let's say in the most primitive of living, biological entities, you are bound to cross over to cultural evolution as well. ( I am no expert on the subject, there are probably other intermittent steps as well). Synergistic effects in the process of evolution may even be considered in Quorum Sensing's most favorite model: Vibrio fischeri.
A simple search on the subject instantly yielded me:

"Evolution of alkaline phosphatase in marine species of Vibrio". J Bacteriol....

In other words: molecular evolution, as being part of the many evolutiony research focuses.
The idea and gross effects of Darwinian evolution are often rather straightforward at first glance. All the little details, that have to be accounted for -with scientific rigor-, as science itself is evolving, are probably where the team-work starts, as do the discussion.
So the only fixture you can count on is team in science.
The introduction to the evolutionary topic at hand, that you would use in an abstract or introduction would depend on the scientific sub-discipline, and would likely already be readily available through peer-publication.


text:
Human body power consumption in still state
I'd like to know what kind of power human body needs to maintain life, in still state (average daily power consumption of an average man is also of interest). In terms of watts.
I've only managed to find one figure - 1700 kcal per day without physical activity. That converts to 80 watts, which seems (intuitively) a bit low, so I wonder if it's the right figure or not.

1700kcal=7000kJ=a lot of ice turned into steam. Actually @Amory 7000KJ isn't going to turn that much ice into steam If you ask how much quantity of heat is required to convert 1 kg of ice into vapour then you have to add latent heat of fusion that is 336 kj/kg and latent heat of vaporization 2257 kj/kg (these two process occur at constant temperature so need to add rise in tempeature) So it will be:
Q= 1×336 + 1× 4.18 ×100 + 1× 2257
Q = 3011 kj Or 3.01 Mj So you can turn ~2.33 KG ice at 0° into steam at 100° with that energy.

You're basically correct.  I don't know if you've found the Wikipedia article on Basal Metabolic Rate but it's got everything you need, including a bunch of formulas you can use to figure out an average value for a given body type.  There are also many online calculators, such as this one.  You can easily figure out averages, which I think is what you want, but between two individuals the number can change quite a bit.
Why does 80 watts sound so low?  This is more of a physics.se answer, but Watts are a unit of power which mean they measure energy use over time; W=J/s, or Joules per second.  Every second.  Have you ever touched a 75 watt lightbulb?  They're hot as hell.  If your human does nothing all day, s/he will be like an inefficient incandescent lightbulb on for a full 24 hours.  Maybe that seems low but electricity is relatively cheap these days.  To use another classic physics experiment, 1700kcal=7000kJ=a lot of ice turned into steam.
No wonder my father always made me turn the light off in the bathroom...

A bulb is exactly what I thought about. Temperature is inversely related to surface area. Body has much higher area than a bulb, so will have much lower temperature given the same power dissipated, and it has to maintain 37C. And not all power consumed by body dissipates as heat. But that's just intuition, like I said. I didn't do the math.


text:
Agony, Hydrophobia and viruses in the light of evolutionary principles
I'm undergraduate physics student, but I've always been interested in biology. So I have a couple of questions about an application of the evolutionary principles to practice.

Agony as the last stage of dying.
Hydrophobia as symptom during Rabies.

Now I'm going to clarify what exactly I do not understand. In the first case it's not clear for me how this mechanism helps to survive, how it can help at all? In the second case it's not obvious why this virus causes such a symptom. As I think virus always create favorable environment for himselve (for reproduction). But how could water prevent it?

These might be better posed as separate questions.

I'm with Kevin. These seem like separate questions. To give you an idea of the first - Evolution via Natural Selection doesn't really 'care' how you die, as long as you've passed on your genes (reproduced) beforehand.

Agony is not always associated with the last stage of death, many pass peacefully - and the agony when it does occur is likely to be caused by the cause of death (ie a symptom) and possible exacerbated by the fact the person knows they are dying... And viruses/disease can have weird side effects on neural pathways which could be why we suffer from unusual neural episodes/behaviors

Maybe you mean fear of death?  I don't see that agony always accompanies death. Could you cite some reference or example?

Viruses and bacteria have a tendency to care mainly about eating and/or dividing. If the host dies, it's often a biproduct of toxin or foreign body accumulation. Agony in death, however, can be either physical or psychological and I'd count that as either too broad, or inaccurate (not everyone agonizes, as in painful symptoms). I wouldn't count the first question as having to do with biology/evolution.

