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x-linked recessive inheritance and correlation for males
I was inspired by a discussion in this thread. Wikipedia lists a number of disorders linked to recessive genes on the x-chromosome. One typical example is red-green color blindness. Now wikipedia says that up to ten percent of men and up to one percent of women suffer from red-green color blindness. This is due to the fact that the recessive gene for red-green color-blindness sits on the x-chromosome and men have only one copy of this chromosome while women have two.
Now if you take a random male that suffers from red-green color blindness there is a ten percent chance that his father also has red-green color blindness. There is also a ten percent chance that his mother has red-green colorblindness. She must have one copy for red-green color blindness, and if so there is a ten percent chance that she is homozygote and thus suffers from color blindness herself.
So if you did not know the gene causing red-green color blindness and investigated, say 1000 red-green color blind males you will find no correlation between their color blindness and the sex of a parent that also have color blindness.
If you do it the other way around you will of course find that 100 percent of the sons of color blind women be color blind, there is total correlation. So you get very different results depending on the way you set up your investigation.
Now there are also polygenetic traits such as length or intelligence that might be affected by recessive genes on the x-chromosome. The y-chromosome is much shorter than the x-chromosome and contains fewer genes than the x-chromosomes so you would naively expect that somewhat more of the variance in polygenetic traits in male are due to genes inherited from their mother than from their father.
Now if you set up a large scale investigation trying to find out how much of the variation in a polygenic trait in a male that is due to genes from his father and from his mother will the contribution from x-linked recessive genes be accurately determined?
If a man has an x-linked recessive gene making him, say, one centimeter taller than if he had another gene variant, there is equal likelyhood that his father and his mother is affected by this gene perhaps making the correlation "invisible"?
If a man does not have a recessive x-linked gene there is zero likelihood that his mother is affected by this gene but his father could still be affected by that gene.
Question:
1. How does the fact that some of the x-linked genes contributing to a polygenic trait are recessive influence large scale investigations based on correlations trying to determine how much of the variation in a polygenic trait in a male that is due to genes inherited from his mother?

Now if you take a random male that suffers from red-green color blindness there is a ten percent chance that his father also has red-green color blindness. [..] She must have one copy for red-green color blindness, and if so there is a ten percent chance that she is homozygote and thus suffers from color blindness herself Can you please somehow justify this claim?

you will of course find that 100 percent of the sons of color blind women be color blind Can you please justify this claim?

If a certain percent of all x-chromosomes in a population contains a certain recessive gene a women must be homozygotic in that gene in order for the gene to be expressed in her. If the women is homozygotic, her son must inherit one copy of that gene and as he receives no copy from his father that gene must be expressed.

@Remi.b It is just conditional probabilities: if the frequency of the recessive X allele is p=0.1, and the son is colorblind, it means his mother definitely has one recessive X allele. The probability that her other X allele is also recessive is then p=0.1. Similarity, the father has only one X allele, which is recessive with provability p=0.1. If a woman is colorblind, her both X alleles are recessive, and her sons will inherit a recessive allele with 100% probability. The described experiment design of simply sampling from population is however flawed.

@Agerhell your argument holds only if fir every child you consider only one parent. Once both parents (or more complicated genealogies) are included, the things become less ambiguous.

@Remi.b If there is a ten percent chance that a random x-chromosome codes for colorblindedness and you know that the mother must carry one of those for her son to be colorblind. Then there is a ten percent chance that her other X-chromosome codes for color blindedness which would make her colorblind. If both her x-chromosomes codes for color blindedness her son must inherit one of them.

I see several separate questions here, please narrow it down to a single discreet question. Honestly most of your questions don't require any of the lead up.

The correlations you are looking are all based on some unusual and arbitrary subset of the data. The one type of correlation that people generally look at is the one that we call heritability.
For a detailed definition of the term heritability, please have a look at this post. In short, heritability (in the narrow sense; again see above link) is the fraction of the overall phenotypic variance (for a specific trait) that is caused by additive genetic variance.


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What makes iodine an effective antiseptic?
I'm thinking about tincture of iodine, potassium iodide (Lugol's), and povidone-iodine (PVP-I) specifically, which, as is my understanding, work by solubilizing elemental iodine in an aqueous solution. These solutions slowly release free iodine, and it is ultimately the free iodine that does the biochemical damage that kills microorganisms.
But how, specifically, does free iodine cause this damage? The Wikipedia page on povidone-iodine says that free iodine:

kills eukaryotic or prokaryotic cells through iodination of lipids and oxidation of cytoplasmic and membrane compounds.

and that:

Slow release of iodine from the PVP-I complex in solution minimizes iodine toxicity towards mammalian cells.

I understand that elemental iodine strips electrons from all kinds of stuff because it is such a strong oxidizing agent, being so close to neutral valency, and obviously that's bad for important macromolecules, but I guess I'm looking for a bit more detail on how it works (or doesn't work) in other respects, with answers to questions such as:

Why does iodination of lipids cause the lipid membrane to fail?
Why does "slow release" make a difference for mammalian cells - are eukaryotic cells somehow better able to handle the damage caused by low concentrations of free iodine than prokaryotic cells?
What makes bacterial spores and protozoan parasites such as Giardia resistant to iodine's antiseptic properties?

Sorry that that's more than one question. But if anyone is able to elaborate on any of these concepts, I'd greatly appreciate it!

Welcome to Biology.SE! This seems like an interesting series of questions, but please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. ——— In particular, please separate your questions — each post should be focused on one question. This helps you get answers to all of your questions and makes those answers more accessible to searching by other users. (You can provide links to the related questions in your text.) Thanks!

The most recent review I could find on this subject was from 1999 — maybe you can use that as a starting point to find out more ...

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How to preserve leaves between sampling (collection) and analysis?
Suppose I spend a day in a forest, collecting different kinds of leaves, which I would like to analyze under a compound microscope. Now, obviously, measures should be taken to preserve the leaves some how. What would be the appropriate procedure? It seems (based on browsing the web..) that refrigeration could be one option. Is it scientific (used in published papers)?

What is the aim of the analysis and what type of traits/features do you want to study?

You may want to see:
Mark W. Chase, Harold H. Hills; Taxon, Vol. 40, No. 2,  1991, pp. 215-220: 'Silica Gel: An Ideal Material for Field Preservation of Leaf Samples for DNA Studies'
Summarized, the process would be the following:

Place the leaves inside ziplock plastic bags;
Add ten times (minium) the weight of the leaves in silica gel;
After 12 hours (after which the degradation of the biological material is more likely), check the leaves by bending them: if they break cleanly, the leaf is dry;
Store in the ziplock bag, inside a box with an hermetic lid;
Refrigerate (if possible).

Note: Freezing by submersion in liquid nitrogen is also a viable approach, yet might be less practical

I was thinking about the same thing with regard to DNA (have used it myself previously), but it sounds like the poster wants to analyse morphology.

This method (although I haven't ever used it, or seen it in use) seems to preserve the shape and physical features of the leaf, essentially "freezing" the leaf. In fact, a quick search for images will show that the biological material is kept more or less intact.

Placing the leaves in wax paper and under the pressure of several books would be beneficial (in terms of a short term preservation).
This method may not be suitable for field preservation, due to the bulky nature of books and other weights, although it might be suitable if using an alternate method of pressure.

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Clumping factor test
I'm come across this question and I'm somewhat confused:
In the test for staphylococci, the clumping factor detects:

staphylothrombin
DNase
mannitol fermentation
Fimbriae
fibrinogen-binding protein

I know that bound coagulase can convert prothrombin into staphylothrombin and eventually fibrinogen into fibrin.
I'm thinking it's staphylothrombin, but when it says ''detects'' does it mean that the test concludes whether staphylothrombin is produced or does it mean that the clumping factor actually ''detects'' a substance?

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Challenges of Industrial-Scale Fermentation
I was reading the wikipedia article on industrial fermentation, and it mentions that

It is well established in the field of industrial microbiology that what works well at the laboratory scale may work poorly or not at all when first attempted at large scale.

Why is that?  What are the barriers to large-scale fermentation of bacterial culture?
Also, I know that cell cultures have distinct phases of growth and decay, but what happens after the cells die?  Would an industrial fermentation process have to "re-culture" the bacteria?


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Protein Design - Target Structure Specification
I'm curious about how protein structures are defined in general, but in particular, I'm wondering how a target structure can be specified without knowing the amino acid sequence.
For example, in protein design (or from what I gather on the wikipedia page http://en.wikipedia.org/wiki/Protein_designs), scientists design a 3D structure that will perform a particular function.  They then try to come up with an amino acid sequence that will fold properly into that structure.
How can a 3D structure be defined if no amino acid sequence (and hence no molecular geometry) has been determined?

You don't create some structure and then try to find the amino acids that will create it; the residues themselves are important. Generally modelling is based on known motifs. The basic steps are: model in silico, test in vitro, fail, repeat.

Hmm, how is de novo protein design done?  From the article: "In de novo design the entire sequence is designed anew, based on no previous sequence"

Right, the sequence is designed anew. I also said generally.

I think that's what I was going for in my question - how can a sequence be designed anew?  I understand the idea of protein prediction - design an amino acid sequence, try to predict how it folds. But protein design is the reverse. Am I misunderstanding the meaning of "target structure"?

Afaik. they use quantum-mechanical models to calculate the active site and probably the whole enzyme structure. Enzyme designing is a very new topic and you'll need a lot of math to understand it.


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Blood Type/Punnett Square
Male: Blood type O   (Genotype written as: i^o i^o since O allele is recessive to the A and B alleles).
Female: Blood type AB
Draw a punnett square to show all of the possible offspring.
I got Ai^o,  Ai^o,  Bi^o,  Bi^o)
What are the possible phenotypes for the children?
I got...
Phenotypes: Blood type A
            Blood type B

What exactly is the question here? Do you want someone to clarify the answers you got?

yes please @iro

as far as simple punnet square is concerned your answer is correct.

