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Are there more descriptive ways of naming genes and gene interactions?
I couldn't help but notice just how non-descriptive the gene names that modern genetics is using. Currently I'm reading "The new science of Evo Devo" by Sean B. Carroll and here are some examples of gene names used:

Fzrb
Krox 20
Hoxa2, Hoxb4
ZPA
FGF8
sonic hedgehog

While these names identify genes uniquely, they do very little to express what and where the gene does, or how it is related to other genes (While FGF8 may be related to FGF7, it's relationship to XYZ10 is not obvious).
I get the need to uniquely identify genes , and the book is an example of just how hard it is to presently write about a lot of genes at once. The author creates a picture of what's going on, but the gene names get in the way. Even in cases where a gene has a semi-descriptive name, like "eyeless", the reader has to remember that it's actually the gene responsible for eye formation.
Are there are any efforts underway to systematize or name genes for a given organism in an expressive manner?
As a programmer, I write code for a living, and having descriptive names makes it easier to look at someone else's code, read about code and even discuss it with novices. For example:

initializeDataModel
createViewHierarchy
userDidSelectLayerAtIndex

Modern programming tools make using descriptive names easier, because of autocomplete - typing in the first few letters of a programming structure completes the rest. Even google has a list of autocomplete suggestions.
We are all familiar with the Internet, where biology.stackexchange.com/questionname resolves into a specific page. Stackexchange is the site we are visiting, and Biology is a subset of that site. There are other biology websites, but biology.stackexchange.com uniquely identifies this site. The use of "biology" in the address gives readers a general idea of what the site is about and relates it to other biology sites. Our web browsers resolve the address into a proper string of bytes and get the right page. What if we name genes like like

com.drosophila.eyeformation
com.chicken.limb.structure.ZPA
com.human.development.geometry/XYZ10

,and whatever technology we use would actually resolve that descriptive name into a gene or a series of gene interactions?

You are absolutely right and gene names are often horrid. Just wanted to point out that one of the genes on your list is actually quite descriptive: FGF8 is fibroblast growth factor 8, doesn't get any better than that.

@terdon Some have really huge full forms e.g. NEDD: Neuronal precursor Expressed Developmentally Downregulated; SNARE: Soluble N-ethyl maleimide-sensitive factor Activated protein REceptor ... :P

Many gene names are descriptive, e.g. DRD1: dopamine receptor D1, TOP2A: DNA topoisomerase 2-alpha, or PTGS1: prostaglandin G/H synthase 1. These are examples of genes that have a clearly defined main function.
The genes you listed are involved in development, and there describing the function of a gene becomes much more difficult. E.g. sonic hedgehog is involved in patterning many organs, from brain structures to teeth. How would you assign a descriptive name?
The analogy to (programming language) functions does not work for many genes, because they were not designed to fulfill one function, but evolved to do many different functions. For genes that have many functions, we just need a unique name. The multitude of functions is catalogued elsewhere.
(Bonus descriptive gene family name: MAPKKK: MAP kinase kinase kinase)

there are actually MAP4Ks as well - Mitogen Activated Protein Kinase Kinase Kinase Kinases :)

Maybe there's a higher level of abstraction then, like gene interactions or cycles that can be given descriptive name?

@AlexStone: there are pathways that can be given a nice name, e.g. http://www.genome.jp/kegg/pathway.html -- but even then there will be more functions to the pathway than what can be encapsulated in the name

In theory, your idea seems reasonable, but I can see at least to problems with implementing it.
First, the situation is complicated by the fact that genes often carry out multiple functions, and a single label is often insufficient to annotate the complete functional repertoire of a gene. @MichaelKuhn made an excellent point with regards to the evolution of gene function. When one stops thinking about a gene (and its protein products) as something that was designed to fulfill a specific purpose, but rather as something that has been adapted (often serendipitously), for better and for worse, to fulfill a particular set of functions, the difficulty with annotating gene function is a lot clearer.
Second, this idea is confounded by the fact that reliable functional annotations are really, really rare. Sure, lots of genes in human and yeast and Drosophila have been extensively studied for decades, and many of their functions are well understood (at least we think they are). But for the vast majority of genes for the vast majority of organisms that have been studied, functional annotations are inferred from sequence similarity to previously annotated genes, without any additional experimental validation. Of course, every genome project would love to functionally classify all of the genes for their pet genome, but this is really expensive, time consuming, and low-throughput. For every extensively studied, well annotated gene, there are literally hundreds of analogous genes in other organisms that have been annotated solely based on sequence similarity to this gene. As disappointing as this is, it doesn't seem like it's going to change any time in the near future (unless there are some drastic improvements in the throughput of gene function annotation). So any proposed nomenclature convention that does not address this reality is quite inadequate in my opinion.

Are there are any efforts underway to systematize or name genes for a given organism in an expressive manner?

As you observed, the genes are named by their discoverers and some genes usually have anecdotes behind their names. Since gene names have to be small it is difficult to systematically describe them completely. But gene nomenclature can adopt a certain way of classification and it has been used extensively in yeast; genes are named by their chromosomal locations (This was done in an age when cytogenetics was more developed than functional genetics. So you can understand why it so happened). Some genes were named after the processes they are involved in. For example cdc2, cdc48 etc (cell cycle control)
Check this site: it has some guidelines for gene nomenclature.
But I completely agree with you that there should be a standard way of nomenclature. Perhaps it shall happen when functional genomics gets saturated.

This is of only peripheral relevance, but I think that you have got the history of yeast genetic nomenclature backwards. For decades yeast genes were defined functionally and were named accordingly. So, for example, the CDC genes (uppercase = dominant form, usually wild-type, lowercase = recessive form, usually mutant) were described by Lee Hartwell in 1970, about 25 years before the yeast genome was sequenced. At this point ALL of the ORFs/genes were given a systematic name (e.g. CDC1 is YDR182W). The aim is, however, still for all genes to be given a name relating to function as well.

I think it seems like a good idea at first but...
You have to take into account that as has been said genes might have multiple roles, sometimes very different and for most of them functions are still unknown.
So It's very difficult to classify a constatly changing promiscuous set of things. Even the gene concept is changing (Hello, ENCODE :)).
To me It's a lot easier to leave names as short as possible with some hints of they role (just the way they are) and if you're interested in the specific function, a very quick visit to a database and using the list as input will provide you with the current description and/or function of the gene.


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How do cells slowly degrade 5,5'-dibromo-4,4'-dichloro-indigo?
5,5'-dibromo-4,4'-dichloro-indigo is the product of X-gal cleavage, often used as a reporter with B-galactosidase. I've made the (unreferenced) observation that it seems as though the blue product slowly degrades over periods of time within the cell, allowing for cells to lose their blue coloration.
What mechanisms can explain the degradation of 5,5'-dibromo-4,4'-dichloro-indigo within cells?

Can be 3 reasons: 1. Dilution 2. Reductive conversion to colorless leuco-indigo 3. Metabolic decay: I suspect the metabolism would be similar to that of purines

^ that was purely speculation

Indigo compounds are so damn insoluble I don't know if you can get it into an enzyme easily. I've made indigo ( not the x-gal indigo in the question, but same core structure ) just for fun while my boss isn't watching, and I haven't found any solvent that will dissolve it. But maybe glutathione can slowly reduce it. When I reduce the indigo I make, I use sodium dithionate and boiling water. GSH wouldn't be as powerful, but you don't need it to work as quickly. More pure speculation.

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Recent and good quality articles on systems biology
I'm a biotechnology student and I have to write a sort of non-experimental thesis (30 pages long) within the end of a three years study.
I'm very interested in the "systems biology" field and I'm searching good (innovative) and recent (max 3-4 years old) articles about this subject, but unfortunately I've found my research more difficult than I expected.
I'd like to focus on not immediate/easy articles and possibly containing new and promising approaches.
Does anybody have suggestions?
PS: it all started from Uri Alon's great lessons on YouTube.

Welcome to Biology SE.  Unfortunately, your question is very broad - there are many topics (not even getting to papers) that fit your criteria.  Are there particular types of techniques (or objectives) that you are interested in?

Maybe we could start with asking for a list of the most interesting problems currently being worked on in systems biology... what do you think Mattia?

Thank you for your answers. I have been broad because i'm not interested in nothing in particular, moreover I don't want to miss something (I'm ignorant in the field, mainly fascinated) that you may think very interesting. I need however that the subject has already been studied in an article. I'm willing to eventually study hard on it for fill my gaps.

I'll have a go at a short list.  This is more of a highlight and primer sort of response to a somewhat subjective question so pardon if this isn't what you wanted. I don't have paper references for all this, but I'll try to come back and add some later - I usually only have half an hour or so to write an answer so bear with me.
Synthetic biology as defined as the use of genes and promoters to engineer cells or even multicellular organisms like devices is a major category.  I like browsing the projects from the iGem Competitions.  A couple of outstanding efforts in this field are the use of photoreceptors to program E coli gene expression and the general effort to create logic and computational circuits in the cell.
A major application in systems biology is engineering cells to produce new chemical compounds or to overproduce compounds.  A classic example (sort of old, but still pretty outstanding) is the engineering of E coli to produce the antimalarial drug artemisinin at levels which would enable world wide release of the drug.  This has inspired efforts to produce fuel from algae and bacteria as well.
If you define Systems biology as being often concerned with modeling some or even all the biological processes of the cell, there are probably too many major efforts to cite, but this is just a list of some favorites.
There are lots of papers focused on flux balance analysis which models how the metabolic machinery processes and synthesizes all the scores of chemical compounds that make up a cell.
Another category of synbio tries to take the genes found in a genome and model the actions of all the genes.  One of the most exciting papers to come out in this sort of systems biology is the whole cell model of Mycobacterium genetalium.  Using data from a massive effort to characterize every gene in this very small genome, the model consists of over 20 specific models which have combined to make a very impressive simulation of the entire cell dividing.
Then there is metagenomics, which looks at the different populations of microorganisms and tries to look at how they vary with different environmental conditions. A recent paper that's exciting is the review of how different bacteria dominate in the gut of obese mice and people (several references in the link).  A tour de force in metagenomics was the global sea survey.