The hydrophobia symptom is most likely a bi-product of the effects the virus has on the brain and not an evolutionarily derived strategy to create an appropriate environment to reproduce in. Just the same as other symptoms the infection causes, like fever for example, is a reaction the body has to the presence of the virus and not something the virus is doing on purpose to set up a better environment.
A bit old, but check out [1]: "Hydrophobia may represent an exaggerated respiratory tract irritant reflex with associated arousal potentiated by the selective destruction of brain stem inhibitory systmes."
So basically the virus is indirectly causing a fear of water. The destruction of brain cells and inflammation caused by the presence of the virus in the central nervous system cause a reflex in the respiratory tract which manifests as muscle spasms and renders the patient, who is already pretty out of it at this stage, unable and very unwilling to drink any fluids [2].
[1] http://europepmc.org/abstract/MED/982512 (Warrell DA, Transactions of the Royal Society of Tropical Medicine and Hygiene [1976, 70(3):188-195])
[2] http://publichealth.lacounty.gov/vet/rabiesmanual/clinical.htm

It's not actually a fear of water. It's that they have spasms on swallowing. Rabid animals will not swallow their saliva either. Hence the frothy mouth.

@anongoodnurse Because the brain prepares the body for swallowing before it occurs, thinking about swallowing may trigger the same reaction, which may appear as a conscious fear of water.

The fact that hydrophobia is a biproduct of the virus's effects on the brain doesn't necessarily mean that it is not evolutionarily selected for.  Rabies is transmitted via saliva in bites, so difficulty swallowing could very well have been selected for by evolutionary pressure (along with other behavioral effects such as increased aggression and hypersalivation).  In effect, the host's altered behavior can be considered part of the "extended phenotype" of the virus!

If your first question means: why is later-life ageing usually a long and painful process of degradation (rather than why do we have existential agony) with diseases of ageing like osteoporosis, heart disease, dementia - then I can offer one answer.
There is an absence (almost) of any selection pressure after reproductive age. Once individuals are past reproductive age, any such diseases, unless they place a great survival burden on the immediate (related) community/family, do not influence fitness of the population.
In other words, perhaps evolution has nothing to say about diseases of ageing, and no 'imperative' to purge our species of these afflictions.


text:
Why do hummingbirds build nests with live ferns instead of dead materials?
Hummingbirds prefer to build their nests with spore-bearing ferns, and mosses. This is helpful for the reproduction of the ferns, which are then better able to spread their seeds. But how is this beneficial for hummingbirds? Building in this manner is more difficult and energy-consuming.
Do live ferns make for better building materials? Is there a scent that these ferns are giving off to attract the hummingbirds? What kinds of research exist on this question?
References:
Carl Zimmer's National Geographic article, "A Living Nest?" (Feb 4, 2014) http://phenomena.nationalgeographic.com/2014/02/04/a-living-nest/
Question by Twitter-user Jessica: @LadyJaya

A wild guess: Where living ferns and mosses thrive it is a damp environment. In a damp environment, dead plant material would start rotting fast. Thus, using living plants guarantees a more durable nest.

From the article titled "Evidence of mutualistic synzoochory between cryptogams and hummingbirds", the specific advantage for the hummingbird is that it gets good nest building material through the selection of cryptograms. The cryptograms though have its seeds dispersed over large distances by birds which is a process called synzoochory.

Great answer / citation! I might rephrase as "the specific advantage given for the hummingbird is good nest building material" - it seems unlikely the authors would call it a mutualism unless they believed that there was a real benefit to both.

@Oreotrephes You are right.. I'll edit it.


text:
Why human cannot stand still in one place?
When a human stands in one place, he cannot stand still but we can see the body slightly swings.
Is this due to the Earth rotation or it has something with biology and muscles relaxations?
I have not been able to find a concrete documents on this thing.

Although at first sight this might seem to be biology rather than physics, maintenance of human posture is an example of control theory. Indeed a quick Google will find many publications on it - I found a good review here.
A standing human is a dynamical system that is not in equilibrium so it requires a (closed loop) feedback system to maintain it. This means sensors in your body detect deviations from your desired posture and muscles contract to return you to it. The problem is that there is a lower limit to the movements you can detect i.e. you body moves a certain distance before your muscles respond and move it back. The result is that even when we try to stand absolutely still we are actually continually moving then correcting that movement.
Some people are better at maintaining posture than others, so some people can stand stiller than others. Plus the ability declines with age, as I can testify from personal experience :-)


text:
Could an organism evolve to adaptively evolve?
Besides chance mutations sticking around because of their utility towards survival and procreation, could an organism evolve the ability to aid this process by mutating more frequently in beneficial directions in response to the environment (e.g. based on some form of past higher order evolutionary experience)?

cephalopods have some funky DNA editing mechanic that you should look into

Also look into humans! :) https://en.wikipedia.org/wiki/Somatic_hypermutation

You mean environmentally-responsive pre-programmed mutations, based on higher order experience? Like an animal in cold weather will tend to have more hairy babies than an animal in warm weather? AFAIK evolution conforms to higher order architectures which are only slightly tweaked in ways which are probably useful, like symmetrical limb lengths vary a lot more than non symmetrical chance mutations.