A noble answer +1


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Are brown eyes healthier than blue eyes?
I have read somewhere brown eyes have more melanin than blue eyes and as melanin protects our body from cancers, I thought that brown eyes are more healthier.

Where did you read this?

I am voting to close until more information has been given on the source of the claim. It is for the moment hard to tackle the truth value of a claim we don't know the origin of.

Might be that melanin in our irises protects our pupils' dilator muscles but not much more.

People conflate "Dominant" traits to mean "healthier" which is a huge misconception. The previous answer provided a good example of how what is adaptive in one environment can be Mal-adaptive in another. Many Disorders can be dominant for example Huntingtons disease or achondriplastic dwarfism.

You're right to draw this distinction. However, polygeny and pleiotropy allow evolution to render many deleterious alleles recessive, and still-dominant examples (including HD) usually affect the individual late in life, resulting in little effect on fitness.

true: gene expression is often more like volume nobs than On/Off switches

Not an answer (I hope an expert provides one), but too long for a comment.
Although I'm unfamiliar with this claim, it's conceivable the optimum melanin content in eyes is subject to a trade-off as it is in skin. In bright areas, skin is dark to prevent damage from ultraviolet light; in dim areas, skin is light to produce enough vitamin D to avoid rickets. Eyes are different in their details, but they too may have adaptive geographical variations (or the distribution of light irises may be due to something more mundane, such as genetic bottlenecks). In theory their optimum colour would trade visual acuity against retinal protection, though I'm dubious about that as light enters through the pupil, not the iris.

@JG I agree with your point regarding adaptive geographical variations. Is there any place wherewe can discuss this more?

@AScientist I have no ideas about it besides those I wrote.

Well,That's a bummer.Do you know anyone who knows this stuff?


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Can humans derive any nutrition from eating the bones of animals?
Bones contain many nutrients like Calcium and phosphorus.
And I'd take a guess that some kind of bones like bones of a chicken(hollow) aren't dense enough to be much of a  problem during digestion.
So,is there any benefit in eating for example say chicken bones?

Just the actual bone, or the marrow as well?

The actual bone.I know we derive nutrition by eating the marrow.

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Why do scabs itch?
I have noticed that scabs formed over wounds itch a lot.
And if the scab comes off then the skin rarely completely heals and a scar is left.
Assuming scabs are important for the healing of skin ,shouldn't the scabs not itch?
Since they itch,we sometimes scratch them off which is detrimental to skin health and also can lead to infections.
If they wouldn't have itched, most people wouldn't scratch them off thus ensuring better health for the organism.

Part of this is due to the immune response to such an injury, which causes some amount of inflammation leading to histamine release - the introduction of this paper has a nice overview. In addition, mechanical stress on nearby nerves due to collagen fibers being reformed may increase the feeling of itch. The sensations of pain and itch are at least partially connected - there are pathways that are specific for each but also some that are shared. This is why pain can actually inhibit itch in some cases - like when you have a mosquito bite and slap it or apply a very hot wetted cloth to it.
This article gives a decent layman's overview of the connection between the two sensations. The sensation of itch still isn't fully understood, and there remains controversy as to how deeply it's actually tied to pain.

Shouldn't there be systems in place to damp this feeling cause it'd be beneficial to the organism if he doesn't scratch the scab?


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Why do mosquitoes hover over our heads?
So I play soccer in evening at a nearby park. I noticed many times that after the game and even during it many mosquitoes hover over some of us. They sort of form a structure like a tornado.
The more the one is sweaty, the more the mosquitoes.
What can  be the possible reason?

Maybe they swarm all around our bodies, but we only notice them near our heads because that's where our eyes and ears are.

mosquitoes are attracted to CO2, lactic acid, and the bacteria that live in sweat (old sweat) physically active human emit all three. It makes sense that blood seeking parasite would be attracted to smells indicating blood containing organisms.

In many mosquito species (and other diptera) males make swarm to attract the females. The vast majority of individuals in swarms are therefore males (but there are always a number of females in them as well).
These swarms are a type of lek mating which is also very common in midges (thanks to @arboviral for this info). Are you sure those you see are mosquitoes and not midges?
In order to produce these swarms, they typically hover a recognizable element in nature to swarm around, such as a small tree, a bush, a big stone, etc... On a soccer field, players are a distinct element to swarm over!
Of course, females are attracted to $CO_2$, warm bodies and odour of sweat but this is IMHO likely not an important factor causing the swarms you see. See @Kiny's answer on the subject.
References:

Takken et al. 2006
Yuval et al. 1994

Also, why is this in the evening?

Mosquitoes typically start mating at the beginning of the evening and then forage during the night. However, this varies quite a bit from species to species. Aedes egypti for example, forage day and night while species of the genus Culex forage only for a few hours after the sun has set.
Such variation in the timing of mating behaviour can lead to (pre-zygotic) reproductive isolation between lineages. Potential reasons for being active at specific times and not others include temperature management, easier to parasite for females during the night (only females bite), timing with flowers (as both males and females feed on nectar). I would not be able to argue for why a specific species shifted its circadian rhythm in a specific way though.

Also, why is this in the evening? Not in the morning or afternoon

@ASuckerinMaths Please see edit

Gah - beaten to it! For reference this is called lek mating. You most commonly see it with midges, rather than mosquitoes, though.

@arboviral Thank you! I edited the post to add the term lek mating.

I found an interesting paper about the subject that could contribute to answering your question.
There are volatile substances that we produce that help attracts and repels mosquitoes such a geranylaceton, octanal, nonanal, and decanal (Logan et al.)
The tests showed that those substances can both be used to attract and repel depending on their concentration with geranylaceton having a constant decrease in attraction.
Curious for more I have decided to look further into the subject and found another paper studying these components which states:

A blend formulated from the four aldehydes and combined with CO2-baited CDC trap without a light bulb doubled to tripled trap captures compared to control traps baited with CO2 alone. David P. et al.

Those four aldehydes referring to heptanal, octanal, nonanal, and decanal. which suggests that their attractive effect is stronger joined than separated.
Therefore, besides the "CO2, lactic acid, and the bacteria that live in sweat" stated by John, the reproductive behaviour stated by Remi.b there is also other volatile substances that make our attraction to mosquitoes stronger(or weaker).
References:
1. James G. Logan, Michael A. Birkett, Suzanne J. Clark, Stephen Powers, Nicola J. Seal, Lester J. Wadhams, A. Jennifer Mordue (Luntz), John A. Pickett. Identification of Human-Derived Volatile Chemicals that Interfere with Attraction of Aedes aegypti Mosquitoes.
2. Tchouassi DP1, Sang R, Sole CL, Bastos AD, Teal PE, Borgemeister C, Torto B. Common host-derived chemicals increase catches of disease-transmitting mosquitoes and can improve early warning systems for Rift Valley fever virus

Oh! Your right! thanks for pointing it out. Indeed after rereading it and without the acess to the paper my post makes little sense. I'll correct this right away.

Again, welcome to Bio and +1 for a well-sourced answer

Kiny, when you write to another user, make sure to add the '@', so to reach Mesentery write ' @Mesentery bladibla ' [I don't recommend adding the bladibla though ;-)

@AliceD Oh! sorry! This is the first time I am partecipating in this sort of websites and as such I have no knowledge of how to properly go about doing things.

@Kiny stop saying sorry! We're here to help

@AliceD Understood xD I'll try to stop. I apreciate the help. It is a pleasure to meet you.

@kiny Thx for the info. By the way, are these substances excreted out of skin?

@ASuckerinMaths Yes, all of those substances where identedied by studying the air around humans (in the first paper, specifically the hands).

"James G" is actually James Logan; it looks like something's happened to the formatting of the author list.

@arboviral did that fix it? Thanks for pointing out a issue. If you see another please let me know.

Partly - I've done the rest and added links to the papers. Thanks!


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chaperone protein names
I am studying chaperon proteins DnaK, DnaJ etc. This question sounds trivial but I would like to know what the acronym stands for. I have looked on google/google scholar. My best guess is that the name comes from the fact that these are genes whose products are necessary for bacteriophage DNA replication. Can this be confirmed? The full name of GroES and GroEL may also be helpful. Thanks!


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What are the disadvantages of myelin
The myelination of axons has plenty of advantages. It increases signal speed in axons, and thereby reduces reaction times. This is, of course, very good for the survival of the animal in question.
Most invertebrates do not have such a myelin coating. I know, that evolution does not just evolve features, because they are useful, but it seems to me, that invertebrates are entirely outclassed by vertebrates, because of how important reaction times are to an animals survival. So if such a trait is not impossible to evolve, it would most likely have evolved multiple times in different animals. If it was as advantagious as I imagine, invertebrates without myelin would have been outcompeted by now.
So there must be a significant disadvantage to having myelin coating.
Can you explain to me, what that is exactly?
Is it just the associated energy cost?

When you say "outclassed", I hope you realize the most numerous and diverse members of the animal kingdom are insects. And please think about your assumption that reaction time only depends on myelination... I think we could agree that flies or mosquitos have faster reaction times than your average mammal due to the architecture of their muscles and cuticular exoskeleton. The efficacy with which they respond with movement is very much quicker than the tugging of a bone by a partially contracting muscle pulling a tendon.

Apologies for the late reply, I kind of forgot about my question. I know, that insects are the most numerous. But at their size, intelligence is not as important as it is for bigger creatures, because of the limited number of neurons.