Thank you for your list, the whole cell model is very exciting! And pardon me for the broad question, I'll keep it in mind in the future.

I personally wish more sorts of questions like this were around more - having a good conversation about ongoing science is kinda hard to find on the internet...

I agree with you, but maybe this is not the right place to discuss of it since my answer has been closed. I'm trying to figure out what is my favourite subject, so I will ask again but with more precision.  For now I am focusing on flux balance analysis and on the cell simulation article (that has an exhaustive 100 pages long supplemental document).

This question is extremely vague, and can't have any real answer without you specifying a question or at least focus. Keep in mind, there is no high-road to research, you will have to dig in and start reading papers to gain understanding of your field. If you want help from others, you should at least take time to list the papers that you have already read and why you liked them to give readers a flavor of your interests.
To start you off, consider this Google Scholar query for systems biology since 2009. If you've read specific older papers that you've liked, for example this popular 2002 minu-survey:
Kitano, H. (2002). Systems biology: a brief overview. Science, 295(5560), 1662-1664.
Then you can learn how the field has advanced since by doing a forward search in Scholar (and restricted to 2009+). Hopefully this will provide you will some ideas so that you can ask a more precise question!

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Is wiping with RNAse Zap enough to destroy RNAse activity?
From the RNAseZap MSDS, it is an SDS at some unknown concentration, maybe with some NaOH?
Some other links suggest there is some NaOH as well.
The Ambion site states that RNAseZap destroys RNAse activity on contact, but they also instruct to rinse with water twice after wiping RNAseZap on the surface being cleaned.
So, does RNAseZap actually destroy RNAse activity, or is it simply a "good detergent" to pick them up and rinse them away?
Thanks!
Carmen

Look up their patent. I remember it was an ammonium salt.

It's hard to know what RNaseZap does since the ingredients list is a trade secret.  However, I expect it is a lot more than just detergent.  RNaseA is extremely hard to destroy; moreover it can easily renature once the denaturant is removed. Therefore, very minute quantities are sufficient to annihilate RNA experiments.  The historical method of purification was to boil solutions of it until all other proteins denatured and could be easily separated. I can personally attest that you can precipitate it in pure alcohols and it will spontaneously refold as soon as it is rehydrated.
I would not trust a simple detergent to get rid of it; you'll need something more volatile to be reliable.  A lot of "home made RNaseZap" recipes on the internet include hydrogen peroxide, which causes a variety of covalent modifications to the protein.  It also has the advantage of cleaning itself up (eventually turning into H2O).  The detergent is useful because you typically don't want any protein residue floating around your experiments, denatured or not.  If you have some dried RNaseA aggregates, it will also help break those up.
I work with RNaseA itself, so I can't personally vouch for the recipe below (since I'm not interested in destroying my sample), but it seems sound.  But if you have the cash to blow, just get the RNaseZap.  It's very widely used by RNA labs and you really don't want to chance a potentially expensive experiment on it.  Especially since you're constantly shedding tons of RNaseA from your skin, being sloppy will probably bite you eventually.

Mechanism of action for H2O2
plausible recipe

The Ambion's RNAseZAP is not a detergent but contains chemicals that denature RNAse, the step of rinsing with water is necessary in order to clean up the chemicals as well as the denatured proteins left.
It is highly recommended as it completely wipes out the RNAse and the experiment can be run safely. No need to risk time, money and samples.
So, to sum up, it is not a detergent, but a solution that denatures proteins.
Good luck!

Thanks! Is this denaturing irreversible?

The MSDS reports to contain only a 'trade secret' surfactant in the range 1-20%. Why you say it is not a detergent?

Which chemicals that denature RNAse could it contain?


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Does bleach destroy RNAse activity, and if so, how does it do it?
I am working with RNA samples, and I'm trying to be very careful about RNAse contamination.
I have some questions about bleach, though. Some people say that a solution of bleach is enough to destroy RNAse activity, but is it really? How does it do it?
I'm not sure if wiping the surface using a solution of bleach would be enough to kill RNAse activity, or if it is necessary to use products such as RNAseZap or RNAseAway.

RNAses are enzymes, and there are various ways to inactivate them. Unfortunately, RNAses are rather stable proteins and autoclaving doesn't completely kill their activity. The common methods to inactivate are unspecific methods that will destroy any enzymes, either through covalent modification or degradation.
The most common methods for RNAse inactivation are:

Treatment with DEPC. This covalently modifies histidine and a few other amino acids, which will inactivate RNAses.
Heating to 200-250 °C for at least an hour, this is most commonly used for metal and glass equipment
Incubation with 1M NaOH for an hour at 37 °C, which will hydrolyze proteins

Using bleach is not a method I've used, but it should work in principle as hypochlorite will react with proteins.

I think they are asking how to clean surfaces like benchtops.
Bleach might work. But a better solution would be to get a box of aluminum foil. The processes for making the foil are very harsh, so it's doubtful any protein would survive the process, not to mention that there are no proteins involved in aluminum manufacture to contaminate the process. Just be sure to always use gloves when handling the foil or you'll contaminate it.


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What is the mechanism by which Melatonin increases dream vividness and intensity in humans?
I'm looking at the wikipedia article on Melatonin and noticed that it mentions vivid dreaming caused by melatonin. I have the "Melatonin and the Biological clock" pamphlet referenced in the article, and it does not go into too much detail of how vivid dreaming is happening.
I've personally experienced vivid dreaming side effects of melatonin today - dream after dream of profound intensity, but completely unrelated content. This makes me interested - how does melatonin influence the intensity of dreaming in humans? Is it by interaction with Serotonin? Or does it get metabolized into something psychoactive?

Check this out. Not accessible to me at this moment.


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Why are certain aneuploidies more common?
Certain aneuploidies such as trisomy-21 (Downs syndrome), trisomy-18 (Edward syndrome), Turner syndrome (XO) etc are more common than others.
I had a vague thought that it is related to chromosome size: the chromosomes which are towards the extremes of size will be affected in an improper segregation event.
Chromosomes 13, 18, 21 and Y are among the smaller chromosomes in humans, and are commonly associated with aneuploidy (but 22 which is also small is not affected). The larger ones are unaffected (X is an anomaly).
I thought that longer ones should be more affected because more cohesin bridges have to be broken, but it seems that is not the case.

Is there any association of chromosome size and frequency of aneuploidy?

EDIT

If the difference is because of differential lethalities then does the length correlation still hold true? Smaller the chromosomes, lesser the genes and hence lesser would be the effect of extra copy on the cellular biochemical networks.

re: lethalities, I'd say it still depends on the genes and the dosage (extra or missing copy). Not all gene and dosage combinations are equally essential/lethal.  I don't think average "biochemical activity" is going to be useful.  What would be interesting is if someone had measured the fitness of specific gene deletions/duplications.  Also, are genes "essential" for the completion of embryonic development equally distributed among the chromosomes? Unequal distribution would obscure any length correlation.

I thought it was just that the other aneuploidies were fatal. They occur as often but miscarry earlier in the term therefore you don't see them. So basically there are only three that are viable 21,18 and the sex chromosome with a number of combinations: XO, XXY, XYY and XXX.
More information here:
http://www.nature.com/scitable/topicpage/chromosomal-abnormalities-aneuploidies-290
With regard to the frequency for each chromosome:
For males (i.e., sperm; source):

The mean disomy frequency is 0.15% for each of the autosomes and 0.26%
  for the sex chromosomes. Most chromosomes analyzed have an equal
  distribution of disomy with the exception of chromosomes 14, 21, 22
  and the sex chromosomes, which display significantly higher disomy
  frequencies.

Size of the chromosome is frequently reported as a factor in the frequency.
For females (i.e., eggs; source):

The data is obviously harder to attain. One study from IVF treatments
  show differences in the frequency of different chromosomes at
  different stages in meiosis.

there is some statistics in the link that you provided.. it doesn't actually say that other aneuploidies were reported in stillbirths or spontaneous abortions

this is still quite a likely explanation - there is very little or no data for pregnancies that terminate before the foetus is smaller than a pea.  Almost all extra chromosomes for instance come from sperms and ova formation and they may simply not compete for fertilization.

This is the answer. They all happen with similar frequency, however most are lethal. The less lethal the more common, hence trisomy 21 or Downs being fairly common; however most trisomy 21 foetuses do die before getting to the second trimester.

@AndroidPenguin.. The two papers in the answer suggest that the probabilities are not uniform..
It seems so that the aneuploidy prone chromosomes are relatively smaller..

