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Is poison venomous and is venom poisonous?
I know the difference between poison and venom AND poisonous and venomous.
But I just want to know if an ingested venom would do harm to humans and if an injected poison would do harm to humans.
I really think that poison is both poisonous and venomous AND venom is both venomous and poisonous.

This wikipedia link might help you understand the difference. https://en.wikipedia.org/wiki/Venom     Read the first two sentences in particular.

I am fully aware of that. But what I am asking is that if poison is injected/venom is ingested would do harm to a person's health.

Related : http://biology.stackexchange.com/questions/53577/are-there-any-animals-there-are-both-poisonous-and-venomous

They had a tough time with venom on SE English Language and Usage here and here.

I think you are both confused about terminology, and asking a very broad question. An organism that produces venom is venomous. Poison is not venomous, the black mamba is venomous. Venom is not venomous.
According to the Wikipedia article on venom,

Venom is a form of toxin secreted by an animal for the purpose of causing harm to another.

A toxin is a poisonous substance produced by a living organism. The article goes on:

Venom is injected into victims by means of a bite, sting or other sharp body feature, which differentiates it from poison (that is absorbed, consumed or inhaled).

However, a toxin is a poison, and poisons are defined (by wiki) as

substances which cause disturbances to organisms, usually by chemical reaction or other activity on the molecular scale, when a sufficient quantity is absorbed by an organism. (emphasis mine)

So, the definitions are kind of circular.
From what I understand of your question, you are wondering whether a venom would still be dangerous if it were, for example, ingested rather than injected, as well as whether a poison would still be dangerous if injected rather than ingested (or inhaled, or whatever), and this is where the "Too Broad" category gets applied. There are thousands if not millions of different types of toxins in the world, ranging from full proteins to peptide-based to small organic molecules to completely different structures, such as lipopolysaccharide (LPS, the component of Gram-negative bacteria that causes septic shock). Some may not survive the digestive tract, others might. Some can act through the skin, others can't be absorbed. Inhalation is the next best thing to injection, but probably not for every single one of them, so it's impossible to make broad statements about their efficacy and median lethal dose via different routes of exposure. The exact same thing applies to the "poisons" category - while something that is damaging when absorbed cutaneously, such as methyl mercury, is probably just as damaging directly injected into the bloodstream, it's impossible to say that with certainty about all poisons.

Most venoms contain a lot of enzymes. These enzymes can be split by the proteases in your stomach. So if they don't have any effect before reaching your stomach, they will probably digested like any other protein. Ofc. there are some proteins which resist digestion.
There are poisons which affect only certain cells in the digestive system, so injecting them probably would not have any effect or it can have a completely different effect. E.g. cholera toxin (if we can call it a poison) affect the glucose transport when injected, while it causes diarrhea when it is produced by the bacteria in the infected guts.
There are toxins which have the same effect from both ways. E.g. botulinum toxin can be deadly both injected and ingested. You probably heard of botox injections...
The effect can vary by delivery method as well. Injected can mean subcutan, intravenous, etc... while ingested can mean drinking, swallowing a capsule, which protects it from the proteases in the stomach, and so on... It depends on the dose as well.
I think MattDMo is right, the question is too broad because there are many different poisons and venoms and delivery methods.

To answer this question first we need to look at what is the definition of a venom and poison. This is somewhat difficult because the definition has changed slightly over the years, but looking over them we can learn of the similarities between the two.
"A venom is typically a mixture of compounds containing one or more toxins, which is produced in venom glands and injected into animal tissues via specialized morphological structures." This meaning that a venom is made and is injected into another organism (both plants and animals can do this).
"A poison is one or more compounds that are toxic. These toxins can be inhaled, absorbed, ingested, or injected. Plants and animals can produced organic poisons; however, poisons can also come directly from the environment." Example: Chlorine or Fluorine gas.
This is where it's tricky with the definitions. A venom can only be injected to be harmful, whereas a poison can be as well; however, a poison has a broader area of effect. Some snakes have venom that can be absorbed or toxins in their flesh making them poisonous to eat. So the issues are first what happened, was it injected or not, next could it have not been injected and still caused harm.
The best logical answer is that all venoms are poisons, but not all poisons are venoms. This is because both can be injected and cause harm, but venoms have to be injected when poisons don't. Like with the above, some snakes have toxins that are commonly injected so they are still called venoms even when they can be absorbed making them poisons by definition.
To conclude, it's a complicated issue that people are still trying to figure out. In the end the main difference between the two is that a venom needs to be injected, when a poison can but doesn't have to be.