I kind of forgot, that insects have increadible reaction times :) Thank you for pointing that out :)

Many invertebrates possess myelin. It is a misconception that invertebrates lack myelin.
The world speed record for a traveling bioelectric signal is held by the myelinated axons in the abdomen of the Penaeus shrimp!
Please take a look at this website or this review to find a highly recommended comprehensive website about invertebrate myelin from about a decade ago. Here you will find a list of references and additional readings if you are so inclined.
As an additional note: invertebrates also possess and very often make use of ensheathing glial cells, such as is the case with sensory neurons in lepidopterans (moths and butterflies) as depicted below. I've labeled the sheathing cells in pink and red. Please understand that it is currently still unclear whether these cells secrete myelin, though they are thought in some way to insulate the neuron. What you are looking at is a hair-shaped sensillum that is innervated by one or several sensory neurons; these are the basic functional units for sensing movement, proprioception, smell and taste and they exist across all invertebrates, often lining the cuticle and across the entire body, e.g. on legs, on the antennae, in genital tracts, etc. They are best studied in hexapod insects.

Thank you very much for the detailed answer (and apologies for the late reply...) I am a complete novice, when it comes to biology, so I have to admit, that I don't fully understand your answer, but I will read through the linked sources more thoroughly, and then post follow up questions, if necessary. Thank you very much for your time :)

Quick follow up question: In what way are intelligence of an animal and signal speed (and myelination) related. If you were to create a mouse with much less myelin in the brain, would it be less intelligent, or would only things like reaction speed decrease? Likewise, could we increase the intelligence of some invertebrates like octopuses by increasing the myelination in their brain?

I think intelligence and myelination are not directly linked. Intelligence is a very complex (multifaceted) word that is typically poorly defined. In evolutionary biology, it typically means the ability to respond to entirely novel problems with a pre-existing machinery; it has little to do with the speed of transmission or speed of thinking. Sloths have myelin too! Maybe you are asking what the effects of hypo- and hyper-myelination would be. Take a look here, it may be of help.

thank you very much :) My idea was, that the brain of the octopus is specialized to achieve high reaction speeds etc despite the lack of myelin. Could it have more neurons, to achieve higher intelligence, because the size of the neurons could be reduced? Also, what are your thoughts on this paper: https://www.sciencedirect.com/science/article/abs/pii/0191886994900493


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lifespan of Nautilus compared to other cephalopods
Most cephalopods live uncharacteristically short lifes compared to other creatures of their size and intelligence. The octopuses with the longest lifespan for example, the giant pacific octopus, only live for up to 5 years.
This is quite long for cephalopods already, as some of them only live for as little as half a year.
The reason for this short lifespan is not aging itself (meaning loss of information in the epigenome and similar effects), but their reproduction. The maturation of their reproductive organs results in the deactivation of their degestive glands, so they basically starve themselves to death.
When the reproductive glands of an octopus are removed, their lifespan increases greatly.
Nautilus are an exception to this low lifespan of cephalopods. They live to be over 20 years old.
Why do nautilus live so long and is it possible to grow other cephalopods with similar lifespans by introducing nautilus genes?

Queen conch can grow to be over a foot long and can live for as long as 30 years. some species have been known to live to 40 or more. It's difficult to see if the nautilus has average or max lifespan of 20 years.

On a basic level, the difference in lifespan is due to the fact that the nautilus has a vastly different reproduction strategy from other living cephalopods.  While most other cephalopods exhibit a rather extreme form of r-Strategy reproduction, the nautilus is, relatively speaking, a K-Strategist.  To explain, r-Strategy is when a species produces many offspring, but puts relatively little investment into each one under the expectation that most will die.  K-Strategy, on the other hand, produces relatively few offspring, but put much greater investment into each one.
As you stated, in most cephalopods, sexual maturity triggers a shutdown of the digestive tract, as they put all their energy into reproduction, during which one spawning episode will result in hundreds or thousands of eggs.  After fertilizing the eggs for males, and for females after laying those eggs (allowing for a delay of a relatively short incubation period in some species, including most or all varieties of octopus), the adults die, having produced enough young to guarantee the next generation.  This lifestyle of a single massive reproduction event before dying is called semelparity.
However, with nautiluses, each mating results in only about a dozen eggs.  These eggs are much larger than the eggs of any other cephalopod, have a considerably longer incubation perios, and by extension, the hatchlings start out larger and better-developed.  However, technically, nautiluses aren't true K-Strategists, like humans or whales, which have only one offspring at a time and put a massive amount of investment into that offspring.  Instead, they are more like cats or dogs, Median Strategists, who fall somewhere between the extremes.  While for r-Strategists like other cephalopods, semelparity can produce enough young to ensure the survival of the species, this is not the case for Median or K-Strategists.  Instead, they must reproduce multiple times over the course of their life, a strategy called iteroparity.
While in all cephalopods, the gonads are destroyed by the process of reproduction, in nautilus females, the gonads regenerate after spawning, allowing them to mate again the next year.
It should also be noted that despite this, the nautilus spends a relatively small portion of its life sexually mature.  It takes roughly fifteen years for a nautilus to reach breeding age.
While my knowledge of genetic engineering is pretty much limited to what appears in the news, based on this information, it seems like to lengthen the lifespan of other cephalopods to be on par with that of a nautilus, you'd have to completely change the way they reproduce and the rate at which they mature, which I tend to suspect is beyond our current abilities.


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How can humans taste saltiness in an aqueous solution of salt (saltwater) if the anions and cations in the salt are dissociated in the solution?
This may sound like a dumb question, but I've always wondered why we can still taste saltiness in a dissolved mixture of saltwater. In an undersaturated, aqueous mixture of salt and water, the salt ions are completely dissociated from each other, meaning that the salt is dismantled into its constituent parts. If this is the case, then why do we taste saltiness when drinking saltwater and not taste the individual tastes of the constituent cations and anions? Why do we taste NaCl instead of Na AND Cl individually?

Why do you think you are tasting the NaCl combined rather than either Na+ or Cl- separately?

And in what context do you think your mouth would ever be exposed to solid NaCl?

Note that there other things besides NaCl that taste salty, like potassium & lithium chlorides.  Also, at least as far as I understand the mechanism of taste (but I am not an expert), things have to be dissolved in water (saliva) for the receptors in the taste buds to work.


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Why bovine serum albumin is used in mass-spectroscopy and how to interpret such data?
In the paper Network organization of the huntingtin proteomic interactome in mammalian brain, there is a description of a mass spectroscopy experiment where Bovine Serum Albumin (BSA) is added to a sample lysate and the same lysate without BSA was used as the control. I have a working knowledge of how mass spectroscopy works but I could not understand why BSA is used in this experiment. Can anyone help me?
This is probably a very trivial question. Excuse my ignorance, I am not a biology major. I tried google search to get an explanation for this but I didn't find anything satisfactory.

Their LC-MS-MS data was only semi-quantitative as gathered, meaning they could compare relative levels of one protein to another in the same sample, but not necessarily between different samples with a high degree of confidence. So, they spiked known amounts of BSA, an extremely well-characterized protein frequently used in the lab, into their samples and created a standard curve across different concentrations that correlated pretty well with the input amounts. They could then use this curve to better quantify the other proteins in their samples among all the different sample types. This in turn allowed them to say with greater certainty that, for example, Protein X was expressed at three-fold higher levels in Sample A than in Sample B. Otherwise, they would only have been able to say that Sample A expression of Protein X was higher than Sample B.

Hi Matt, Thank you very much for the answer. Your explanation sounds reasonable to me. Thanks again!

@incrediblesulk You're welcome. BSA is an extremely common reagent in biochemistry/molecular biology/cell biology labs, as it's useful for all sorts of things, including as a standard in many concentration measurements.


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Are genetic crosses between asexual organisms possible?
To my knowledge (Please correct me if I am wrong), genetic basis is the key in defining species. When we encounter an unknown species, we can sequence it's genome and compare the genome with other known organisms from the genome data bank and see if there is a significant similarity. If no significance were found then we can call it a newly discovered organism. Also careful study of genetic crosses between species pairs and partially isolated sub species to identify general patterns in the genetics and origin of reproductive isolation helps to answer the question of speciation. Then how would we cross asexual organisms like many bacteria or protists? Is it possible to cross asexual organisms? If not, how do scientists study their genetics and define species of asexual organisms?

What do you mean by "genetic basis is the key in defining species"? If you are assuming that the "definition" of a species is related to the ability of individuals to produce fertile offspring then you need to learn more about 'species concepts'. You could start with this post. This post is also very relevant.

When it comes to viruses and bacteria, genetic cross is just as a vaguely defined concept as species. The latter is often defined on the percentage of the sequence similarity (for viruses) or the percentage of common genes (for bacteria).
If we speak about simply mixing genomes of different organisms, there are many possibilities, how this could happen. Just to give a couple of examples:

Some viruses integrate their genome into the host genome. In some cases these integrated genomes cease being functional viruses, and may evolve to be functional genes of the host. This is truly a genetic cross. See here, for example.
Bacteria and viruses routinely undergo horisontal gene transfer in which genes from one bacteria are integrated into the genome of the other one. A typical bacterial species has a few hundred core genes, and thousands of genes that are present only in some specimen or borrowed from other species, which significantly vary from one bacteria to another. Thus, every individual bacteria or bacterial community can be thought of as a genetic cross.

Thank you very much for the write up. I knew about the reverse transcription process (I leant about it while studying HIV) and also horizontal gene transfer. But never thought these concepts could be related to crossing in any manner. It seems to me defining a species that do not undergo sexual reproduction is even more difficult. Especially with polyploidy and multinuclear cases.


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How to do research in bioinformatics without wet lab experiments?
I graduated in physics from Bangladesh and keen to work in the field of biology. Like, systems biology, computational biology, bioinformatics or systems medicine. I have not produced any research work in such fields as of now. I am studying sequence alignment and RNAseq and later plan to study flow cytometry bioinformatics. I have no affiliation with any institute now in my country as they don't accept students from other disciplines. Is it possible for me to do research on my own by using databases available? If so, I would be really grateful if anyone can suggest how to approach my research topic/work.