IMHO, the whole genome replication/recombination/mutation process and arrangement has evolved to increase the likelihood that changes will be beneficial or at least neutral.  In chromosome recombination, for example, new chromosome combinations are constructed from old, tested, gene sequences, while making sure that the new pieces are homologous to corresponding pieces in the parents' and grandparents' chromosomes.


text:
How to classify equilibrium points
I have the two differential equations:
$$\frac{dN_1}{dt} = N_1(2 - N_1 - 2N_2)$$
$$\frac{dN_2}{dt} = N_2(3 - N_2 - 3N_1).$$
I worked out the equilibrium points to be at $N_1 = 0, \frac{4}{5}$ and $N_2 = 0, \frac{3}{5}$. I then calculated all the Jacobi matrices and worked out the eigenvalues (and eigenvectors). I now have to classify these equilibria. How do I do that? Is there a set of rules I follow to classify them?
Also, the next part says:

Sketch the phase portrait of this system in the biologically sensible region: draw the the null- clines of the system and determine the crude directions of trajectories in parts of the phase plane cut by the null clines, designate the equilibria in the phase plane, and sketch a few typical trajectories.

I can do the null - clines and I think once I have found out the stability of the equilibria, I can determine the directions of trajectories of the bits cut by the null -cline, but how would I sketch the trajectories of the equilibria?

The fundamental question here is math, not biology, even though it may have been presented as a biological system. You may have better luck on math SE.

Classification of equilibrium points is done on the basis of the eigenvalues.

If the two eigenvalues have no real parts, it is a hyperbolic fixed point and represents undamped oscillation.
If both have a negative real part, it is a stable fixed point. If any of the eigenvalues has an imaginary part then it represents damped oscillations (in that case the equilibrium point is called a focus).
If one or both eigenvalue have a positive real part, it is an unstable fixed point.
If one eigenvalue has a positive real part and the other a negative real part, it is a saddle point.*

You sketch the trajectories of the equilibria by starting a tiny distance away from the point (where it is not in equilibrium) and trace the quiver plot. Drawing trajectories around unstable points is tricky and you have to plot the function in negative time i.e. instead of plotting f(x1,x2,t), you plot -f(x1,x2,t).  This page has representative trajectories for the different types of equilibrium points.  This page has a more thorough explanation, generalized to multiple dimensions.
*This classification appears to be slightly variable (more or less categories), on the basis of the two links I found.  I think the one I list is the simplest version, but any classification should suffice.  They are all based on the same principles. You can refer to some books on non-linear dynamics:

Nonlinear Systems by Hassan Khalil
Nonlinear Dynamics and Chaos by Steven Strogatz

@WYSIWYG added the references and some additional information -  I would like to second the recommendation for Strogatz's book.

yeah.. its such an easy and comfortable read..


text:
Why do cyanide and arsenic smell like almonds and garlic, respectively?
Why do humans smell arsenic as garlic or cyanide as almonds? Do both smells activate the same receptor? Is there any reason why our brain interprets these smells the same?

Why do you think almonds have a smell?

@jamesqf volatile organic compound

@murmansk: Do you really think the human nose is capable of detecting all volatile organic compounds?  Different people can smell different things.  For instance, my ex thought alyssum (the flower) had a wonderful fragrance, but I can barely detect a sort of grass-like smell.  Same with almonds: to me, they have no smell at all.  I've never tried cyanide, though.

This question already has been asked on https://chemistry.stackexchange.com/questions/80564/do-almonds-smell-like-they-do-because-of-cyanide

According to CDC.gov and Toxnet, bitter almonds contain cyanide, which, gives them the characteristic odor, but this can be also due to benzaldehyde (PubChem), which is, by the way, used as almond flavor for cooking (Wikipedia).
Garlic has its odor due to allyl methyl sulfide (Wikipedia) and not due to arsenic, which is not present in garlic in significant amounts. Arsenic as such does not have garlic odor and foods high in arsenic, such as rice, chicken, fish, beer and wine (Prevention) do not smell like garlic.
However, poisoning by toxins, such as arsenic, thallium, organophosphate pesticides, selenium and tellurium (FPNotebook, PubMed) is followed by addition of the methyl group (CH3) to them by normal intestinal bacteria, which gives them the garlic-like odor.
So, the connection between the garlic odor of garlic and arsenic (or other) poisoning is in the presence of methylated substances: allyl methyl sulfide in garlic, trimethylarsine in arsenic poisoning, dimethylselenide in selenium poisoning, etc (PubMed).


text:
Are there any exceptional cases in which a person with O negative blood group cannot donate?
Are there any exceptional cases in which a person with O negative blood group cannot donate or any case in which compatibility might not be established between O negative an any other blood group?

There are some situations, where, depending on the interpretation of Rh status, an exception could become possible. Rh +/- commonly refers to the D antigen. However, the Rh group has many antigens in it, including C and E. One can become sensitized to these other antigens and develop a hemolytic response to incompatible C or E type.
Dean L. Blood Groups and Red Cell Antigens [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2005. Chapter 7, The Rh blood group.