Trisomy 13 also doesn't always lead to miscarriage / stillbirth


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Highly spherical Radiolaria; does this image accurately depict the organism?
If I understand correctly, Cenosphaera spp. is a type of Radiolaria, which is a type of zooplankton.  The following is an image of Cenosphaera spp. is from the supplementary material (Figure S2) of the following paper:

F. Lejzerowicz et al., Ancient DNA complements microfossil record in deep-sea subsurface sediments, Biol. Lett. (9) 2013.

Question: Does this image accurately depict the organism?

More specifically, in other images of this organism, there are numerous thorns pointing outwards.  Is this thorn-less version a natural variation (or e.g. the result of the process of imaging the organism)?  Also, is it largely a sphere with a hollow inside?
The authors give the following description of the process involved in obtaining these images.

Eighteen sediment samples were wet washed over 63 μm and 20 μm sieves. The >63 μm residua were dried and picked for radiolaria and foraminifera. From most samples all specimens were picked. Rich samples were divided with a dry microsplitter into fractions, from which at least 100 specimens were picked for each group. Specimens were arranged by taxa on micropaleontological slides. Radiolaria are classified on the generic level, according to the classification utilized by [8]. Foraminifera above the species level are classified according to [9]. In addition, for radiolaria, the 20-63 μm fractions were soaked in peroxide, then washed with tap water and propanol. For each sample, a few drops of suspended material was left on a glass to dry, covered with Durcupan ACM resin and a cover glass. The micropaleontological slides were analyzed under Olympus BX50 light microscope (electronic supplementary material, figures S2 and S3).

In terms of their hollowness, they all (at least, when they're alive) will have the actual cytoplasmic mass (the organic bits) inside. What we see in the picture, and classify them by, is the mineral exoskeleton.

According to the Marine Species Identification portal, the presence of these thorns is variable.  They also vary in size, shape, and the presence of polygonal frames.  I don't think there is anything about the imaging process described that would result in the uniform loss of spines (unless the sieve/microsplitter broke them all, but I think that would be a non-uniform loss).
Re: whether it's hollow or not, that appears to be variable too.  One species is filled with oil, while another appears to be hollow.

The genus Cenosphaera has indeed been used to qualify fossils of Spumellarians (an order of polycystine Radiolarians) that consists of a single, hollow, spherical shell. The biological meaningfulness of this definition is however unknown.
The very small external thorns that one can see on the picture you're showing are thought to be secondary growth and therefore variable with the age of the specimen, the availability of silicon in the specimen water column and the state of preservation (if it is a fossil).
When alive those species fo course are not hollow inside. The cytology of spumellarians is not as well known as the cytology of Nasselarians (read papers from Cachon, Hollande or Enjumet if you're interested or this nice review from Suzuki & Aita) but they do possess for sure a cytoplasm separated by a capsular wall into a dense endoplasm and a loose ectoplasm.
NB: The reexamination of the specimens Ehrenberg used to described his first species of Cenosphaera (Cenosphaera plutonis, de facto type-species) showed that this specimen was not actually a single-shelled spumellarian, hinting that this genus name have been probably misused in 150 years of radiolarian research.


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Which X-Y chromosomes have the developmental genes for mammals?
I know that for a given mammal, half the chromosomes come from father and half from mother. This is typically denoted as x-y. I've recently read about "toolkit" genes that control how a cell develops into an embryo into an organism. I'm interested which set of chromosomes(x,y or both) contains these toolkit genes for development of an organism from a fertilized cell?
In other words, does an X chromosome know how to build a female and Y chromosome how to build a male, or is it some "overriding" of developmental instructions that Takes place when Y is present?

Can you clarify what "toolkit" genes you are referring to? Do you have a link/citation for the source you read about them from? I'm guessing you are not referring to the toolkit genes listed here, so a bit more clarity might be helpful.

That sounds like the toolkit genes I'm referring to

First, while half the chromosomes come from each of the two parents, these two sets of chromosomes are not termed X and Y (they would usually be called maternal and paternal).  The terms X and Y refer to potential members of just one pair of the 23 pairs (in humans) of chromosomes, and X chromosomes can come from either the mother or the father.  The presence or absence of a Y chromosome determines sex in mammals.
The Y chromosome contains one gene, SRY, which determines sex, and almost no nother genes.  SRY simply switches on the "make a male" program in the cells.
Essentially all other genes, including any toolbox genes, come from both parents, one copy from each.  (An exception, in males, are those genes on the X chromosome, which in males are present in only one copy and which came from the mother.  Another exception is mitochondrial genes.)

In addition to @mgkrebbs response, I'd add that many genes are controlled by epigenetic mechanisms which may mask one of the parental copies by methylation.  This can be a specific effect where, the active gene is specifically from either the father or the mother. Mosaicism, where one copy of gene is randomly inactivated in any given cell, is also possible.  The classic example of this is X chromosome mosaicism, where the entire X chromosome in each cell of a female is silenced. (At least in the case of humans and animals like humans)

There's also this really cool example of a gene for a voltage-gated potassium channel, in which the paternal copy is methylated by a paternally-expressed ncRNA from the same locus (that site is methylated maternally).  If this is disrupted, it results in developmental defects. <Shameless plug for an unanswered question of mine that has the relevant links.>

There are surveys of such genes from mouse studies, my favorite is MEST. I took a shot at that one @dd3 :)


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Does biofuel production by microalgae need an extra source of CO₂?
It is necessary to have extra source of CO2 i.e. from a nuclear reactor or factory chimney to produce bio-fuel by microalgae or is it able to do it with the normal CO2 density in the atmosphere?

I think your question needs some clarification to be answerable.  Algae need $CO_2$ as a carbon source for photosynthesis but the source is irrelevant.  Are you asking if industrial scale biofuel production can be sustained at atmospheric $CO_2$ concentrations?

@KennyPeanuts: Exactly. Is it possible to produce bio-fuel from  micro-algae at industrial scale at atmospheric Co2 concentrations?

That is definitely an interesting question but I am not sure it is a biological question as much as an engineering question.

I asked this because it is claimed to change the world by providing green fuel, but if it needs high concentration of Co2 then it cannot exist in a complete green world (needs pollution for existance)

OK so that sounds like a slightly different question... it sounds more like you are asking if algal biofuel production could lower atmospheric $CO_2$ concentrations to the point where it is no longer possible.  I think the issue here is that the industrial process that "farms" the algae could concentrate the $CO_2$ in the bioreactor so that the atmospheric $CO_2$ concentration isn't that important.  There was certainly lots of algal production when atmospheric $CO_2$ was 280 ppm, so that is plenty to get them to grow.

@KennyPeanuts: So it is possible at industrial scale with normal Co2 atmospheric concentrations. If it is true, write it as answer and I'll accept, thanks for your time.

Maybe this is easiest understood comparing to our current rate of CO2 consumption to the possible industrial CO2 absorption rate.
Human non biological CO2 production is 29 Gtons.  A little more than four tons of carbon per human being each year.  The natural carbon cycle on the planet through CO2 is otherwise about 788 Gtons.

Is it possible to grow enough algae to balance our current rate of industrial production? I think so - it would be an additional 2% of the current carbon cycle.  In a first pass, that implies turning 2% of the non-productive earth surface into an average patch of ocean or forest/jungle.
This is possible, but it would be expensive.  we're talking about flooding a desert basin for algae production. (numbers are from google).
2% * (area of earth surface = 197million miles^2) = 3.9 M miles^2.
Sounds doable, but remember that 70% of the earth's surface is already water and producing algae at a pretty good clip.  We'd be using ~6% of all the land for the algae farm:
For comparison,  3.9M miles^2 is larger than the continent of Australia.  (2.97 Million miles ^2), and bigger than the Sahara desert (3.6 M miles^2).
just to get into the questions raised in the comments.... To DEPLETE the CO2 level in the atmosphere, we'd have to produce more fuel from the algae than we use - which seems to be impractical from a market standpoint - the fuel would be sitting around in warehouses while the plants die.  I can't imagine anyone making any money from this, and it would be expensive... so it'd be a strange set of circumstances that would deplete the atmosphere from carbon dioxide.  Also more oxygen probably would encourage more combustion and more animals too... so hard to see this happening.

Amazing answer. This is not my field of specialty but listening at a conference, the bio-fuel plants were planned to be near factories and nuclear reactors to use their extra Co2, so I was curious to know, if we produce enough bio-fuel then there would be no need for reactors/factories and is it possible to continue producing bio-fuel without these source of pollutions or bio-fuel plants get shutdown.

nice answer....

Thanks, both! I think we'd still need power plants to convert the biofuel to energy (unless its bioelectricity or biohydrogen). With a projected population of 12 billion, demand for fuel is just going to go up. I think they were saying that from the plants/factories you can pump the CO2 directly into the pools of algae. I'd like to see numbers on how this might prevent the CO2 from getting into the atmosphere. Could help... we used to bubble CO2 into the algae in the lab to help it grow. I would be surprised if it changed the efficiency of an effort this size by more than a few %..?


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The Eye, and Camera Lenses
How do near sightedness, farsightedness, and normal sightedness work? If the eye is accustomed to one small focal point, how can it manage a wall of light? And also, how does it process the small pinpoint that it normally does?