Doing actually valuable bioinformatics research completely on your own after graduating from university (I am assuming that this corresponds to a master's degree) is somewhere between impossible and very unlikely - even for someone who actually studied bioinformatics.
In order to really do research (in almost any field) you will have to become a PhD student first - and for that studying the relevant topics on your own, like you are already doing, is probably the best preparation.
If there are truly no 'cross discipline' applications possible where you are from, you'll probably have to apply for programs or positions abroad. It is, however, becoming increasingly common for bioinformatic research groups to hire people from various different backgrounds - ranging from wet lab biology to physics. I would advise you to actively look for such interdisciplinary research groups (ideally purely computational groups as a physics background will be more valuable there than in a mixed dry/wet-lab group) and potentially directly contact the group leader if the university/institutes don't offer any programs that would allow you to apply.

Thank you very much Nicolai

It seems to me that all you really need to do bioinformatics research is a computer. Of course it would be easier with formal training, but I don’t see that it is impossible without it. Sincerely, a wet lab biologist.

@canadianer I'm not saying it's completely impossible, but (as an analogy) all you need to do mathematical research is a pen and some paper - but honestly how many people who just graduated university can (nowadays) actually produce something worthwhile?


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What happens if a speciation event causes the new species to evolve out its clade's defining trait?
If a speciation event occurs to a member of the strepsirrhine clade in such a way that its rhinarium is selected out, would it stay a strepsirrhine?

Yes, it would. A clade is defined as an ancestor and all of its descendants regardless of whether they look alike or not. Now, it is of course up to us (humans) to decide what we want to call strepsirrhine. If we decide that the new species that has no rhinarium is not a strepsirrhine, then strepsirrhine will stop being the name of a clade but will be the name for a paraphyletic group (and we would probably need a new name for the current clade of strepsirrhine).
You can get more information about phylogeny in this post and much more info in an intro class to evolutionary biology such as Understanding Evolution for example.


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Retrovirus Production
I have been having difficulties with low transduction efficiencies of my retrovirus production. I expand my plasmid of interest (on MiG-GFP plasmid) in DH5α E Coli for ~24 hours, purify with Qiagen midi prep kits, then put on ~90% confluent 293FT cells with either retronectin or polybrene for 24 hours. I then change media and harvest supernatant at 48 and 72 hours of incubation with the 293FT cells. I then expose 3T3 cells to varying volumes of the virus containing 293FT media and am able to transduce about 10% of the 3T3 cells, which is really low. That being said, here and there I am able to get very high transduction efficiencies on the 3T3 cells, but for unknown reasons. I have tried concentrating the virus but transduction efficiencies don't increase all that much. And I have tried growing up the plasmid in Stbl3 cells, which if anything gives me worse virus.
Anything here jump out as being responsible for low transduction efficiencies. Or is there another way somebody does this that works really well?

Have you tried using a transduction agent? I personally suggest effectene if you decide to try your luck there. What titre are you using? How much did you change the titre when you concentrated it?

I also use polybrene as a transduction agent and have used 5-FU to get my cells cycling prior to transduction. But I have not tested effectene, I appreciate the suggestion. And when I concentrated the virus the titre tested on 3T3 when up by about 5-10% with what I would have expected to be a 10X concentration.

Hmm, that titre should definitely have increased the efficiency by quite a bit. I'm not sure what could be restricting that. Well if you want to keep the retroviral vector (of course effectene is only good for free DNA) there are several reliable brands of transduction agents you could try.

In my experience, transduction efficiencies skyrocketed when I applied a spin-infection procedure. A 30 min low speed centrifuge with the virus changed a lot. Here is the TRC protocol for this: http://www.broadinstitute.org/rnai/public/dir/download?dirpath=protocols/production&filename=TRC%20viral%20infection%20200909.pdf

I have tried this. I have even spinfected for 2hr followed by a 3hr 37C incubation and it does make a slight difference, but still doesn't solve the problem.

In this case, using ideal (nontoxic) dose of polybrene and spinfection, I'd look for an optimal stage on the growth curve of your 3T3s. It's been a while since I've worked with that line. But in other cases of transfection, establishing the curve on uniformly spread cells (with polydL coating or so) helped a lot. (I am aware of transfection&transduction differences, yet I find that fast growing helps with the latter as well.

Also, try titering your virus in HEKs or HeLas, just to make sure that your production is not the issue here. Protocol here: http://ow.ly/LFQHe
There are qRT-PCR titering methods as well saving effort; such as this one:http://ow.ly/LFQK2


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Different names in paired-end sequence files
I am aligning paired end sequence reads using bwa mem and I get an error saying that paired reads have different names: "M01814:86:000000000-A6MU9:1:1101:15545:1335", "M01814:86:000000000-A6MU9:1:1101:16059:1338" So it looks like the locations for some of the reads don't quite match up. Is there a way to ignore these reads? Or to use them but not treat them as pairs?

are those Illumina reads?

Yes from the MiSeq

Ok, just wanted to confirm. Will look into it.

Do you have equal number of reads in your files (I assume you have separate files for the two ends).

Yep exact same number in each file.

According to this document : http://support.illumina.com/help/SequencingAnalysisWorkflow/Content/Vault/Informatics/Sequencing_Analysis/CASAVA/swSEQ_mCA_FASTQFiles.htm the position of your reads on the sequencing tile don't match, but I think you've figured that out if i'm not mistaken by " it looks like the locations for some of the reads don't quite match up" You could delete these reads to solve the problem. I have no other suggestion without knowing more of your setup.

Yeah I did already figure that out. And deleting the reads would be less than ideal, but may be the route I need to go. Thanks anyway for the help.

I assumed that you've figured this, but wanted to make sure, so that I don't make mistakes while trying to help you. I found some links that might help you resync your files : https://www.biostars.org/p/6925/#6928
https://www.biostars.org/p/12576/#12578 http://seqanswers.com/forums/showpost.php?p=141460&postcount=45
originally from here:http://seqanswers.com/forums/showthread.php?t=46538

Let us continue this discussion in chat.

Paired reads do not have different headers. Most likely these are singletons. You can provide an option to your aligner to not align singletons.

@TheNightman How many singletons do you have? Just parse and see.

I'm not sure how to see how many singletons I have. Do you know how to do this?


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Are the processes on afferent neurons that go from the sensory receptor to the cell body considered axons or dendrites?
References on pain fibers say impulses move along axons to the CNS, but I thought that by definition axons carry impulses away from the cell body.

They are considered axons. Pseudounipolar cells have a bit of an odd morphology.
The reason you consider the entire length an axon is because it all grows from a single process from the soma which then branches. Terminology is just terminology, so "rules" are often made to be broken in biology: yes, an axon typically carries information away from the soma, but that's not the case here for neurons where the information sort of bypasses the soma.
Besides the developmental origin from a single process, the initiation site for an action potential is out in the distal end of the axon, rather than at an axon hillock connected to the soma, and if you had a section of axon on either side of the soma it wouldn't be apparent which end you were looking at.

Tandrup, T. (1995). Are the neurons in the dorsal root ganglion pseudounipolar? A comparison of the number of neurons and number of myelinated and unmyelinated fibres in the dorsal root. Journal of Comparative Neurology, 357(3), 341-347.


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How is Pseudomonas aeruginosa diagnosed?
I know that P. aeruginosa is cultured on an agar plate, but which media or assays make it distinct from other Gram-negative bacteria?

Welcome to SE BIology. Please take the time to take the Tour and find out about this site. After that, the Help on asking questions should be your next call.  You need to show that you have done some research for yourself first before posting here. Tell us where you have searched an dwhat you have or have not found.


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‘Inoculum’ vs ‘inoculant’ – which one is it?
I’m currently writing the report of a study which looked at commercial soil inoculants (Rhizobium sp.). However, I’m confused about the differences between the words inoculum and inoculant and when to use which.

ask on http://english.stackexchange.com/ please

If the dictionary definitions do not tell you which one to use, I doubt anyone at english.se would know either.

I'm voting to close this question as off-topic because it is a question about the english language.

@GeraldEdgar I disagree. There are a number of people over at english.se who write some excellent answers about usage, suffixes, and the like. I expect that's the best SE site for this question about when to use the direct latin ending inoculum, vs. the suffix -ant

Further to @DeNovo, I would say that on SE English Language and Usage you will be expected to provide a sample sentence in which you wish to use the word. You will also be expected to report what you found in dictionaries and explain why it didn't help. It would help to know what the leading scientific journals are in your field, so that anyone with access to a (e.g. University) subscription can search for actual usage of the word if you cannot. Also Google ngram viewer may be a useful tool for that in relation to books.


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Cell Line With DNMT3a Mutation
I am looking for a cell line (preferably hematopoietic) that has an inactivating DNMT3a mutation. I have checked the Cancer Cell Line Encyclopedia but of all the hematopoietic cell lines I know I can't find any with a DNMT3a mutation.
It would be great if somebody knows of a cell line with a DNMT3a mutation, but it would also be helpful if somebody knows of a database that I could use to find this information in the future. Thanks.

Why not just induce one? There are quite easy-to-use CRISPR/Cas kits available nowadays.

While that would work, it would be much cheaper and easier to identify which of the cell lines at my disposal contain such a mutation.

All I'm saying is if you can't find a cell line that meets your needs, it would be quite cost-effective to generate one on your own. There are some extra costs outside of the kit, but this Life Technologies kit is only US$514, whereas purchasing a new cell line from ATCC not in your collection may cost an approximately equivalent amount, depending on the line, what kind of institution you're at, etc. Worth thinking about.

For CRISPR-Cas you don't even need the kit. Just have a plasmid for containing the Cas9 gene from where you can IVT the Cas9 mRNA. Co-transfect this with the donor plasmid.

Or for only $60 from AddGene


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Effects of Fixation on Cell Membrane
Why does fixing of cells with something like formaldehyde disrupt the membrane enough for probes, antibodies, and dyes to get into the cell?