When the donor has some infections in the blood (HBsAg, HIV, HCV, VDRL etc positive)the blood cannot be donated. For otherwise normal donor, there is no such theoretical contraindication. However, it is always good to do a cross match test before blood transfusion, as there is always some possibility of cross reaction.


text:
For Penicillin Binding Proteins, why is the enzyme-peptide complex less stable than the enzyme-β-lactam complex?
I'm trying to figure this out. I cannot find any publications that go into good detail about the chemistry of PBP inhibition by β-lactam antibiotics.
PBPs cross-link adjacent pentapeptides to form peptidoglycan. My understanding is that, in most bacteria, this pentapeptide has a terminal D-Ala-D-Ala dipeptide. The enzyme removes the terminal D-Ala and forms a D-Ala-Enzyme complex, where the enzyme is linked to the rest of the peptide via ester bond to the D-Ala.
However, when PBPs bind to β-lactams, they also form a β-lactam-ester-enzyme complex. However, this complex is more stable so the β-lactam remains in the active site. Why?
Any good publications are also very welcome.
I would also like to ask, is there any reason the "β-lactamoyl-enzyme" complex can't be hydrolysed?

According to Foyes Principle of Medicinal Chemistry, the significant difference is the crowding of the active site by the cycle next to the lactam ring, which prevent attack on the ester and release of the drug from the PBP.

Reversing the reaction to the beta-lactam is unfavorable given the resulting ring strain.
I would personally expect the ester to be hydrolysable (water being much smaller), but not very rapidly given the active site somewhat shields the complex from water. Foyes disagrees on that. ("Water is also an insufficiently effective nucleophile and cannot hydrolyze the complex either.")


text:
What's the difference between proliferation and diffusion when talking about changes in tumor density?
Cell proliferation and cell diffusion seem to be important quantities to estimate when trying to understand or measure tumor growth, but I don't really understand a) the difference between them or b) their relationship to tumor growth.
Cell proliferation refers to cellular subdivision. This doesn't necessarily mean tumor growth because something can subdivide but still have the same net mass, right?
Cell diffusion on the other hand, refers to changes in cell density. Supposing cell proliferation is constant and we have positive diffusion, that would mean that cells are 'spreading out' (ie the mass is less dense but bigger). Is this correct? Would positive diffusion be equivalent to tumor growth?
This question came up when reading this paper. It talks about estimating diffusion and proliferation parameters in order to solve the reaction-diffusion equation which is, in turn, used to model tumor growth.

I would also like to see a reference to these terms if you have one.

A tumor by definition is an abnormal proliferation of cells but I don't think diffusion has anything to do with cells actually diffusing. Rather, the carrying capacity of a tumor depends on such parameters as nutrients or oxygen, which must diffuse further inwards until they cannot reach cells. Hence, the core of large solid tumors tends to be necrotic. It's also my understanding that there is a natural pressure that forces older cells inwards to the core of the tumor, as the outside layers continue to divide and grow outwards, increasing the diameter of the tumor.


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Are neurons roughly a magnetic dipole?
I would like to make a simulation (concerning genetic evolution) and I want to use a very simplistic model of neurons.
I don't really care there are different kinds of neurons, I don't care much that the extracellular field is different at axons-dendrites and initially, I don't even care that the spike is transferred through the axon. What I really want to know, is whether I can approximate (very roughly) the field with a magnetic dipole pointing at the direction of the axon. Or are the directions of the MF and the axon unrelated?
I have looked around for some image depicting such a relation, but I didn't find any. Is there any resource of some kind available?

Have a look at the cable model. It models neurons as electrical cables. Modelling them as dipoles would be super excessively simplistic and very far from reality. In fact, such a reduction would not even be useful in any context.

in my research, i am trying to see if magnetic fields have any effect in some aspects of the evolution of the brain. If i was to use the cable model to deduce the magnetic fields, i would have to use a "cylindrical" cable model in order to be precise at a fields level. That of course would be really expensive at a computational level especially for a genetic algorithm. I will though try to simulate a cylindrical cable model to see what comes out. thanks.

They surely are not magnetic dipoles, but they can be modelled as magnetic dipoles (more or less accurately). I believe your question would have been received even better (at least by me) if you had asked it this way: "How accurately can neurons be modelled as magnetic dipoles?" But maybe I'm just a penny pincher.

Yes, neurons can be modeled as magnetic dipoles.  In fact, that is the basis of MEG.  Here is an example of a paper that instantiates a computational model of magnetic dipoles in order to explain MEG data Neural mechanisms of transient neocortical beta rhythms: Converging evidence from humans, computational modeling, monkeys, and mice.

ok, so i see i have to use current dipoles instead on magnetic ones. After some thought i guess it makes more sense...


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What causes skewed ladder bands on an agarose gel?
I frequently ran into an issue where the bands of my ladder become skewed. What causes this?
Here's an example: 0.7% agarose gel, 100V, 60 minutes. Same problem occurs with 1%. I loaded 10 ul of a 20 ul PCR reaction.