This question has brief explanation of some common problems with focussing

I think I understand what your issue is here.
Often, in diagrams of lens systems and eyes, the diagram will only show rays parallel to the optical axis (see here). Although many optical systems are designed so they are optimal for this axis, off axis rays respond in a fairly predictable way too. This figure shows an off-axis point source, which focuses at a corresponding off-axis point on the other side of the lens.
So, there is "one focal point", as you say, for each position of the object relative to the optical axis. In optics we generally talk about a focal plane rather than a point, as the focal point only refers to cases of idealized point sources, lasers etc.
Now, the aperture (pupil) is a completely different matter. This provides a limit to how well an optical system can focus. When the aperture is small, it can focus really well, but not much light can get in. When it is large, the ability to focus is reduced but it allows one to see better in the dark (increasing the signal to noise ratio). Focusing requires all the rays from a source to end up at the same point on the retina/film, the aperture, when it is as small as possible "selects" only those rays that will end up focusing at exactly the right place (assuming the lens focuses to the right place, which it does not in the case of the short or long sighted). This selection cuts out a lot of the light, and often it is good to trade off the ability to focus for the amount of light. Without going into detail, this large aperture results in the focal ability of the optical being strongly dependent on how far away the object is (see this).
Your question is rather open ended, but I hope this is what you were getting at.


text:
What is an epistasis group?
I have been trying to wrap my head around the concept of epistasis for a couple of days now, and I think I understand it, at least at a basic level, but I still don't understand some of the ways that the term is used.
What does it mean if gene A is epistatic to gene B? Does this simply mean that gene A masks the phenotype of gene B when expressed? or is there more to it?
Also, what does it mean when genes are in the same epistasis group? I am currently studying the transcriptional up-regulation of PSY3 in yeast as a result of UV treatment. PSY3 codes for a protein that forms the Shu complex along with 3 other proteins. One paper I am reading states that PSY3, is in the same epistasis group as the three other genes that code for these other proteins. What does this mean?

What does it mean if gene A is epistatic to gene B? Does this simply mean that gene A masks the phenotype of gene B when expressed?

Yes.  Note that this does not say anything about mechanism. If A converts 1 to 2, and B converts 2 to 3, then A is epistatic to B, but A is also upstream of B.  In a signaling pathway, say B inhibits A and prevents it from signaling. A mutation in B allows A to signal. A mutation in A means there is no signaling. Mutations in both A and B means there is no signaling: A is epistatic to B, but A is downstream of B.
An epistasis group is a group of genes in the same pathway.  Knocking out any combination of these genes will not result in a more severe phenotype than knocking out the most "sensitive" of these genes (the single mutant with the most severe phenotype).


text:
How long can a naked human survive on Mars?
How long can a naked human survive at the surface of the Mars planet?
For instance, let's say a worker's base takes fire while he sleeps, the building is totally ablaze and he can do nothing but run to the emergency building 200 meters away without any respiratory equipment, pressure suit, UV protections or anything.
Maybe a human could survive for a rather long time, and apnea time is the real limiting factor?
Climate:

Temperature: 27 °C to −50 °C (base is at a rather warm location, on Equator)
Pressure: 0.006 bar (Earth: 1 bar)

I think two things might be the issue: 1) lack of atmospheric oxygen and 2) the dust.

@dd3: Don't hesitate to propose an answer around this :-)

Frost Burns are likely to be the real killer here. Lack of blood flow due to constricting vessels means that cells and tissue could freeze solid from the dramatic temperatures

"You should only ask practical, answerable questions based on actual problems that you face" - I'd take care if you're planning to test this ;-)

@RoryM: It is actually a problem that might be faced: http://mars-one.com Of course, more serious research must be performed eventually :-)

@NicolasRaoul ah glad im not the only one aware of this site! You planning to apply hence the question?

I did wonder if it was related to Mars One :L

Long story short, the astronaut probably wouldn't make it, and would first loose consciousness then suffocate.
There is a lot of myth and hollywood dramatization regarding this kind of thing. Here are some:

You will explode. This is just ridiculous. The skin is air tight (relatively speaking). It is also very elastic and can pull and bend quite a great deal before tearing. Through quite a few, equally durable, tissues, it is connected to the bones, which are unaffected by negative air pressure.
Your blood will boil. The circulatory system is also a closed system. It is not directly exposed to the environment. Also, the blood pressure in a healthy person is averaged around 100 mmHg and Earth's atmosphere at sea level is 700 mmHg. There is already a massive disparity, yet Earth's atmosphere doesn't go pouring into our veins at random. Likewise, the blood in a person's veins won't go pouring out into the atmosphere simply because the pressure is extremely low.
Any air in your lungs will be forcibly sucked out of you. Again, this is a closed system, if you hold your breath. As long as you don't try to breathe there is nothing forcing the air from your lungs.
Your eyes will be sucked from their sockets. Thank you Total Recall (the original) for this myth. The eyes are very firmly in place. You might feel a pull on them, but they aren't going anywhere.

Absolutely none of these would happen in the vacuum of space and certainly not on the Martian surface.
Here's what will happen:
Any liquid material on the surface of your body will vaporize. All sweat, saliva (if you open your mouth), water in the mucous, and tears on the eyes, will nearly instantly vaporize. It would be quite uncomfortable, especially the eyes, but very survivable. Long term exposure to a vacuum might damage the eyes eventually, but in this scenario there are far more pressing matters.
The negative pressure may also cause your eardrums to rupture. Try to imagine the feeling your ears get on the plane at 30 thousand feet times about 100. Since you can't close your ears, plugging them with your fingers may help, but likely just postpone the inevitable pressure disparity, which will lead to at least great discomfort and possible drum rupture.
If you had the chance, you should take a deep breath before jumping out and avoid trying to breathe at all costs. Opening your lungs for a breath would very quickly draw whatever breath you had in them out into the atmosphere and also vaporize any fluid that was in them. Considering the rapid pace of this event, you would surely have permanent damage from this and begin suffocating and will die in a minute or two unless you get medical attention. There seems to be conflict in the procedure for this, with some sources suggesting that emptying your lungs would be better to avoid this. Considering the astronaut in your example is about to do a 200 meter dash he is going to need all the O2 he can get.
The cold is also a treacherous factor. At -50C the heat from your body would dissipate so rapidly that it would likely be very debilitating, perhaps causing you to seize up and clutch your extremities to your chest. It would also be excruciatingly painful. It might cause you to fall into shock. In a total vacuum however, this does not exist. A vacuum is actually very insulating, but on Mars' what little atmosphere is there is enough for you to feel the chill.
The lack of oxygen and high CO2 would be what would eventually kill you. You would eventually try to breathe and loose consciousness within a breath or two (or you might loose consciousness first then your body would try to breathe naturally). Your body would try to keep you alive as long as possible by pumping your heart faster and increasing your blood pressure, but your heart would eventually fail and you would die within seconds after that.
Evaluating your particular scenario
There are first a few things about the scenario that seem unlikely.

The astronaut would not be naked. They remain in some of their protective gear in case of emergencies like this. He would have some protection against the cold if he had to run out without it.
Certain things like extinguishers are always nearby. The idea that one was unreachable is a little silly.
Space vehicles, shuttles, and buildings all are compartmentalized like a submarine. They could simply close off the affected areas.
Fire only burns in the presence of oxygen (with few exceptions). After being closed off, compartments can be decompressed, halting the fire immediately. They can then begin refilling them with breathable atmosphere. This poses the same vacuum problem if the astronaut is in the affected area, but he won't be trying to run across the surface naked. People have survived rapid decompressions before without a single injury, as listed in my second source, however, others have never regained consciousness.
Assuming you made it to the other building, they usually only open from the inside. So unless someone saw you coming and opened the door for you, your last minutes would be better spent desperately fighting the fire until it consumed you rather than banging on the neighbor's door.

But let's say all of this breaks down and poor Astronaut Joe finds himself making a mad, streaker's dash across the Martian surface.
We should assume that our astronaut is both quite athletic and knowledgeable about the environment outside of his shelter, knowing that he should take a deep breath before heading out, but literally has no time to grab a shirt, goggles, breathing mask, or anything. Just him and Mars.
If he's lucky, it's not too cold and he doesn't seize up and fall into the fetal position within a few steps. Let's say it's -20C, which is pretty darn cold, but tolerable for a minute or two. I next see him flailing across the surface, trying to run in Mars' low gravity (no easy task). He begins to loose vision as a cloud of steam of what should be tears pours from his dry eyes. His eyelids then begin to stick to his eyeballs because there is no longer any lubrication. He is desperate to reach the other building, and his movements get more and more erratic, as his body is rapidly using all of the available oxygen. All the while, he is still holding his breath, knowing that if he attempts to breathe he will likely collapse within seconds and perish. But the more he struggles to make it, the more his innate urge to breathe overpowers his conscious thought to prevent it. Eventually, against his own willpower, he gasps and attempts to inhale deeply. He takes two or three dying breaths, if they can be called that, then falls to the ground unconscious. He dies shortly after when his heart stops and his brain tissues die.
The whole ordeal lasts under 30 seconds and he is 100 meters at most away from his shelter. If he did get lucky and actually made it to the other building, he would likely have frostbite over much of his body, permanent damage to his eyes and ears, and possibly deadly exposure to cosmic rays.
The event would be very similar to being drug by a fishing line to the bottom of the sea and drowning.
Sources:
A fun questionnaire to see how long you would last in space
What really happens in a vacuum

Temps vary between 80F and -199F, averaging -64F. So while it's cold on average, the temperature could certainly be reasonable enough to not be a factor, and it's reasonable to assume that a habitation would be on the equator, so would be warm at least at midday.
I'd argue a fit, healthy, trained person with time to aerate in the air lock and who's life depends on it could hold their breath for three minutes at a push. At walking pace on earth, it takes almost three minutes to walk 200m. Cutting it close, but it's a problem of low pressure, gravity, and oxygen, not necessarily temps.