It doesn't. You generally also need to permeabilize with a detergent in order to do antibody staining. Fluorescent dyes are very small when compared to antibodies or large nucleic acids, and so can diffuse across the membrane or fit through very small pores created by (para)formaldehyde fixation.

In my experience, somehow antibodies are accessible to the inside of cells without permiabilization. But I do not know the explanation.

243 is right, however fixing tissues with formaldehyde or PAF usually leads to the formation of methylen bridges cross linking proteins and potentially masking epitopes. Therefore in most of the cases you'll need an antigen retrieval step based on heat induced or proteolytic protocols to properly access to the antigens. While working with cell some chemical will at the same time fix and permeabilize your cells (like aceton)


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How can a sequence be downloaded from UCSC genome browser
If I have genome coordinates is there a simple way to download the entire intervening sequence from the UCSC genome browser? I found some fancy way of using ftp but I can't figure it out.

Yes. Table browser allows you to do that.
In the dropdown box called output format select sequence and click the button named get output. You'll get the sequence.
If you don't think it works then this is the output that I am getting. (Fist few lines):
>hg19_gold_AL096773.6 range=chr1:115207623-115347729 5'pad=0 3'pad=0 strand=- repeatMasking=none
GATCTGCCAGCGTCCACCTCCCGAGGTGCCGGGATTGCAGACGGAGTCTG
GTTCACTCAGTGCTCAATGGTGCCCAGGCTGGAGTGCAGTGGCGTGATCT
CGGCTCGCTACAACCTCCACCTCCCAGCCGCCTGCCCTGGCCTCCCAAAG
TGCCGAGATTGCAGCCTCTGCCCAGCCGCCACCCCGTCTGGGAAGTGAGG
AGCATCTCTGCCTGGCCGCCCATCATCTGGGATGTGAGGAGCCCCTCTGC
CTGGCTGCCCAGTCTGGGAAGTGAGGAGCGCCTCTTCCCGGCCGCCATCC

Actually Table browser is quite useful as you can get different kinds of data for a given genomic region which include annotations, variation, transcription factor binding sites etc.

Actually this does not seem to give me intervening sequence for coordinates. (I'm trying this: chr1:115227814-115227978) It just outputs some coordinates.

@TheNightman In the dropdown box called output format select sequence and click the button named get output. You'll get the sequence.

I did find a way of doing this using UCSC das. If the pertinent info is changed in the page address here, it will output the intervening sequence between two locations:
http://genome.ucsc.edu/cgi-bin/das/hg19/dna?segment=chr1:100,200


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Why does low sequence diversity cause sequencing problems
When sequencers are processing sequence fragments, if there is little diversity at a particular bp locus this can cause problems for the sequencer. I have the superficial understanding that when a flow cell contains a significant percentage of a single base on any given cycle, it has difficulty deciding what base is present in each sequence. Why is this?

I think the problem is more that the software has a hard time identifying individual clusters if way more than a quarter of them are lighting up for a given base.  If you have more diversity in the first few cycles, when the cluster coordinates are being identified, I think this is less of a problem.


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What is the meaning of oIMR
In reference to genotyping primers, often some are labeling with 'oIMR'. It seems that this often refers to internal positive control primers, but I'm not sure. What does this stand for?

it stands for oligo Induced Mutant Resource.


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Expected dS/dN ratio for exome
I am trying to determine whether or not my sequencing data has more/less non-synonymous mutations than would be expected. My understanding is that there is some fixed ds/dn ratio for the human exome that I can use to calculate this. Is this true? And how might I calculate this?

The page linked behind the anchor "ratio" has gone stale. Can you fix that?

There isn't a fixed value for the human exome AFAIK, nor would it be a good idea to have a fixed value for the exome because different regions and genes can be under different selective pressures.
The norm is to compute the ds/dn ratio and then test against a null hypothesis of the ratio being 1 to infer if your region is under selection or not. If it is greater than 1 it indicates positive selection and if it is less than 1 purifying selection.
You can find a  decent introductory treatment here.


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Troubleshooting PCR Steps
I am troubleshooting a PCR reaction that gives me no product, and there are a lot of different approaches that I can find in books and just in google searching (things like running a gradient, increasing cycle number, etc.). But it would be really nice if somebody could list out in order the steps they take to troubleshoot a PCR reaction. Thanks.

Did you observe a small band due to primer dimers but not your target? or you got nothing at all? For the first one, redesigning primers is a possible solution as well as modifying the annealing temp. For the later, try running a positive control PCR to make sure your reagents are working.

This question is broad. You can troubleshoot PCR in a thousand ways depending on what the problem is. Can you ask a specific question?

I think 30 cycle PCR is maximum to see bands by electrophoresis in most of cases, because under the ideal efficiency, one copy could be detectable by 34 cycles of PCR. However, if your expected products are longer than 1 kbp, you might extend several cycles.
I usually add DMSO 5% in any PCR reaction. In my experience, DMSO would not interfere PCR reaction--you can amplify your fragments without DMSO; you could get PCR products with DMSO. Betaine sometimes work better than DMSO, so I am shifting my default reaction mix from 5%DMSO to 5%DMSO and 0.5M betaine.
For annealing temp, you can not tell which is better, lower or higher than the first trial which showed nothing. When increasing the annealing temp, primers may be able to access your target sequence more and you could get efficient amplification. So you might want to try both. If you have a PCR machine set various temperatures at once by gradient. You could include lower and higher temp together.
Alternatively, I sometimes use the touch-down method. You do not need to determine the best annealing temp in this case. If you just want amplified products, this could be a quick solution.
Additionally, hot start is also my default condition, because this could not ruin PCR reaction without hot start.
Basically, I change annealing temp. If I do not get good amplification and specificity, I change PCR enzymes. Changing PCR enzymes could mean changing buffer conditions because companies try to give unique features for their products.

Generally I start with a temperature gradient running in 2 deg steps above and below the calculated Tm (which I calculate by the simple 2AT4GC method). If that fails, I might try something similar along with PCR "enhancers" - usually some variation on DMSO or betaine. Depending on the problem (detection/cloning from a reverse transcription reaction? Sequencable fragment from genomic DNA?) I might try redesigning the primers, changing the type of PCR polymerase, or improving the template in some way.


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HSC Cycling Rates
I would like to know how often human hematopoietic stem cells go into cycle in the bone marrow niche (with a paper reference). I have heard they cycle 1-2 times per year but has anyone robustly measured this?

Not knowledgeable in this respect myself, is this what I should be looking for? http://www.bloodjournal.org/content/117/17/4460?sso-checked=true

That is helpful but I would like something where the dynamics are directly measured if it has been done.


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Can storing food in a de-pressurized container result in anaerobic bacteria growth?
I was looking for a way to store for longer some products which go bad quickly. I found a stainless steel container made with a hermetic lid that you can remove air through (using a pump) so you create a vacuum of sorts (I don't know to what level can the internal air pressure be reduced). The issue is whether storing food which isn't specially sterilized, such as vegetables or spices, can result in the growth of pathogens such as Clostridium botulinum? What I originally looked to buy such a container for is soy lecithin, as I read these go bad very quickly even if stored in a cool, dry place as advised.

Any sealed container can become anaerobic relatively quickly if there are oxygen consuming organisms inside (which there probably are if it's not sterilized). So, growth of anaerobes should always be a concern when using a sealed container for food storage, and proper temperatures for such storage should be considered.
A container like the one you describe would probably be good for extending the shelf life of dry foods that are sensitive to oxidation (coffee, spices, or your soy lecithin powder), and might even help stave off aerobic spoilage organisms (like molds), but it probably won't do anything to prevent growth of anaerobes like C. bolulinum or C. perfringins.

So it can increase the probability of anaerobic growth? It seems the usual aerobic spoilage is not potentially lethal, but stuff like botulism is.

I'm not sure that it would actually increase the anaerobic growth, but it probably won't help prevent it. The trouble there is that anaerobic spoilage can be less obvious than, say, mold growing on your food. Might be why C. perfringens is among the leading causes of food poisoning. Good news is that botulinum and perfringens don't grow well at colder temps, so keeping food in the fridge or freezer, when possible, is a good way to prevent them from growing.

Thanks. Though, I think within the freezer at -20 Celsius no bacteria or mold should develop anyway whether there's vacuum or not. Within the fridge (3–4 Celsius) be, how effectively can it prevent such anaerobic growth? The non-freezing temperatures probably don't halt it completely, so if the stored product is something that takes months to finish, what might happen?


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Rescuing a virus from naked (c)DNA
Reading the articles it seems that for several human virus strains, synthesizing the full-length genome then electroporating into vero cells and incubating a few days gave birth to living viruses that can infect people as well as the original do (thus offering an easy way to add some mutation and make chimeric virus)
Am I correct and what are the few facts to know about this ? For example influenza would need more efforts, transfecting either seven separated plasmids, or the full genome plus infecting with a living virus producing the influenza RNA polymerase.


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Understanding ancestry testing mathematically
Forgive me if this question has been asked here before, because it is something which should be very easy to find, but I can't seem to find an answer no matter where I search.
The question is simply where to learn the mathematics that goes into things like popular ancestry tests, and also more academic things like determining ancestry components of historical groups (e.g. usage of the terms Ancient North Eurasian, Eastern European Hunter-Gatherers and all that).
It is clear that if someone gets an ancestry test saying say 32% Scandinavian, then of course that doesn't mean 32% of their base pairs have a convenient "Scandinavian" label attached to them, rather there is some statistical inference going on behind these percentages, and I would like to understand that.
Suppose I have the raw data of my own fully sequenced genome, and also a database of the genomes of many individuals from various populations (of course grouping them into populations is already something that involves some assumptions that I would like to learn more about). Where would I learn how to analyze that myself to produce something like the results of an ancestry test? Is there a textbook someone could recommend that gets into the actual algorithms used?