As you can see, the problem is not smiling per se. The lanes themselves are fairly vertical and straight. Just the bands themselves appear warped. What could cause this issue?

The ladder and lane next to it look overloaded. Try to use less. Also, if possible, don't use the lanes on the sides of the gels, leave those empty if you can. Are you reusing the buffer? You might need to replace it more often.

0.2u Filter the solutions you use to make your gels, and don't overload the gel, this is overloaded.

@user137 Why do you recommend not using the side lanes?

@Chris It might just be coincidence, but it seems like I'm more likely to get a problem with the ladder if I put it in the side lines. Maybe it's just the electrodes in my gel box, or maybe it was a problem with my early gels before I knew not to overload the lanes, but I avoid the side lanes when possible and have had fewer issues.

I have never seen this problem when the gel box was ok. Boxes which caused multiple gels to run funny usually had problems with the wiring of the electrodes.

Can you please accept an answer which satisfatorily answer your question? This is a nice gesture towards the people who provide the answers. You still have a lot of open questions with proper answers. If the answer is not ok, use the comments or edit the question.


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What is the best file format to store gel images?
I store many gel images which are included in my Latex notebooks. The geldoc software normally produces TIFF files, however, Latex only accepts PNG or JPEG.
If I am going to store only a single copy of my DNA agarose gel images, which format is a good idea? PNG, or JPEG? Is there a good reason to keep one copy in TIFF and one copy in another format for every gel?

I asked this here because an answer would require understanding of what sorts of information is recorded when a gel photo is taken, and how valuable they are for research purposes. I'm open to the idea of migrating it elsewhere (for instance SuperUser) if that seems more appopriate.

JPEG is a lossy format. So save it as PNG. All these are raster graphics; all of them store images as pixels only. The differences lie in the compression methods and resolution.

BTW This question appears to be off-topic because it is about image formats which is not in the realm of this forum.

You have to convert it into a .png. This is accepted by PDFLaTeX and since it is also a loss-less format this shouldn't be a problem. As this is a LaTeX question, this is off-topic here, and should be asked at tex.stackexchange.com, which I can really recommend for all sorts of questions around LaTeX.

@Chris I think the major issue here is not TeX-specific, it is more about good practices for documentation of scientific data.

@MadScientist Agreed.

I agree with Mad Scientist response. More often than not the images I produce from microscopy or imaging are TIFF (my raw data files) and TIFF (the raw data) is more reliable for things such as pixel densitometry analysis (used for quantification analysis).

Always keep the raw data files! This is always a good idea for scientific data, and the only exception should be if the raw data is prohibitively large and it is not feasible to store it completely. This is not the case for gel images, so I would always keep the originals, and then use a cropped and edited copy in a suitable format for documents.
The original image has the full amount of data, any conversion can potentially destroy data. For example, some imaging systems produce images with more than 8 bit color depth. Converting to another format will in many cases reduce the color depth to 8 bit as many programs and some image formats like JPEG don't support higher color depths.
JPEG is lossy compression, I would always prefer PNG. You might have to use JPEG at some point because of the file size, but that should be at the latest point possible.

No reason to ever use jpg. PNG is also a compressed format.

But Jpeg can compress by an order of magnitude more, by the nature of its lossy compression. PNG will compress in a similar manner to ZIP and so the gains are fair less.

@terdon The lossless compression of PNGs still results in much larger images than JPEG. I personally use PNGs for almost everything, but there are situations where you need smaller files and where JPEG can be acceptable.

True. I'm just leery of JPG since they can easily get corrupted. Personally, I'd probably just convert the TIFFs to EPS and deal with those.


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What good is the MinION?
This year, Oxford Nanopore MinION has been shipped to some researchers for testing.
The advantage of a table-top sequencer for diagnostics and personalized medicine is obvious. Similarly, research "in the field" and forensic science could be aided greatly by this device. My question is about the applications in the research lab.
What does MinION do that a well-equipped lab with access to Sanger and next-gen sequencing cannot already do?
How well does the MinION work? How powerful is it?
What important scientific discoveries are being made using the MinION?
While the website of Oxford Nanopore has a list of publications, the most recent one is from 2013. This is before the early access program began - I am particularly interested in developments since February 2014.

I don't know a lot about it, but basically there is an electrically resistant membrane into which protein pores are inserted. An electric field is applied across the membrane which creates a current through the pore as ions flow through. As DNA passes through the pore, it blocks the flow of ions and thus reduces the current. Each base causes a characteristic current reduction. Its big advantage is that it is fast: it reduces amplification and assembly and can sequence something like 100 000 nts/s. However, it only has (last I heard) ~95% accuracy and so multiple passes are required.