Then again, I'm going by my experience while swimming - and the diving reflex is a thing, so you may be right about the 30 secs, after all.

I joined this community just to add this comment, this answer is wrong in so many ways, please disregard it and don't consider it's length as merit for it's correctness.  @fredsbend, please consider deleting -

@ccook I certainly will consider deleting it ... once you show why it's wrong. If it really is wrong in "so many ways" then I think an answer showing what is the correct answer would be the best course.

@fredsbend, in short: 1. chest cavity explodes from 14 psi over large surface area of lungs.  2. It's a gauge pressure difference, your blood pressure is higher than atmospheric, second, gases release due to partial pressure releasing dissolved gases.  This is called the Bends.  3. This is just physically wrong, just like a balloon you will expel the gas in your lungs through your mouth if you dont rupture elsewhere.  You cannot hold 14 psig.  4.  This is true because your head and eyes are made of liquids, which are incompressible (right conclusion, wrong reason).  [1 of 2]

@fredsbend [2 of 2] for the what will happen paragraphs 1. Closing your mouth will not allow you to hold any appreciable pressure.  Try getting a pressure gauge to read 1 psig by blowing on it. 2. This is conjecture, where ironically, opening your mouth serves to protect your eardrums (yawning to fix ear pain in flight.  3. This is against all general advice.  4. Thermal and pressure scales are dramatically different, one is at the speed of sound, the other takes many minutes - pressure gets you not temperature.  5. It takes more than a breath or two to run out of oxygen (its pressure related)

@fredsbend and see this for cases showing survival in vacuum on the scale of minutes:  http://www.scientificamerican.com/article/survival-in-space-unprotected-possible/

@ccook Thank you for responding. From the article: "Vacuums are indeed lethal: Under extremely low pressure air trapped in the lungs expands, tearing the tender gas-exchange tissues. This is especially grave if you are holding your breath or inhaling deeply when the pressure drops." I believe one of my sources mentions this, yet also mentions it may not be the case. Whether to hold your breath or not seems to be a point of contention. I suggest a breath because he's about to sprint; he'll need the oxygen.

As for the rest of your comments, I'm having trouble seeing what you are referring to. Perhaps starting a chat room would be best, then you can quote the part of the answer you object to, then list your objections.

And, yes, some have survived minutes of vacuum exposure, but all I know of have lost consciousness in under 30 seconds.

Mars is at about 1% Earth atmosphere. Space is much less and the pressures in the tests that article mentions says did it at about 0.25%. I figure the extra pressure allows a bit more time of consciousness. Indeed, it is true that he may lose consciousness before trying to breathe, but that paragraph is a dramatization, not necessarily textbook reaction. All the other stuff in the answer is.

Perhaps a few things can be clarified, specifically, you're likely to lose consciousness in the first 30 seconds due to the pressures, but we don't know for sure if the extra pressures on Mars is enough to keep you conscious longer. I may edit this weekend if I have time.

@fredsbend When doing an emergency ascent from 10m (2 atm), divers are told to exhale constantly and steadily to prevent lung over-pressure. (See Pulmonary Barotrauma, CESA).

I really like the effort put into this answer, and it was eye-opening for me in several ways. However, I still gave a downvote because there was still a big issue unresolved: "closed system, if you hold your breath. As long as you don't try to breathe there is nothing forcing the air from your lungs...Absolutely none of these would happen in the vacuum of space". Actually, air would still get out. There are more orifices other than one's mouth, and they can never be all closed perfectly tightly, especially since the man is naked.

@rhyaeris If you hold your breath, how much air can actually escape in 30 seconds. Half a breath? A quarter breath? I'm betting much smaller. Is it significant enough to mention?

@fredsbend https://m.youtube.com/watch?v=pm6df_SExVw please see 1:53. In vacuum, air can escape quickly through several orifices, simply due to the vast pressure difference.

One other important event that can kill the person is that the atmospheric pressure on Mars surface is less than one percent that of earth at ground level. Suddden exposure to extremely low atmospheric pressure will immediately release dissloved gases within blood and and other body fluids as bubbles and the individual is likely to get a very severe form of Decompression sickness as in divers coming up too fast. The person is likely to lose conciousness and die within a couple of meters after leaving the shelter.

That sounds like the fastest factor so far, thanks! Is there any reference or research on the topic? Accepting this answer.

The pressure difference human normal atmosphere - near vaccuum is about 1bar or the same as 10m of water. Are you sure this is enough to cause divers sickness?

@mart When ascending from 10m, divers will usually do a stop at 5m, then 3m to avoid any issues. That said, an emergency swimming ascent from 10m without stopping is part of the training (but obv not recommended). One thing to consider is that short (air) dives often don't last long enough for nitrogen levels to reach saturation levels in tissue, so presumably the situation on Mars would be worse.

Less then a minute breathing in the atmosphere (and a very painful death). Mars' atmosphere is >95% CO2 with only trivial O2. These are atmospheric conditions similar to those used to euthanize laboratory animals. He probably wouldn't even make it 200 meters before suffocating.

i havent done the math but you can hold your breath longer than a minute, i think you would die of freezing to death long before you suffocated though

Certainly humans can hold their breath longer than a minute, but can they run 200 m while holding their breath given the elevated heart rate and blood pressure resulting from general sympathetic response resulting from their sleeping quarters being on fire? They won't freeze at 27 C.

27 degrees is the highest recorded temperature on mars, the average temperature of the surface is -55 degrees C

the time to death after being submerged in ice water is not that short.  I'd say asphyxiation (< 5 minutes) would do it first.  This is kinda a bar-bet conversation... but still interesting.

@kmm: "These are atmospheric conditions similar to those used to euthanize laboratory animals" ← Very interesting! That should give us a pretty good idea of the time, right? Has this euthanisia method ever been used on a big monkey for instance? How long is usually necessary?

@shigeta ice water is around about 0 degrees, this is -55 degrees were talking about, the difference will yank that heat out of you in seconds

If the atmospheric conditions are similar to those used to euthanize animals, why is it such a painful death?

the article you link also mentions that mars' atmosphere has 0.6% the pressure of earth' atmosphere, so you only get 0.6% of the CO2 per lungful as the lab animals on earth - I doubt that you get enough to die of poisoning before freezing.

Coming up with the exact number is likely to be very difficult but i would put it in the range of 1-2 minutes to impossible.
Let's ignore the lack of oxygen and assume you could hold your breath long enough to reach the safe haven.
The extreme cold would easily drop your core temperature to the realm of severe hypothermia within minutes.
If that doesn't kill you first then the extreme cold has already caused your blood vessels to shrink before you can even take more than a few steps. On top of this the extreme cold is enough to freeze solid any muscles and other tissue, making movement painful / difficult / impossible.
Now lets assume that through some miracle none of that kills you and you make it to the safe haven. The distinct lack of a magnetic field around the planet exposes you to high levels of UV radiation. Being completely naked and having your entire body exposed to this level of UV is likely to cause lots of mutations throughout your cells. Which in itself will kill you.
So your chances aren't looking good for anything beyond a minute!

good point - big difference between sunlight and day/night conditions, but there is a limit to how quickly the body can lose heat....

Interesting! At http://www.sciencebuddies.org/science-fair-projects/project_ideas/MicroBio_p017.shtml I see that UV kill bacteria in 6 days, I guess it Mars UV are more violent but would UV alone really result in such a sudden death?

@NicolasRaoul i will find the link, the UV exposure levels on mars are something like 10 thousand times greater than what we are exposed to on earth

You have a point RhysW, it sort of depends on whether you are talking about the most extreme conditions, average , or what.

U.S. standards limit an astronaut’s lifetime radiation exposure to 1 Sievert and http://news.discovery.com/space/mars-radiation-astronauts-health-threat-130530.htm says "even the shortest roundtrips to Mars would get radiation doses of about 662 millisieverts". While the number is impressive, it also means that UV-death won't occur before a few days, which means long after suffocation.

http://www.hou.usra.edu/meetings/ppw2015/pdf/1011.pdf "The UV flux on equatorial Mars has been modeled by several teams [e.g., 1,6,7] and yields approximate fluence rates for UVA(400-320 nm), UVB(320-280 nm), and UVC (280-200 nm) of 38, 8, and 3 W/m2at the mean orbital distance from the sun.  These fluence rates are then decreased or increased by ~18% at aphelion and perihelion, respectiveluy[sic], during the martian orbit"
That's Watts, not kiloWatts. Fine for a stroll, but you will get sunburn from prolonged exposure. UV is not a significant risk in this scenario.


text:
Introductory text for primatology
I'm looking for a book that provides a good overview of primatology, one aimed more at researchers rather than a popular science book. Ideally, I'd like something with an ethology/ecology angle with an eye towards phylogeny.
My preference would be for an e-book.

Lucas, I put more of a professional spin on this so it's not as much of a "shopping"-type question.

@jonsca I appreciate your effort, but you did change the nature of my question. I definitely want a good book, that is very important, it really does not matter if it is a canonical text or not. The ability to soundly judge things good or bad is the true value of professionalism ;)

well, maybe of expertise, but that didn't fit :)

Your changes to it are fine, thanks for your feedback!