I'll give here a simple, non-technical answer because I'm assuming you don't need to actually perform an analysis of ancestry.
So, detecting ancestry is a non-trivial task. Given your genome sequence, you would need to compare some "informative" regions of the genome with the homologous sequences of some population (say, of a database with other genomes). These informative regions are usually some parts of the genome that vary across individuals (variation is used because differences are informative: some populations vary on particular sites, distinct from other populations). At the core, this is a question on how to compare "character strings" (DNA is composed of 4 characters, namely, A, T, C, and G). But these strings exist in a complicated structure: a human genome is partitioned in 23 pairs of chromosomes, within each individual. However, the question of ancestry is not about individual sequences really, but about population-level changes in DNA composition. So, in fact, you need to consider population-level factors: size of the populations to consider, the rates of recombination (DNA exchange across chromosomic pairs), mutation rates, and even population structure (people move geographically!).
Given these (and, many other) factors, people build models of "coalescence": given a sequence of interest, how likely is that it shares some ancestor with another query sequence? So, the models try to relate these two sequences (say, the one you are interested), with a query (say, a "consensus" Scandinavian sequence), and then make a model of a 3rd sequence (the ancestor!). This process is repeated to test many hypothesis, so you end up with many probabilities. On top of this, you can estimate the ancestry for any given part of your genome, and this is what most companies do (say, 23 and me).
In summary, you are correct that a "% Scandinavian" does not mean sequence similarity per se. It implies an estimation of common ancestry. This estimation comes from models of shared ancestry. If you're unsatisfied with this simple answer, and want a more technical answer, I recommend reading this paper. An intermediate-level explanation is found here.

What is ancestry?
I think some of the confusion in ancestry proportions stems from the fact that 'ancestry' can really mean several different things in different contexts. I would really encourage people to read this short piece, as it does a good job of clarifying what the different terms mean https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1008624
What something like 23andme is trying to do is to infer how much of your genome most closely matches the genome of a particular pre-specified reference population. This is relatively easy to interpret if one parent if from Nigeria and the other is from Norway, since it will roughly be 50% Norwegian and 50% Nigeria, but becomes more complex to interpret when someone is 70% Norwegian, 20% Danish and 10% Swedish, for example.
Summary of the 23andme process
Since you specifically asked about 23andme, I will try and give you a relatively simple explanation of how they end with the numbers that you might have got on the report.
What 23andme are trying to achieve is essentially a 'classification' problem - they have a genome from an individual of unknown ancestry (call this the target individual), and they would like to describe it in terms of some pre-defined set of different ancestries (like 'Norwegian' or 'Nigerian'). To achieve this, they first need to assemble some kind of reference dataset of individuals of whom they know in advance to be of a certain country. For this, they will choose individuals who they know have e.g. all of their grandparents and great grandparents from Norway - so they genomes of these individuals will be reflective of general Norwegian ancestry.
They use something called Support vector machine Learning, which is just a fancy computational method, to 'learn' what segments of Norwegian ancestry look like. This is analagous to the AI algorithms which are able to tell the difference between an image of a cat and a dog. If you 'train' the AI with enough labelled examples, it can accurately classify new images. In the same way, if you train the SVM algorithm with enough examples of what Norwegian or Nigerian DNA segments look like, it can classify the probability that a new segment comes from a particular reference population.
They then take the genome of target individuals and split it up into chunks along the genome (something like 100 chunks per chromosomes). They then apply the SVM algorithm to calculate the probability that a particular chunk comes from a particular reference population. So for example, there might be a certain chunk of the genome which has a 70% chance of coming from the Norwegian reference population and a 30% chance from come from a Danish reference population. If the individual is admixed, the the next window may have a 90% chance of coming from the Nigerian reference population and a 10% chance of coming from the Cameroonian reference population.
They will then go across the genome and look for windows of 'high-confidence', where the probability of the window coming from a particular reference population may be higher than say 90%. If you add up the high confidence windows across the genome for each reference population, you will end up with your overall ancestry proportion for that population.
Other ways of inferring ancestry
There are many, many other ways of inferring ancestry proportions/components. For example, Principle Component Analysis, ADMIXTURE analysis, clustering methods, all of which have different strengths and weaknesses.


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Reason for aquatic plant roots
My question is about why aquatic plants have roots. At first they seem a bit superfluous to me because leaves of the plants could just absorb nutrients directly from the water thereby skipping a need for root function that land plants have to pull nutrients from the soil. I then wonder if nutrient trafficking is the reason for the root system as diffusion may not occur efficiently through thick leaves.

Also consider alternative uses, such as anchoring/staying in one place.

I did consider that and that makes sense but doesn't solve why roots still are the nutrient absorbing part of the plants rather than the entire plant.

According to this article, Bladderworts have evolved this ability.


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Longevity Experiments
I realize this is a bit of a long shot, but sometime this year I was reading a paper about experiments that I believe were performed in Drosophila (may have been planaria) where breeding was delayed until late adulthood through separation of the sexes. After a number of generations there was significant lifespan increase.
Anybody come across this that can point me to it?

Planaria are hermaphrodites.

Look into Michael Rose's work at UC Irvine. No sure if this is what you were thinking of.


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Sources of Mutations
I'm looking for a reference that gives some information quantifying sources of mutations that occur within cells. These can be general, but I'm interested in some percentage of mutations caused by external vs internal sources (like mutagens vs replication errors).

This is going to strongly depend on the cell type, where it's located in the body, the type of organism, etc. Are you interested in looking at cancer, which occurs in pretty much all cell types, or heredity, in which the mutations must occur in the germ cells, or what?

There is an issue of epistemology when talking about the "sources of mutations". The question makes little sense and you should rather be asking about the "factors causing variation in mutation rates".

See this: http://dx.doi.org/10.1038/nature12477

An extensive collection of the various mutation rates (from which you could reverse-engineer their fraction on the total share of mutations):
http://www.bionumbers.hms.harvard.edu/search.aspx?log=y&task=searchbytrmorg&trm=mutations&org=&rpp=100

cool site I'll take a look.

I actually found this in the following paper:
http://science.sciencemag.org/content/348/6237/880.full
This group shows estimated governing forces in mutation incidence by tissue types.


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Estimate of total number of oncogenic mutations
So there are a number of ways point mutations can hyperactivate or inactivate genes. But realistically there are only some small number of point mutations ever observed for a particular gene in cancers. An example is the JAK2 mutation: c.1849G>T p.V617F chr9:5073770 which is almost the only JAK2 base substitution observed in leukemias.
Is there some estimate of the number of substitution loci ever observed in cancers?

you can visit the TCGA website, but be warned navigating that mess is a giant pain

@KoustavPal yeah I've played with TCGA a lot, but that I can find there is no sum total estimate of this.


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Infant Death Adjusted Historical Human Lifespan
I had found a good paper at one point to describe this but I can't seem to locate something similar now. I am looking for a manuscript that describes average human lifespans throughout history/prehistory especially adjusted for infant and child deaths but it would be nice if there was un-adjusted data as well. Does anybody know of a reference with this information?

Related Q/A with some relevant references: Survival curve in early humans

I assume you are asking about expected (mean/median) age of death, for people that survived young childhood(?).

@fileunderwater Unless I'm missing it I do not see the answer at the linked page, but yes I am looking for mean/median age of death for those that survived childhood compared across time (ideally prehistoric times up until recent times).

The link goes directly to the answer (Q above). This doesn't directly answer your question though, but contains some information on infant/child mortality in different types of human societies.


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Primer Design With Primer-BLAST
I am trying to design primers for sanger sequencing snp detection. In the past I have used Primer-BLAST, but I'm trying to pick up KRAS codon 12 mutations. The problem is that in Primer-BLAST you specify refseq gene ID and so it doesn't seem to design primers outside of the gene locus. This means that my primers will sit on the SNP. Is there a way to tell Primer-BLAST the exact locus I am trying to sequence? Or is there a better way of doing this? Thanks.

You can manually restrict the design ranges in Primer-BLAST screen.

First of all you should enter the targeted sequence. In this case, it will be NC_000012.12 which corresponds to chromosome 12 that has KRAS gene.
You should determine the position of variant that you interested in that chromosome. The KRAS G12D -or rs121913529- variant is in 25245350. position. You can find the position of specific variant on dbSNP.
For Sanger sequencing, the recommended size is 600-1000 bp. So, we should select ranges +/- 300-500 bp apart from the variant position.
For the left primer we choose From:25244850 To:25245050; for the right primer we choose From:25245650 To:25245850. And then submit.
Here are the primer-sets that you are looking for. :)

So actually for the way I phrased the question, this is the correct answer and I appreciate it this works for me trying to get G12D. But the problem I am trying to get at as well is what if the variant I am trying to pick up is in one of the first 100 bases listed in the RefSeq accession number. So the for primer 'From' number should be something like -350. Can this be done?

I understand your question. Unfortunately, it is not possible. I suggest that instead of using RefSeq ID, you can enter larger sequence -such as chromosome-.

yeah that makes sense, that's sort of what I figured. Thanks.

For sequencing primers, I've always used this tool to great effect. You can set up how many bases you want to include before your target, and define how to divide large exons and set up no. of overlapping bases. I think this is what you ask for in your comment to the previous answer.
http://ihg.gsf.de/ihg/ExonPrimer.html

glad to be of service :)


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Would Ants and Termites be considered r or K strategists?
My initial assumption is that most swarm species would fall under r strategists due to their prodigious number of offspring, but it also occurred to me that since worker types are non-propagating we would only consider the queen/drones which would be K. So which viewpoint is correct?

Its not an either or question, r and K are directions on a line scale.

@John I know, I just had some trouble phrasing the question. My question is more would the non-propagating workers affect the conclusion, or are only viable offspring factored into r/K?

What are r or K strategists? Your question is unclear to me.