This blog post may be useful https://biomickwatson.wordpress.com/2014/09/07/thoughts-on-oxford-nanopores-minion-mobile-dna-sequencer/

Also http://omicsomics.blogspot.co.uk/2014/09/oxford-takes-some-flak-fires-back.html?spref=tw


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What's the worst that can happen from too much sleep deprivation? Can you die?
It is well known that sleep deprivation causes considerable discomfort in humans (and has even used as a form of torture), but nevertheless there have been people who went through protracted sleep deprivation, apparently with no long term consequence.
I've noticed that sleep deprivation seems to trigger an intense sense of "this is bad for me" - yet given the apparent lack of ill effects (beyond the obvious) I cannot say whether this is merely anxiety over discomfort, as opposed to a genuine perception of physiological damage.
What if you were to go without sleep for as long as possible, despite the discomfort? Is it possible to commit suicide in this way (and what would be the cause of death)? Would you fail because you eventually ignore whatever stimulus was preventing sleep, and sleep anyway? Would artificially counteracting the temporary debilitating physiological effects (such as loss of body temperature) allow you to survive sleep deprivation of arbitrary length?

yes, you can die!

I heard something on the radio the other day that mentioned studies on rats that eventually died after sleep deprivation, but it took some effort to keep them awake that long, can't remember the reference. IACUC probably wouldn't approve it today.

@user137 There are in fact several such studies (for rats, they usually rotate them into shallow water which forces the rats to wake up and move). The first problem is that these are in rats (or rats, flies, etc) and I am asking about humans. The second problem is that I haven't been able to figure out how exactly it is that these rats die: Do they just drop dead, or do they fall into such deep sleep that they are unable to wake up even as they drown in the water?

I believe one of Michael Jackson's causes of death was lack of sleep - that's why his doctor was sedating him. Trouble was, anesthesia isn't the same as sleep. Sorry, don't have a ref ATM, which is why this is a comment

@Superbest the rats die from hypothermia. Sleep deprivation increases the organism's need for energy. At first, sleep deprived animals overeat, but at some time, they cannot compensate and die. After the metabolism has reached the point of no return, you can even let the rats sleep and they will die soon nevertheless. See the popular science book Sleep thieves for a nice summary of the studies.

The short answer is: Yes.
Fatal familial insomnia is a genetically passed down disease that at some random point in a carriers life will suddenly stop them from sleeping, ever, they die within 7 to 18 months
I know you did not ask about the disease, but it shows (even without illegal war tests) that it will kill you eventually, even in humans.
I believe in humans without the disease a complete lack of sleep may kill them within weeks, but who knows? maybe it was the drug.

Eventually your brain will start to break down and malfunction.

Chronic poor sleep puts us at increased risk for serious medical conditions, such as obesity, heart disease, and diabetes. During sleep, our bodies secrete hormones that help control appetite, metabolism, and glucose processing. Poor sleep can lead to an increase in the body's production of cortisol, also known as the stress hormone. In addition, skimping on sleep seems to throw other body hormones out of whack. Less insulin is released after you eat, and this along with the increased cortisol may lead to too much glucose in the bloodstream and thus an increased risk for type 2 diabetes.

At 24 Hours: Impaired Coordination, Memory, and Judgment
At 36 Hours: Physical Health Starts to Be Negatively Impacted
At 48 Hours: Microsleeps and Disorientation
At 72 Hours: Major Cognitive Deficits and Hallucinations
After even longer, your brain deteriorates and eventually you will die.


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Identify this vertebra
I was walking on the beach in New Jersey (U.S.), at about 40 degrees longitude, and found this bone. It's not a fish. The long process in the front is interesting. It is likely a C2 vertebra. I looked on the web, but could not find anything aquatic that it might match. Certainly not a dolphin. It is 2 inches long (50 mm), and 2.5 inches high and wide (64 mm). I guess it need not be aquatic, and New York City (20 miles North of here) used to dump garbage in the ocean. It looks old. Can you help me identify it?

Looks very much like an axis (C2) vertebra. The give away is the odontoid process (aka "dens") clearly visible on the bottom of each photo. Spinous process looks uniquely shaped (keel like) which might help your search. Size sounds too large for dog/cat, but who knows. Definitely not human.

www.boneid.net provides a great searchable database of identified bones

I found a picture with various cow vertebrae here: https://www.chichesterinc.com/Images2012/1172-40-V1-Lg.jpg Not sure your's is there.

Still disappointed that I can't figure out what this is. Is it pretty difficult to identify a single vertebra?

By the size you said and using the bonid site mentioned, it can looks also like a wild boar C2. But do you have wild boar in NJ?

Looks like Lumbar Vertebrae or Sacral Vertebrae of a Cow like @Brian Hanson Said above.
Studying closely in laboratory can elaborate more secrets about the bones.

This is not a lumbar or sacral vertebra. It doesn't even look like it's from a cow: http://www.boneid.net/product/lateral-view-cattle-c2-vertebrae/


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Could inhibition of progerin formation slow the rate at which a body ages?
According to wikipedia, progerin is activated in senescent cells. The protein itself is known to be the cause of a rare affliction 'progeria' - a disease marked by accelerated aging of the body. This disease is not accompanied by neurodegeneration.