I've had some experience with Karen Strier's 'Primate Behavioural Ecology', and it's solid. It's a nice overview with (obviously) a strong ecology/ethology bent. I don't think it comes in ebook though.
Here's the Amazon link.

Sweet Jesus that's expensive. Not unusually so, but I'd managed to forget how much academic books are.


text:
How long human can survive with just drinking water everyday
Can humans live without eating food, just by drinking water?  How long can we survive just by drinking water everyday?

116 "Singh finally heeded a resolution of the Congress party and the request of his father, ending ended his 116-day hunger strike on 5 October 1929"
You can see this on: link: http://en.wikipedia.org/wiki/Bhagat_Singh In section: "Hunger strike and Lahore conspiracy case" last paragraph

About 52 to 74 days according to hunger strike wiki page.
This wiki page bases its data on 8 persons who died due to hunger strike:
Days survived by each person: 66, 59, 61, 61, 61, 46, 71, 73, 62, 60.

Where does the 74 come from? The highest referenced number there is 73. Did you get 74 from another source or was that just a typo?

@RhysW: Last line of Medical View says: There are examples of hunger strikers dying after 52 to 74 days of strike.

nice find... I imagine the average is a bit lower than this, but the record kind of tells you how long we can endure without food if we're well hydrated and not otherwise stressed.

This timeframe is similar to one mentioned in malnutrition lectures I've had

This would vary a LOT depending on the amount of stored fat, previous diet, the weather and even the water drunk.  Weeks though there is a good chance that a loss of electrolytes can cause health problems.  (that's why I mention the water you drink, because many bottled water brands and wells have a bit of salt in them.)
Its hard to say from anecdotal experience. There are claims of 3 weeks being easy, but a medical study would be unethical because of the risks posed to the subjects.

You can remember this easily as the rule of threes:
You can survive:

3 minutes without air. (death by asphyxiation)
3 hours without shelter (death by hypothermia, heatstroke).
3 days without water. (death by dehydration)
3 weeks without food. (death by starvation)

Going beyond those guidelines will generally do you permanent damage.
Further reading: http://www.wildernesscollege.com/basic-survival-skills.html

Hi cpendlebury, here at Biology.SE we like answers to reference the claims they make.  For more information on this, see meta.

Noted and fixed.

1 year and 17 days only on water and electrolytes.
Actually, he went water only for about 75 days (read that elsewhere, can't remember) and then they supplemented his water only diet with electrolytes. He's done it under medical supervision and gained 7 KG in 5 years after the fast. So the weight does stay off (obviously, if you go and stay into a healthier diet).

"He did not eat any food, but the staff gave him yeast for the first 10 months and multi-vitamins every day. Potassium is essential for the proper working of the heart, and when his potassium levels got a little low around the 100-day mark, he was given potassium tablets for about 70 days."  Certainly not just water.

@Amory Well, if it's any consolation, he pushed further than anyone mentioned here on water alone. I've also read this in a research PDF and they mention at least 75 days on water alone. If I'll find it again, I'll link it here.


text:
Why is saltatory conduction in myelinated axons faster than continuous conduction in unmyelinated axons?
How does spacing apart sodium and potassium channels allow the action potential to travel faster down the axon? This is the reason always cited for saltatory conduction and myelination, but my mental model of conduction tells me that the density of ion gates along the axon should not affect the speed of the AP.
To illustrate, consider a myelinated axon. A wave of Na$^+$ from action potential site 1, a node of Ranvier, rushes into and quickly diffuses down the axon. (It travels in both directions, but backwards is still in the refractory period.) It diffuses through the myelinated region, its concentration always diminishing. Before it attenuates too much, however, it happens upon node of Ranvier 2, where it triggers another action potential. A new wave of Na$^+$ rushes in and the cycle repeats. This should be plain so far.
Now imagine that there is actually a node of Ranvier halfway between node 1 and 2, called node 1.5. The wave of Na$^+$, on its way to node 2, happens to trigger an action potential at node 1.5, from which a wave of Na$^+$ pours in and either boosts the original wave or replaces it by taking its momentum. Now the reinforced wave proceeds to node 2 and triggers it just as soon as, perhaps even sooner than, if node 1.5 had not existed. Repeatedly insert nodes at higher densities until the situation is simply lack of myelination, and we conclude that unmyelinated axons can transmit an action-potential-triggering wave of Na+ as fast as or faster than a myelinated one.
In short, my point of confusion is this: I cannot see how a higher density of gated channels can possibly slow down the wavefront of Na+ that triggers action potentials. If anything, the additional influxes of Na+ should speed up the all-important wavefront, assuming that new waves really "either boost the original wave or replace it by taking its momentum", and also assuming that the wavefront of Na$^+$ is really all-important for signal transmission, and also assuming that the mere presence of (voltage?) gated ion channels in the membrane does not significantly retard the wavefront.
But the usual explanation for why saltatory conduction is faster than continuous conduction (a fact I hope is empirically and unambiguously established) relies on the putative slowing effect of ion channels on the signal fore. Please explain this effect in more detail, if it is not a misconception.

This is similar to, but I think slightly different than http://biology.stackexchange.com/questions/8026/what-is-the-function-of-nodes-of-ranvier-in-axons

@kmm Actually, my question is in some sense the polar opposite of that question. That one asks why the whole axon is not completely covered in myelin, whereas mine asks why myelin is useful at all. I can understand that without regularly replenishing the Na+ inside the axon, the signal attenuates. Its wavefront is not a 'block'; like the Romans (pardon the analogy), it diffuses its previous territory as well as advancing its border, weakening itself.

My best guess is that people actually don't know. I'm usually quite good at comprehending science when it is there. In the absence of true models or explanations though it is impossible to comprehend. Take a simple thing like how hydronium ions drive osmosis, without knowing that and people just saying "water evens out its concentration", you cannot possibly wrap your head around it.. http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.618.291&rep=rep1&type=pdf

 Short Answer
Myelination acts as an electrical insulator and allows saltatory propagation.

By reducing membrane capacitance and increasing membrane resistance, myelination increases the velocity of signal (i.e., Action Potential) propagation.

If you want to see a really wonderfully simplified explanation, see this Quora post by Edward Claro Mader. Four great figures that Edward created show this phenomenon simply:
Decreased Membrane Capacitance:

Increased Membrane Resistance:

 Long Answer
So you're right: myelination speeds up electrical conduction. Unmyelinated axon conduction velocities range from about 0.5 - 10 m/s, while myelinated axons can conduct at velocities up to 150 m/s -- that's 10-30x faster!!
But why? ...
 Let's Look at Action Potentials & Signal Propagation:

You can get a background of this process in numerous places (e.g., here), so I will just mention this briefly:

When the neuron is at rest, ions are distributed so that the inside of the neuron cell is more negatively charged than the outside. This creates an electrical potential, called the resting membrane potential, across the cell membrane.

Sodium and potassium channels in the cell membrane control the flow of positively charged sodium (NA$^+$) and potassium (K$^+$) ions in/out of the cell to maintain this negative charge.

During depolarization, the cell membrane essentially becomes more permeable allowing NA$^+$ to enter the cell. This causes that section of axon to have a positive charge relative to the outside.

When this positive voltage is great enough (i.e., when an action potential is created), the influx triggers the same behavior in the neighboring section of the axon. Gradually, this positive charge on the inside of the cell moves down the length of the axon to the axon terminals.

 The Main Takeaway:
In this process, action potential generation occurs repeatedly along the length of the axon.
It's important to note two things about action potential propagation:

Each action potential takes time to occur.
The charge (i.e., voltage) that is created dissipates with $ \uparrow $ distance.

 Time for some Math & Physics:
In fact, we have equations to calculate both the time a voltage change takes to occur and how current flow decreases with distance.

You can read more about the mathematics behind this and passive membrane properties in general here and here.

Importantly, these equations rely on two constants: length and time.
The time constant, $\tau$, characterizes how rapidly current flow changes the membrane potential. $\tau$ is calculated as:
$$\tau = r_mc_m$$
where r$_m$ and c$_m$ are the resistance and capacitance, respectively, of the plasma membrane.

Resistance? Capacitance? Huh?...

Resistance = the measure of the difficulty to pass an electric current through a conductor.

Capacitance = the ability of a structure to store electrical charge.

A capacitor consists of two conducting regions separated by an insulator. A capacitor works by accumulating a charge on one of the conducting surfaces, which ultimately results in an accumulation of oppositely charged ions on the other side of the surface. In a cellular sense, increased capacitance requires a greater ion concentration difference across the membrane.

The values of r$_m$ and c$_m$ depend, in part, on the size of the neuron:

Larger cells have lower resistances and larger capacitances.

Importantly, however, is that these variables also rely on membrane structure.

c$_m$ (the capacitance of the membrane) decreases as you separate the positive and negative charges. This could be the result of additional cellular structures (e.g., sheaths of fat) separating intracellular and extracellular charges.

r$_m$ (the resistance of the membrane potential) is the inverse of the permeability of the membrane.

The higher the permeability, the lower the resistance.