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Is intelligence correlated with neural calorie usage?
The human brain uses a lot of calories in comparison to other species, that is usually explained by referencing the intelligence disparity between Humans and other Animals. My question is how far does that go? Do individuals with radically improved intelligence also use radically more calories? And peripherally, does that caloric need place an upper limit on human intelligence?

Have often wondered this myself. Looking forward to an answer! People say the brain atrophies without use, like muscle, and its certainly true that bigger/more active muscles use more calories, so one would think this might be the case with the brain...

Bigger brains take more calories to build, and brain size has been conclusively shown to correlate with intelligence. The relationship is not strong, only very modest, perhaps a correlation of around $r \approx .3$. There is no doubt, however, that the relationship exists.

There is also, however, some evidence that more efficient brains are more intelligent. Efficient meaning here that they use less energy per processing power. This is not quite as clear as there is inconsistent evidence. See, for example, Richard Haier's book The Neuroscience of Intelligence.


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What exactly happens to animals that fail mating rituals?
Quite a few animals (usually males) participate in various mating rituals to showcase their fertility as mates. While presumably, the successful ones get a chance to mate with females, it occurred to me that I don't actually know what happens to the ones that fail. I would assume that not all the ones that fail don't mate, as that would result in roughly 50% of the male population being frustrated sexually. But I can't figure out an alternative, do they get another chance to fight other losers? Do they just mate anyway at a lower rate?

I think it follows a bell curve with the most successful individuals having more than average and the less having less, and some having none.

this depends on the species, it ranges from death to try again to alternative mating strategy. Many spiders that fail get eaten.

A bit late to the party here but something important to note is that females aren't always strictly faithful to the "winners" of animals. In many cases losers actually employ a "losing" strategy where, while continuing to lose, mate with females on the side not immediately taken up by the winner. This is very common in social animals as far as I know but I am aware of species, especially individualistic ones, where (as the previous answer says) mating follows a more bellcurve pattern leaning towards winners meaning the females are just looking for the best options, and in rarer cases, only winners mate while losers don't get to at all. If only winners mated, it'd mess up the gene pool pretty fast, so females will mate with winners as a first choice, and then also try with next best options. Hopefully that helps answer your question, but I'm not a doctor in bio (yet) so take it with a grain of salt. Source: my Intro to Evolutionary Bio Cornell class, yada yada, and a few Youtube videos I'm unwilling to dig up.

What exactly do you mean by "if only winners mated, that would mess up the gene pool pretty fast"? Many animals produce huge numbers of offspring, very few of which end up reproducing. E.g. octopuses hatch tens of thousands of eggs. Genetically, it doesn't matter why an animal didn't reproduce; failure at a mating ritual is the same as failure to avoid predation.


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Why do children not have the Acid Mantle?
Post puberty humans begin to secrete a substance called Sebum which changes the neutral PH of our skin from ~7 to 4.5-5.5. This has that advantage of serving as a protective line against pathogens and discourages larger organism like lice. My question is given these benefits, why are children not born with these advantages?

Kids don't have many dermal infections, mostly flu, respiratory and digestive infections. the acid mantle didn't prevent the black death fleas and the flu epidemics.

This question is wrong. Sebum isn't a "protective line", in fact excess sebum production (an exceedingly common problem) invites pathogenic bacteria to feed, causing acne and pimples. I don't see any evidence of sebum protecting against lice. See my question at https://medicalsciences.stackexchange.com/questions/13862/why-isnt-there-a-larger-effort-to-reverse-and-block-the-effects-of-androgens-on for an explanation of how damaging puberty is for skin.

@user1258361 The Acid Mantle is a very well accepted phenomenon subject to a great deal of peer-reviewed research (see here: https://www.ncbi.nlm.nih.gov/pubmed/30125885). The prominence of Lice on children is acceptably attributed to the lack of the acid layer, but if you have a source that suggests otherwise, please provide. And your linked question is somewhat irrelevant, excess of anything is negative, that doesn't negate the positive effects that proper distribution has.

You -do- realize that secretion of cetylpyridinium chloride would be a far superior barrier against pathogens, right?

I'm fairly certain that constant contact with cetylpyridinium chloride would result in quite a few negative side-effects, and I'm certain that the human body doesn't have the mechanism needed to synthesize cetylpyridinium chloride.


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Why are the hormones dopamine, adrenaline, noradrenaline and serotonin so ubiquitous across the animal kingdom?
As far as I know there is no reason for the makeup of a given hormone to be universal as it merely serves as a carrier from one part of the brain to another. So why are the above hormones seen across the entirety of the animal kingdom, and used in more or less the same way?

Evolution.
This is not special to hormones: receptors and ligands of all types are highly conserved across not only the animal kingdom, but also to single-celled organisms. The degree of conservation is typically dependent on the closeness of evolutionary relationship: more related organisms share more homology.
Because species evolve from common ancestors, they tend to share a lot of the same 'tools.' Changing the purpose of a hormone would likely require some sort of selective pressure, some new reason to use that molecule in a different way, and if the old and new roles conflict then there needs to be a replacement. This can happen, but it's complex and requires just the right conditions. More often, minor changes occur: among the steroid hormones, for example, you will find many small biochemical tweaks that make new molecules that have different functions.
Certainly the functions of some hormones are not entirely conserved, and if you look at the nervous systems of, for example, insects versus mammals, you will find some major differences, but the closer in evolutionary time you look the more similarity you will find.

Thank you for the answer, I assumed it was something like that, I just had trouble with the idea of a shared ancestor between all these animals that still retained the complexity of hormones and neurotransmitters, do we have any idea what animal that is?
P.S. I'm new here, is there anything I need to do to close the question or am I fine?

@ShmuelNewmark If an answer is helpful you should upvote it with the up arrow next to the answer; if a question has been solved by an answer you should accept it with the check mark. Sponges are the simplest extant animals, though they may or may not be in precisely the same lineage as the other animals, but even they have some rudimentary use of molecules like serotonin and dopamine - the purposes are almost certain different, but these things are very very old. C elegans is a roundworm and common model organism - you could start there. The actual common ancestor is long gone.


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Is drinking your urine an effective way to stay hydrated in a hostile environment?
There are quite a few stories about people trapped or otherwise incapacitated resorting to drinking their own urine in an attempt to stave off dehydration, ignoring the long term consequences, my problem with this idea is that the main cause of death when dehydrated is kidney failure, resulting from the buildup of urea and uric acid when the body can't package those chemicals with water to execrate them. Because of this, I'm tempted to assume that drinking your urine (without somehow purifying it) is a futile action as you are consuming both the water and the exact chemicals you need to remove with the water. I'm however not confident with this analysis, so any sources on the subject would be appreciated.

Drinking urine could help you stay hydrated a bit longer, maybe a day, but only when you are well hydrated at the start. You could get about 0.5-1 liter extra water this way. This doesn't work anymore when you start drinking urine the 2nd or 3rd day without water - the amount of urine will be very small and will be too concentrated at that time.
A man, drinking his urine has survived for 6 days under the ruins of the earthquake (Slate.com). However, people have survived for as long as 8 days without water or drinking urine: a 7 and 11 years old kids under the ruins of 2010 Haiti earthquake, and a 35 years old woman trapped in a lift.
According to Guyton and Hall Textbook of Medical Physiology:
...to excrete an average amount of waste products, let's say 600 mOsmols, your kidneys need to excrete at least 500 mL of urine, because they have a limited ability to concentrate urine.
If you drink 1 liter of urine with 600 mOsmols of waste products, you will need to excrete 500 mL of urine to excrete those 600 mOsmols and additional 500 mL to excrete 600 mOsmols from your normal metabolism. So, drinking 1 liter urine forces you to lose 1 liter of water, which means no water gain.
If you are very well hydrated at the time of first urination, your urine will be more diluted, so containing less than 600 mL of urine (minimally about 50 mOsmols/kg according to Wikipedia). Drinking such urine can provide net hydration, but your next batch of urine will be much more concentrated and will provide much less hydration. At the point when the kidneys need to excrete more water to eliminate the waste than you have drunk by urine, you will be in the negative water balance.

You may want to emphasise in your first sentence that this is only true if you are very well hydrated to start off with.

OK, I did......

Thank you, sadly a lot of people will just read for first sentence than downvote which would be unfair

Oh, I don't know. I actually don't want to encourage anyone to drink urine, to be honest; it's just to answer that it makes some logical sense, but then, one could vomit or get diarrhea after drinking urine, which would make dehydration worse. Also, most of those people who said they drank urine and survived, would probably survive without drinking it, anyway.

Under the vast majority of survival situations it is counterproductive, people do it and survive survive despite doing it. but under the super rare circumstance where someone is super hydrated the urine can be used to recover water, but as you said it is a small one time benefit that relies on you basically not needing the water in the first place.

I agree, and no medical or military guideline recommends it.

@Jan I thought I already accepted this answer, I'm sorry it took so long

@ShmuelNewmark...to me it's like "just now."


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During a large forest fire, what is the evacuation behavior of birds?
I'm interested in birds' behavior during large forest fires. Do they fly away as soon as they smell smoke, or wait until seeing fire itself? Do they fly away in flocks, or individually? Do they ever try to return to the area later, or just abandon it for good?
Interested mostly in average forest birds like jays, cardinals, finches, etc.

The exact behaviour of birds during a wildfire is unclear and there is little scientific evidence on their exact behaviour. Anecdotal notes from eye witness observations indicate that healthy birds fly away from the affected area before they are in danger. Birds that are unable to fly or move out of danger from the fire such as chicks in nest and indisposed birds are likely to die. Different species are likely to react differently to fire, species that flock normally will probably flock together as they fly and species that are more solitary are not likely to flock. Most fires happen in late summer and fall, just after the breeding season for most birds and during their migration, meaning they can escape the area. If the fire is very widespread, the birds may not be able to find appropriate shelter and food and would likely die as a result.
Wildfires are a natural phenomenon and birds have evolved to adapt strategies to deal with them. Some birds benefit from wildfires as they are a normal part of ecological succession.