Is progerin the key factor in the aging process?
If yes, could inhibition of progerin formation control the rate at which a body ages?

Progeria (and related) syndromes are essentially a collection of 'accelerated aging' phenotypes caused by single mutations; Progerin is a shortened version of the protein Lamin A, and is therefore not found in individuals without a loss-of-function mutation in the LMNA gene (the wiki page you reference). As far as we are aware these genes do not 'cause' aging in individuals without the mutations.
LMNA is a normal component of the nuclear lamina (a structure inherent to the nucleus). This review discusses the various diseases associated with mutations in this gene, some of which present 'accelerated aging' phenotypes. However, as far as I know, there is limited evidence to suggest that LMNA, or indeed any Lamina associated protein, is involved in 'normal aging'. A recent GWAS meta-analysis found a variant in LMNA that is associated with longevity in humans, however the association is relatively weak (OR=1.18, P=7(x10)-4), so even if this is a true association, it seems that (as usual in aging research) there are many other factors to consider, and it is not a single gene that is doing the aging.
So to stress the point: progerin has no function in 'normal' human aging - it is a defective protein caused by a germline (or novel) mutation in the LMNA gene.  Accelerated aging is the symptom of this genetic disorder, and is not completely analogous to normal aging (as you point out, there is no cognitive decline that is associated with normal human aging).

Could the LMNA be a catalyst, or a key element in the pathway though?

A catalyst to what, and what pathway? If you mean aging, there is no 'aging pathway'

Also note that although the symptoms of progeria resemble aging it is not true that aging results in the same cellular problems (for a start, progerin is not physiologically produced in old age)


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Where do kombucha SCOBYs get nitrogen?
Kombucha can be brewed even with tiny amounts of inocculate, such as the little bit of sediment at the bottom of store-bought kombuchas. Over 1-2 weeks, this can grow into an inch thick film covering the entire surface of the brew; a very striking accumulation of biomass. Where is the material for this biomass coming from?
It seems like most recipes for kombucha brew consist of:

5.7% sugar
0.7% black tea
10-30% of a previous, "finished" kombucha
SCOBY (optional, the kombucha in the previous step is sufficient)

I can see how the sugar provides carbon, oxygen, hydrogen and energy. Of course, merely providing the elements is not necessarily sufficient, since often enough cells require specific compounds as well. But I'll assume the SCOBY community, in aggregate, is able to transform the sugar into every CHO compound it needs. However, what about nitrogen? The amount of tea seems minute, and tea seems like not a very rich source of protein/amino acids. Sugar doesn't contain nitrogen, and while dead SCOBY constituents from the initial kombucha can conceivably be cannibalized, the cannibalism cannot account for dramatic increase of SCOBY biomass because of conservation of mass.

Short answer:
Nitrogen fixation (i.e, atmospheric nitrogen)
Longer answer:
Nitrogen fixation is the process by which atmospheric nitrogen is converted to forms usable by further biochemical reactions. Some bacteria are capable of nitrogen fixation (and some plants have symbiotic relationships with nitrogen-fixing bacteria); all the others rely on those species directly or indirectly to provide nitrogen.
The microorganisms involve in brewing kombucha tea are actually a collection of different species of bacteria and yeast. The bacteria that are found in kombucha tea include Acetobacter nitrogenifigens and Gluconacetobacter kombuchae, both of which are capable of nitrogen-fixation (and there may be others).
Molasses is also often used as the sugar source for kombucha, and molasses includes some nitrogen-containing compounds.
See the following review for more information:
Jayabalan, R., Malbaša, R. V., Lončar, E. S., Vitas, J. S., & Sathishkumar, M. (2014). A review on kombucha tea—microbiology, composition, fermentation, beneficial effects, toxicity, and tea fungus. Comprehensive Reviews in Food Science and Food Safety, 13(4), 538-550.

I hadn't considered nitrogen from the air, wow!


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What is the practical difference between SC, SD and CSM?
Is there some logic to how SC, SD and CSM yeast dropout media differ from each other? I have encountered these three formulations in Sunrise Science Products' catalog, and it appears that the composition differs quite a bit, but I couldn't find any information on what the purpose of these media is.
Obviously, any nutrients that are "dropped out" (e.g. -Ura) will select yeast cells on the basis of that marker. However, what about SD-Ura, SC-Ura and CSM-Ura?

sunrisescience.com/yeast-media-faq. I assume these simply may have arisen from different labs coming up with different chemically defined medias before these were commercially available (perhaps see refs on sunrise link)


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How does electroporation mediated recombination work?
For yeast and other organisms, DNA can be readily taken up into the cell naturally or through membrane disruption. What does applying a voltage to cells do exactly that allows more recombination to occur?

Electroporation is a fairly common way to introduce exogenous nucleic acids into cells. Its name essentially describes the process - an electric voltage potential is applied across a biological membrane, eventually leading to the production of conducting hydrophilic pores. The image below is from the Wikipedia page linked above, showing non-conducting (upper) hydrophobic and conducting (lower) hydrophilic pores. Depending on the voltage, membrane composition, and other factors, these pores can eventually "heal" and close back up, or join together and lead to the rupture of the cell.