Lower membrane resistance means you lose ions quicker and therefore signals travel less far

But why? This is where that length constant becomes important. The length constant, $\lambda$, can be simplified to:
$$ \lambda = \sqrt {\frac {r_m}{r_e + r_i} } $$
where, again r$_m$ represents the resistance of the membrane and r$_e$ and r$_i$ are the extracellular and intracellular resistances, respectively. (Note: r$_e$ and r$_i$ are typically very small).
Basically, if the membrane resistance r$_m$ is increased (perhaps due to lower  average "leakage" of current across the membrane) $\lambda$ becomes larger (i.e., the distance ions travel before "leaking" out of the cell increases), and the distance a voltage travels gets longer.
 Why am I telling you all of this??
How are the time constant and the space constant related to propagation velocity of action potentials?
The propagation velocity is directly proportional to the space constant and inversely proportional to the time constant. In summary:

The smaller the time constant, the more rapidly a depolarization will affect the adjacent region. If a depolarization more rapidly affects an adjacent region, it will bring the adjacent region to threshold sooner.

Therefore, the smaller the time constant, the more rapid will be the propagation velocity.

If the space constant is large, a potential change at one point would spread a greater distance along the axon and bring distance regions to threshold sooner.

Therefore, the greater the space constant, the more rapidly distant regions will be brought to threshold and the more rapid will be the propagation velocity.

Sooo....

If you increase the layer of cells around the membrane, you decrease the electric field imparted by extracellular ions, which allows intracellular ions to move more freely in the axon. In other words, you decrease the capacitance.

As a result, you have more cations available to depolarize other parts of the membrane.

If you decrease the permeability of the membrane (i.e., if you prevent ion channels from moving ions in/out of the axon), you increase the resistance of the axon membrane, which allows for the voltage created in the action potential to travel farther before dissipating.

By allowing the voltage to spread farther before necessitating the generation of another action potential, you reduce the time it takes for signal propagation.

In other words, if you "block" ion channels and decrease the concentration of anions near the axon membrane, you increase  membrane resistance (r$_m$) and decrease membrane capacitance (c$_m$), respectively. Together, this decreases the time of electronic conductance through the axon (and thus increase conduction velocity).
 Finally, to Myelin!
Myelin greatly speeds up action potential conduction because of exactly that reason: myelin acts as an electrical insulator!

Myelin sheath reduces membrane capacitance and increases membrane resistance in the inter-node intervals, thus allowing a fast, saltatory movement of action potentials from node to node.

Essentially, myelination of axons reduces the ability for electrical current to leak out of the axon. More specifically, myelin prevents ions from entering or leaving the axon along myelinated segments. As a result, a local current can flow passively along a greater distance of axon.

So instead of having to contantly generate new action potentials along each  segment of the axon, the ionic current from an action potential at one node of Ranvier provokes another action potential at the next node. This apparent "hopping" of the action potential from node to node is known as saltatory conduction.

 So Why not Just Myelinate the Entire Axon??
The length of axons' myelinated segments is important to the success of saltatory conduction. They should be as long as possible to maximize the speed of conduction, but not so long that the arriving signal is too weak to provoke an action potential at the next node of Ranvier. The nodes also can't be too frequent because, although adding a new node to the axon would increase its ability to generate sodium current, it would also increase the capacitance and thus diminish the effectiveness of other nearby nodes.

Sources:

Purves D, Augustine GJ, Fitzpatrick D, et al., eds. (2001). Neuroscience. 2nd edition. Sinauer Associates, Sunderland, MA.

The Brain: Understanding Neurobiology

Byrne, J.H. Chapter 3: Propagation of the Action Potential. Neuroscience Online. Univ. Texas.

Understanding the Passive Properties of a Simple Neuron

Quora

Wikipedia

This question is also relevant on the topic of how myelin actually influences membrane capacitance.

So in brief, myelin makes the axon less "leaky" and less "sticky" for ions, by increasing membrane resistance and reducing membrane capacitance, respectively. Thank you for this simple and fairly complete answer!

I realize that I originally assumed the cell could just try to avoid placing non-gated ion channels along the membrane, to keep the conductance low, but it must be much more practicable to myelinate the whole thing than to attempt uneven distribution of proteins. In my model, the axon could "spam" action potentials, and the super high concentration of ions would speed up diffusion and offset any slowing effects of R-C. LOL but that would be metabolically backbreaking, and extremely salty.

Great effort to write such big answer !

see Graded Potentials, Action Potentials, Electrotonic Conduction, Myelin on YouTube  [harrywitchel, 14.5 min]

There are two factors that need to be taken into account here:
1. Myelination decreases membrance capacitance.
The rate at which sodium influx through a node can depolarize the axon at the next node is related to both the current and capacitance across the membrane (in addition to a few other factors). So while adding a new node to the axon would indeed increase its ability to generate sodium current, it would also increase the capacitance and thus diminish the effectiveness of other nearby nodes. So it doesn't help to move the nodes closer together. What if instead we increase the distance between nodes? In that case, the trade-off is reversed and conduction velocity is again decreased. So there is some optimal internodal distance at which conduction velocity is maximized, and it turns out most axons happen to have just that geometry. [See: Waxman, SG. 1980]
2. Action potentials are metabolically expensive.
The brain uses a lot of energy (about 20% of the body's metabolism at rest)! Maintaining the proper balance of ions inside the neuron is the major reason for this energy usage. Every action potential incurs metabolic cost and if we double the number of nodes along an axon, we (nearly) double the metabolic cost of propagating spikes down that axon. So although conduction velocity appears to be the primary determinant in the choice of internodal distance, it is important to remember that it is not the only factor the organism must take into account.

Hi Luke! Thanks for the answer. StackExchange notified me about it only a couple of days ago, which is why I've taken a week to respond. I would like to add another important factor, which I had overlooked when I first posted: ion leakage (specifically, outgoing ion pumps). Myelination prevents leakage, which may slow down the wavefront IF we assume that an attenuated (less concentrated) wave travels slower down the axon.

Certainly minimizing membrane conductance is another potential benefit of myelination. To maximize conduction velocity, we would ideally want the inter-nodal membrane to have very high resistance. I did not include that as part of the answer because the cell could (and in some cases does) achieve the same effect by simply localizing channels to the nodes. This could be done without myelin at all, so I'm not sure it should be considered one of the primary actions of myelin.

Wow! It is fascinating that the cell can localize channels to small points along the axon without myelin. Thanks a BUNDLE for taking the time to post. Although I give this answer the check mark, I certainly hope others are not discouraged from contributing their knowledge.

I'd just like to add that, if your information is accurate, this discussion should be pretty interesting, since usually people seem to take it for granted that myelination simply allows the action potential to somehow "hop" from node to node, and therefore the signal is faster. That may be a useful abstraction somewhere, somewhen, but it has no physical meaning, I think.

Regarding 1. You write: "... while adding a new node to the axon would indeed increase its ability to generate sodium current, it would also increase the capacitance ...". Why or how would it increase capacitance? Regarding 2. How does that (help to) answer the question at all?

While Luke's answer is perfectly correct, the answer can be given in a more intuitive manner.
First, the main point is that it is increased positive voltage (inside the axon) that opens the sodium ion channels to propagate the action potential. The question is: how fast can this voltage get to the sodium channels?
In an unmyelinated axon, the movement of voltage across the membrane is due to ion flux (i.e the flow of ions through the channels, the current), and this movement is limited by the time it takes for the sodium ions to diffuse into the axon.
On the other hand, in a myelinated axon, the first bolus of sodium enters at the axon hillock.  Because the capacitance is low, this means that the voltage can propagate down the axon, not by ion diffusion, but as an electrical field.  The electrical field carries the voltage force much much faster than ion diffusion. Therefore, when the ions first enter, the voltage force moves, basically at the speed of light to the next node, where the voltage force opens the sodium ion channels there.
So, by allowing the voltage to be carried by the electrical field, the effect is that the distance between the nodes is effectively eliminated.  Myelinated axons conduct faster because they are >>effectively<< much shorter than unmyelinated axons.
Finally, the optimized distance between nodes mentioned by Luke is exactly that distance in a given type of neuron's axon where the voltage force decays to the bare minimum needed to activate the sodium ion channels at the next node.

Hello Don! Again, StackExchange emails are sluggish.... That's a really dam good explanation, and if it had been given early I might have checkmarked it. I like how it truly explains 'hopping'. However, my understanding of capacitance is not as good as it should be, so I cannot totally grasp the mechanism here. Therefore I am a little skeptical. Could you point me to a resource confirming and developing your answer, so I can study it more closely?

What stops the voltage from propagating down the axon as an electrical field in an unmyelinated axon?

"this means that the voltage can propagate down the axon, not by ion diffusion, but as an electrical field." This is a main point for me. Would you have a reference discussing this?

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


text:
How does a pinched nerve cause pain (at the molecular level)?
Is this due to pressure differentials in the surrounding tissue? (Is it possible to have a pinched nerve without compression of the surrounding tissues, and does this cause pain?)
What are the molecules/cell types involved in this process? Is the pain dependent on the compression of axons from mechanosensitive or nociceptive neurons?

Typically nerve compression or a "pinched" nerve is due to inflammation in the tissue through which a nerve passes. The gap is already quite narrow so any inflammation is quite potent. Inflammation causes you to feel things as more painful (hyperalgesia). In a similar way to how of you burn your hand then poke it, it hurts, when cells are damaged the receptors surrounding them are sensitised to be more reactive. Binding of many ligands involved in inflammation leads to higher than normal sodium influxes which means you feel pain as this impulse is sent. I could be a lot more detailed but not sure what level you want, however for much more detail see this review.

I thought it might be that! Thanks for the review.