Ecological succession is the gradual process by which ecosystems
  change and develop over time in response to a disturbance or
  colonization of new habitat.

Fire essentially creates a new habitat in which not all the same birds will use. Blue Jays prefer forests, but if a wildfire burns a forest, it will likely become a shrubby field afterwards and may take years to regrow into a forest. The Blue Jays will not likely return in large numbers until the habitat is a forest again.
A remarkable bird that is dependent on forest fires is the Kirtland’s Warbler. They breed in Jack Pine forests that are a certain height, once the forests mature; the habitat is no longer suitable. The jack pines themselves only release their seeds from cones in hot fires as they are serotinous and only open when exposed to intense heat, greater than or equal to 50 °C, the typical case is in a fire. The wildfires then create a succession cycle to always have suitable habitat for the Kirtland’s Warbler. Fire suppression of forests by humans has been listed as one of the reasons that led to large declines of this species.
Additional reading:
How Wildfires affects Birds?
Jack Pine Information

Very interesting that forest fires usually happen around the migratory season for birds. And the Jack Pine / Warbler relationship is fascinating. How would the seeds laying on the ground survive the fire itself? Does the Warbler eat the seeds and leave?

The seeds are not fire-resistant, but fire adapted. The Jack Pine cones have a waxy coat that protects them from being burned outright. The Jack-Pine cone can survive temperatures of 800F for 5 minutes. The heat melts the wax which allows the cone to open up, the seeds are not all released right away and there is a time period until they drop. They are adapted to drop after the fire has left the area, removing competing plants and putting nutrients in the soil. The Kirtland's Warbler does not eat seeds, only insects and berries, it relies on fires to regenerate new forest that it nests within.


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How does a spider's legs not get caught in silk when wrapping prey?
When a spider catches a prey, it wraps it up in silk. It uses its legs to do this. So how does its own legs not get stuck on the silk?
Note: I'm not talking about walking around the web. There are non-sticky anchor strands of silk to walk on. I'm talking about when the spider actually wraps something up.

There are two parts to this answer.
Spider Legs
First, I would like to mention that spiders avoid sticking to their webs by more means than just non-sticky anchor strands to walk on.  To help keep the glue from sticking to their legs, an oily substance apparently covers spider legs.  Furthermore, the same study found that:

In addition, Eberhard and Briceno also noted that the spider’s gait seemed specially designed, such that it “reduced the area of contact between the sticky droplets and the setae [spiny leg hairs].” This, combined with the fact that the thread touched many (rather than only a few) branching hairs, made it very unlikely that any glue would slide all the way down the hairs to make contact with the main part of the leg – which would have made permanent adherence more likely.

Spider Wrapping Silk Fiber is Different
The main reason spiders do not get stuck to their silk when wrapping prey is because wrapping silks are different from silks used to make webbing.  There there are seven known types of silk that spiders can produce.  Aciniform, or wrapping silks are the strongest silk from a spider and specifically designed for wrapping.  This silk is typically dry, and does not contain the high amounts of N-acetylgalactosamine which give the distinctive quality of being sticky.   For a very detailed study on wrapping silk architecture, please see this recent study from 2015.

There there are over seven types of silk that spiders can produce. So does that mean there are 8 forms? Please be precise. I assume you are taking this information from your last link, which states Spiders can produce up to seven types of silk [...] in the first sentence of the introduction.


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Why is the Mongolian Horse superior in stamina?
I've heard a lot about the Mongolian Horse over the years, especially that it has more stamina than the Arabian Horse. It's a little smaller/lighter than an Arabian.

Apparently the Mongol Horse can outlast an Arabian, despite having a lower top speed, due to stamina. NOTE: I could not find a good source for this, especially when talking about medieval times. It's very hard to find a true apples-to-apples comparison, because of things like a heavy Knight vs a lightly-armored Mongol, and back then Arabian horses were a little different anyway.
The Mongolian Horse can subsist on grass alone, whereas the Arabian Horse needs a lot of oats if its gonna do heavy hauling or riding.
The Mongolian Horse doesn't need horseshoes, since for some reason the hoof doesn't wear down much over its lifetime.

Source 1, Source 2
I would like to know, what biological differences can explain this? Do they have a different kind of muscle? Is their heart or lungs significantly different? Bones?
And the granddaddy point: What percentage difference exists between the DNA of a Mongolian Horse versus an Arabian Horse? For reference, the difference between a human and a chimp is about 1.2% .

This question appears a bit broad. You should consider narrowing it down.


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How to search for a DNA sequence in a genome on ENA (European Nucleotide Archive)?
I have to do a search for small DNA sequences in the genome of an organism in ENA. I have the accession number and project id. However, I can't download the whole genome because of the download size and would prefer to do it online if possible. I have a rough idea of the part of the genome I wish to scan in, don't know if that's relevant.

Do you want an exact match? Did you try BLAST? You can adjust the parameters according to your needs.

Have you already tried to submit accession number into advanced search? https://www.ebi.ac.uk/ena/data/warehouse/search

@WYSIWYG Yes I  do need exact matches. BLAST would search it against multiple sequences wouldn't it? I don't see how you can find DNA sequences in a particular genome using it

While it is much better/easier to download and do the exact search on your own, it is possible to do something similar, online. You can use NCBI-BLAST and increase the word length and mismatch/gap penalty. It also allows restricting the subject space; you can even align two sequences. The BLAST on ENA does not have much flexibility (subject restriction/word length). Perhaps you can look for a duplicate sequence on NCBI.
If this genome is available on UCSC genome browser then you can use BLAT too. However, it only accepts sequences larger than 19nt.


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What's the amount of blood passing through heart every second at Max Heart Rate?
How many mL of blood passes through the heart every second at maximum heart rate?
Is there any formula to calculate the amount of blood flowing through the heart per sec at say for example 70% of the max heart rate?
I didn't ask
Let's assume that the person in question is a fit 23 yo Caucasian male(if there are differences for various ethnicities)

· Heart Beat Rate

The normal heart has a rate of 72 beats per minute, but in infants the
  rate may be as high as 120 beats, and in children about 90 beats, per
  minute.

Lets say the heart beats at an average pace of 70 bpm (beats per minute)
(~100.000 times a day)

· Cardiac Output
Volume of blood pumped by the heart in a minute.
CO = HR X SV (heart rate multiplied by the stroke volume)
Cardiac output is the volume of blood being pumped by the heart in a minute. It is equal to the heart rate multiplied by the stroke volume. So if there are 70 beats per minute, and 70 ml blood is ejected with each beat of the heart, the cardiac output is 4900 ml/minute. This value is typical for an average adult at rest, although cardiac output may reach up to 30 liters/ minute during extreme exercise.
So for an average adult at rest the estimate is around 5 litres of blood per minute (~1.33 gallons)

· Cardiac Outout / second
There are 60 seconds in a minute so simply :
divide amount pumped per minute by 60
0,083̅3̅  L of blood per second
(83,33 mL of blood per second)
But this is just an average with specific variables defined... so maybe you have to take into account other factors that may vary this value.

· Factors Affecting Cardiac Output

Factors affecting cardiac output in a healthy but untrained individual
  could be:
Increase/ decreased in heart rate
Change of posture
Sympathetic nervous system activity
Parasympathetic nervous system activity can also affect cardiac output.

Heart rate can vary by a factor of approximately 3, between 60 and 180
  beats per minute, whilst stroke volume can vary between 70 and 120 ml,
  a factor of only 1.5.

You can read more here & here

How's the SV like at high rates?


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Can sleep be replaced by chemical supliments?
If adenosine makes a person sleepy to rebuild chemicals in the brain, than is it possible to inhibit adenosine and externally produce and inject the needed chemicals?

There is not only one substance involved in sleep (which is a sophisticated process); orexins and others have a contributory role. How would you know what to inject without a more complete understanding of sleep and its function?

Also, rebuilding chemicals is not the only function of sleep: it is also a method to remove toxic wastes, relax the body, and (possibly) maintaining & creating memories. So, no SLEEP cannot be substituted with chemical supplements.


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Can a protein kinase phosphorylate both a threonine and tyrosine residue?
I know that some kinases can phosporylate both serine and threonine residues because of their structural similarities, but can such a kinase phosphorylate a tyrosine residue as well?
If not, then why?

Ony a few protein kinases can phosphorylate all three amino acids — these are classified as dual-specific kinases (EC 2.7.12.1). Examples are APK1 from Arabidopsis or MEK kinases in mammals.
As with other enzymes, the residues at the substrate binding site determine which substrates can be accomodated there. Structures or Ser- Thr- and Tyr-kinases are available for inspection, should you wish to explore them.

Do you have a reference showing that the same catalytic domain in, for example, the MEK kinases phosphorylates both the Thr and Tyr simultaneously? I do know from working extensively with the MAPKs (Erk1/2 in particular) that the two residues can be under independent regulation. Part of that is obviously a function of different phosphatases, but I suspect there can be independent phosphorylation as well. Just not sure if it's by MEK1/2 or not.

Phosphorylation of MAP kinase by MEK at tyrosine 185 (pY185) and threonine 183 (pT183)...., ref: http://www.ncbi.nlm.nih.gov/books/NBK21529/

I have edited your original answer because, although essentially correct (+1), it had a mistakes in the EC number, and the Kegg link was specifically for MAPKs, whereas the Wiki page considers dual-specificity kinases, specifically. I also put in a link to the structures. As you had done the heavy lifting, I don't want to steal your thunder by posting an alternative answer. Do revert as you see fit.

Thanks for the edit! Can I give you half the credit?

@Ashafix yes, I'm aware of the "classical" understanding of the pathway, I'm talking about what really goes on in vivo.

Well, I guess more qualified people with some real hands on experience should comment on that.

@Ashafix OK, just wondering if you knew...