Electroporation is used in the lab as a method of transfecting or transporting nucleic acids (usually DNA) into cells, to make them express genes they otherwise wouldn't, or to otherwise alter the genetic machinery. The transfected DNA can either remain in its own structure (such as a plasmid), or be incorporated (recombined) into the host genome, similar to what happens during a retrovirus infection. Whether or not this happens is dependent on the structure and sequence of the construct being introduced, not the method of introduction.
So, in reference to your question, electroporation doesn't do anything that directly allows more recombination to occur - all it is is a method of transportation. However, electroporation may allow for certain constructs to be introduced into the host more efficiently, or for a larger quantity of them to be introduced, leading to a greater transformation efficiency. Some cells, especially primary cells like neurons, for example, may only be transfected with any sort of efficiency with electroporation. However, electroporation can also have its down sides, as it can be rather stressful to the cells, and if the voltages and timing aren't properly adjusted can lead to high levels of cell death.


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Why do humans retain two kidneys?
If one kidney can function just as well as two, why do humans have two kidneys? The cost of growing two kidneys must surely be quite high, especially since one kidney is all that is really needed.

Perhaps because humans are pretty much bilaterally symmetric, and have two of almost everything: arms, legs, eyes, lungs... even two brain lobes.  A better question might be why we don't have two hearts or livers...

All vertebrates have two kidneys. There's no selection pressure to reduce to one.

@james the answer to that is kinda cool you might want to ask it, it has to do with the fact the ancestral circulatory system is not paired but one way with a single central vessel going in each direction, and the heart evolved from a portion of the vessel. the liver as part of the digestive system has a similar reason.

One of the easiest answers to the question; "Why do we have ____?" is "Because our ancestors did". This is not trivial or flippant, as it is a significantly important answer that is so often overlooked. Humans are members of Bilataria; a deep branch of the animal tree that is characterized by bilateral symmetry. Humans are typical of other vertebrates in having two kidneys. Selective pressure to reduce to one of two organs is typical in snakes, whose body form favors reduction. But even snakes have two kidneys. Natural selection does not reduce features we don't need unless such a reduction would increase fitness.

So are you saying it would cost more energy-wise to evolve to one kidney and possibly restructure the body than it would save to only have to grow and maintain one?

Its about dying before you can produce all the offspring possible. So if the second kidney does not kill you, there would be no need to optimize the numbers. How would a single kidney result in more offspring? "Energy savings" would be pretty slim.

And having a second kidney is at least useful at the margins.


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Does all of life on Earth use the same DNA compounds for all species?
If an organism on Earth has got DNA, would it always have C,T,G,A?

I have left school 16 years ago and this question is not homework related. I had no idea how to approach googling this question. I like SE a lot and the answer I got here is great.

If an organism on Earth has got DNA, would it always have C,T,G,A?

Yes! All three domains of life (Archaea, Bacteria and Eukaryota) as well as all DNA viruses use these four same nucleotides.
Genetic code variations
There are however slight variations in the genetic code. In other words, there are variation in the meaning of a sequence of nucleotides and the corresponding protein sequence. See Alternative_genetic_codes.
RNA based life
There are also viruses (which you may and may not want to consider alive) that use RNA (and hence U instead of T) instead of DNA. See RNA virus.

Yes, there are no variations on this. There are 3 domains of life; Archaea, Bacteria and Eukaryota. All use these identical nucleotides. All use all four of them, and this is one of many lines of evidence for the single origin of life on Earth.

No, you can check out non-canonical bases on Wikipedia. I believe that most organisms, including E. coli and Homo sapiens have base modifications. In E. coli, the base modifications help them identify phage DNA and destroy it using restriction enzymes. In humans, many base modifications exist. A prominent modification, methylcytosine, can influence the state of chromatin and hence the expression of genes. Wikipedia mentions more obscure cases, e.g. a phage that has 2,6-diaminopurines instead of adenines.
I think that one should clarify the nomenclature in each context. I would envisage two cases:

a simplified case where base modifications are not considered, here methylcytosine = cytosine, methyladenine = adenine
a stricter case where modifications are considered, here methylC does not equal cytosine

Our simplified view of the reality of nucleotidic bases can be justified and explained by the limitations of current sequencing methods. It is impossible, as far as I know, for Illumina sequencers to differentiate modified from unmodified bases. Even sequencers like PacBio's Sequel or Oxford Nanopore's MinION that can detect modified bases can do so only at very high coverages and with some errors.

Methylation does not make nucleotides not "ACTG". I don't believe that was the question. AGCTs are in everything.

@KarlKjer, well I don't know the exact definition of 'ACTG'. That's a bit vague and it would be clearer to say 'adenine, cytosine, guanine, thymine' bases.