As AndroidPenguin described the nociceptive pathways are activated by inflammation or noxious chemicals.
Sometimes pain can arise independent of active nociceptive pathways. Most evident in cases of Neuralgia and perhaps in case of Pseudoneuromas.
In certain cases the injured nerve causes disinhibition of the pain pathways arising from the dorsal horn of spinal cord. This disinhibition is because of loss of the nerve function.
Sometimes increased nociceptor drive can activate dorsal horn of spinal cord which will now respond to normal mechanosensation also [1].
Phenotypic switching is also possible [2].
PS: Both these articles are inaccessible to me at this moment. Refer them for more details.


text:
How can I save bacillus strains on filter paper without an -80 degree freezer?
I want to save my bacillus strains but I don't have access to a -80 degree freezer.  What are possible alternatives?

Use agar stubs: pour some Nutrient agar (or any suitable agar medium) in a test tube (~10% of the tube volume) and punch your inoculum halfway into it using a pipette tip or inoculation loop. Store it in 4⁰C.
Glycerol stocks can be made and stored in -20⁰C also.

How long can you store them in agar stubs? Also we use -70 to -80°C to store our glycerol stocks.

I had stored them for a couple of months but i think it can withstand one more month..


text:
Can I purify polyhydroxyalkanoates by heating the cells extensively?
Traditional methods of purifying polyhydroxyalkanoates (PHAs) and other bioplastics made by bacteria involve washing the cells with harsh chemicals or strong bases.I'm interested in maintaining the spatial position of the PHA globules relative to one another. Therefore, I'm hypothesizing that by heating these cells extensively, I can lyse/degrade the cellular matter and be left with only PHAs, especially given that some PHAs have melting points up to 180 degrees.
Is this approach to purifying PHAs plausible? Has it ever been done?


text:
What could account for an apparent loss of mass at death?
An interesting tidbit floating around the internet these days is that Dr. Duncan MacDougall apparently weighed people shortly before and after death, and found an average of a 21 gram discrepancy, to which he attributed to be the soul departing. As we all know, this certainly can't be the right explanation.
Putting aside likely extreme bias and instrumental/experimental error, is there any bodily process at death that could potentially explain a small decrease in observed mass?

Snopes.com gives a discussion of possible issues with the original experiment.  Evaporation or bowel or body movements for instance.  I think the biggest complaint about the experiment is that it has not been reproducible and that the original experiment was flawed.  MacDougall only took six measurements and he threw two of them out in his original work.  The Wikipedia link you give cites a paper where sheep were found to gain weight at least for a time after death.  Dogs are found to have no weight change.
MacDougall and his contemporaries were inclined to interpret their results such that animals simply do not have souls, or have different sorts of souls.  But if you look at an average of all experiments cited, it could also be said that the average weight loss up on death averages to zero.  3/4 of an ounce of a human being (or a sheep) over the course of something like a death is not an easy measurement.  You can't give them a drink of water, you worry that they are breathing too much and losing water.  Its not an easy experiment, at least for human beings where you can't control the circumstances of death so well.
In any case this really needs to be measured better.  In 90 years it doesn't seem that there's been a real rush to do it.
I just stumbled across this blog post that talks about an effort to measure a change in blood flow to the brain when in intense mental activity popularized in the late 19th century.  The investigator Mosso claimed he measured a difference, but the result is disputed today.  It could not have been more than a few grams. In any case a description of how difficult this measurement can be.

Sheep souls are buoyant, I guess. This sort of thing is tricky to do, even today. I'd be amazed if his scale was even accurate to 21 grams over a 100 kilo human.

I would too - especially after I had kids and tried to weigh them at their checkups :)

Well, did anybody found a centre in a brain that could be called "soul"? If not, and the soul is considered to be some state of current consciousness (of mind), is that what the body loses?

its likely that no real weight is lost... sorry.  if they were able to show this beyond a doubt it would definitely be strong with the internet!

There will be a quantifiable change in mass in any living object dies and then more with decomposition. The loss of energy from the living organisms changes the kinetic mass of the original subject. When death occurs other the process of decomposition now begins converting the organic materials of the organism into inorganic material and energy which in turn changes the kinetic mass of the subject

It would be much appreciated if you could cite your sources for the various points in your answer.


text:
By what mechanism does an obstructed bile duct cause excess fat in the stool?
By what mechanism does an obstructed bile duct (for example gallstones) cause steatorrhoea (excess fat in the stool)?

The function of bile produced by the liver and concentrated in the gall bladder is to aid in fat digestion.  Bile acts as an emulsifier to allow the fat to be packaged into small droplets, micelles.  The breakdown of fats into small micelles greatly increases the surface area for lipases produced by the pancreas have to act on.  These are then absorbed across the intestinal wall.

Bile breaking down large fats into small micelles
If this first step of bile production and transport is lacking (due to liver dysfunction or obstruction anywhere in the biliary tree), the fats are not packaged into micelles and are consequently very hard to digest.  They pass through the entire alimentary canal virtually undigested causing steatorrhoea, fatty, bulky and foul smelling stool.

The Biliary Tree

Gallstones 'block' the plumbing system (i.e. the biliary tree) that drains bile produced in the liver from flowing into the duodenum through the ampulla of Vater. Since bile is a dietary detergent for fats (cholesterol, triglycerides, free fatty acids), the blockage of bile impairs fat absorption in the small intestine and the fat passes into the large intestine and then into the stool. There is always a small amount of fat that passes into the feces (typically very low though), but if bile is not present to aid fat absorption then you get "fatty stool" aka steatorrhea.

Thanks also here for your answer. This seems like common reasoning, but some references of, e.g., supporting websites are still helpful. +1. I added one web link as an example. You use plenty of jargon, which is OK, but linking some terms may greatly improve readability.

AliceD - what 'grade level' are you supposed to answer on? Do you personalize that to the language being used in the question? Thanks for your advice!

Now that is a truly great question. We have a meta site http://meta.biology.stackexchange.com/ and I really encourage you to post this (I can do it for you if you wish). In general, personally, I scan the question and if the level of OP is obviously rock bottom I adapt my language accordingly. In general, this site is targeted for MSc students and grad students. But younger folks tend to be attracted for sure, as well as older ones like me :) Btw - this post is really accessible.


text:
Can stress echocardiography show coronary blood flow difference before and after exercise?
Stress echocardiography means a pair of cardiac ultrasound imaging examinations, before and after exercise. I assume that coronary blood flow is increased after exercise. Is cardiac ultrasound technology capable of showing this blood flow difference?

Update: I emphasize that my question concerns stress echocardiography, i.e. two echocardiography sessions before and after exercise (or pharmacological stress test) - not simply echocardiography.

No, echocardiography is not sensitive enough to do so. For tracing coronary arteries directly flow angiography is the choice.

To a related question of mine AndroidPenguin yesterday answered that with stress echocardiography we could "see how it responds to increased exercise (does the blood flow increase by the same amount everywhere?)". Was AndroidPenguin wrong?

Coronary artery disease thickens the wall. Flow is dramatically affected by thickness (radius to the fourth power). In an echo you observe the heart muscle i.e. does it contract normally using the surrounding muscle and baseline as a comparison. If the wall is thickened, this will cause a decrease in perfusion which will result in the heart muscle contracting abnormally. Xaqron is right, it doesn't show you flow directly, but what it does show you is a quick and cheap way to estimate if the artery is blocked enough that it will cause a noticeable difference. If the heart muscle doesn't beat that means it really isn't getting oxygen (but could be because of abnormal conduction), and if it beats suboptimally it is getting less oxygen than it requires.


text:
Why is elevated homocysteine considered a risk factor for angina?
Elevated homocysteine levels are listed among risk factors for angina. How is homocysteine related to the heart? Or the coronary arteries? How do these relationships make it a risk factor for angina?

In his answer to a related question Alan Boyd has given the mechanism how homocysteine inhibited (1)Protein C activation and the (2)binding of free thrombin, both ways promoting coagulation and thrombosis. According to the answer of Xaqron below there are further mechanisms. Not all of them are linked to angina yet.

Homocysteine:

Causes endothelial dysfunction and damage
Accelerates thrombin formation
Inhibits native thrombolysis
Promotes lipid peroxidation through free radical formation
Induces vascular smooth muscle proliferation
Promotes monocyte chemotaxis

Many observational epidemiological studies indicate that individuals with higher Homocysteine levels have increased risks of cardiovascular disease.

How can the effects on lipid peroxidation, smooth muscle proliferation and monocytes lead to angina?

Did you mean thrombUS formation (rather than thrombIN)?

@winerd: No, if it accelerates thrombus formation then it would be more dangerous. I meant thrombin formation as already said in answer.

I guess that the effects on endothel, thrombin and thrombolysis may contribute to coronary thrombus formation, and that's the link towards angina. Am I right?

@winerd: Mechanism is unknown at the time but these factors make a good basis for thrombus formation. Your questions are more medical than biologic, consider voting on Medicine in area51

@Xaqron I'd say this is on topic for us.  I can see how the factors you've listed would be clear risk factors for myocardial infarction but, with the possible exception of 5, I'm not seeing a clear link to Angina (stable or otherwise).  Could you elaborate further?

@RoryM: Smooth muscle proliferation => lower internal diameter of vessels.

Citing a reference for this would make for a slightly stronger answer as well, just a suggestion, though.

@Xaqron: RoryM mentioned 'smooth muscle proliferation' as the one where (s)he sees a link, not where (s)he does not.