Welcome to Biology.SE! Your answer sounds reasonable (although it isn't clear to me what it adds anything to the existing answers), however, it is likely to receive a more favorable response if you include supporting references (primary literature is best, but a textbook available online would seem sufficient for this question). In particular, the quotes you make must have references to the original sources. ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!

Some substances can be both venom and/or poison.  According to Wikipedia, the source of all knowledge in this internet age, Blue Ring octopi are dangerous to humans if provoked because their venom contains the powerful neurotoxin tetrodotoxin.  According to the same reliable source, Pufferfish are dangerous to humans if eaten because their flesh contains the powerful neurotoxin tetrodotoxin*.
*Summations, not quotes.

Welcome to Biology.SE. The community is looking for more developed answers like the first ones in the list (they include references and citations).


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Problems in optimisation with applications to biology?
I will soon have around 8 weeks to do a research project of my choosing  as I am finishing my undergrad in computer science.
My experience is mostly in optimisation algorithms (mostly combinatorial/discrete optimisation).
I have an interest in applying computer science to biology (mostly human biology).
I would like to ask if anyone knows optimisation problems with applications to biology which would benefit current research.
Although I have read a lot about biology in my free time, I am not too knowledgeable about the current state of the research and so it is a bit hard for me to find a good topic.
Some examples to spark the discussion are string problems in genetics (alignment problems), and community detection in graphs (to find proteins in the same functional group).
Thank you!

Optimization algorithms have lot of scope in computational biology. 'Almost' all parameter fitting requires one or another of such algorithms. I would say look into some computational biology, bioinformatics journals, you will find tons of examples.

Optimization is ubiquitous in all sciences and engineering, and biology is no exception. Many statistical models in neuroscience require optimization for example (my area).

It is probably worth picking one such algorithm and make an answer out of it.

Note that genetic algorithms are a type of optimisation algorithm that is inspired from evolutionary biology. Some people used the knowledge the computer scientist have acquired in studying these algorithms to understand evolutionary biology. For example, questions such as "What fraction of the space of possibilities is explored before reaching an optima?" can be of interest.

Depends on your area of expertise --- continuous / local optimization, or discrete, combinatorial problems? There are many discrete problems in next-generation sequencing applications and network (graph) models. Continuous optimization problems frequently arise in various statistical models (maximum likelihood fitting to data). Optimization is a large field, so would be helpful if you can be more specific as to your area of interest.

I think that either @Resonating answer is satisfying or the question is too broad.

@Roland I editted the question. Discrete/combinatorial optimisation is my focus in general

Maximum likelihood phylogenetic trees. The trees are easily scored but the tree space is so large that finding optimal phylogenetic trees is extremely difficult. There's some research but there haven't been very many actual breakthroughs, so it's probably a pretty rich field.

Well I guess this is a nice example! There's tons of papers on the subject. Here is one and another one.

Here are some examples:

Sequence (DNA, protein) alignment. With the development of next-generation sequencing methods, this is an important and active field.
Genome distance calculation by genome rearrangements
The phasing problem for single nucleotide polymorphism data (determining haplotypes)
Factor blocking problems in statistical experiment design
Network (graph) analysis. Many biological data sets can be expressed as networks, for example pairwise protein interactions, which give rise to a variety of discrete problems, like finding maximum connected subgraphs, graph flow problems, etc.
Biclustering of data matrices, notably gene expression data
Inference on phylogenetic trees was already mentioned.

I'm sure there are many more, this is just off the top of my head. Happy googling! :)

source: Stack Exchange

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Where in the world does blue eyed whites originate from?
I know that there were no blue eyed people until ~6000 years ago due to a mutation and all blue eyed people have a single common anchestor.
But where in the world does it originate? I assume it originates from somewhere in Europe but is it known more specifically where like Scandinavia, Eastern Europe, and so on or is it impossible to know?

Wikipedia has your answer already !

@Dexter Exactly where is the answer to the "Where in the world..." question?

@fileunderwater Reference no 46

@Dexter How about elaborating on that instead of posting an uninformative link to a wikipedia page. I also dont see how the finding of a blue eyed human in Spain from 5000BC is answering the question of the origin of blue eyes. Are there other 5000BC hunter-gatherers from other parts of Europe with sequenced genomes (where the allele wasn't found) used as comparisons? Otherwise it is only showing that the allele is more than 7000y old and occuring in Spain at that time.

@fileunderwater I agree I didn't elaborate. Sorry about that. However that doesn't mean I posted uninformative link. Link suggests 7000 y old skeleton with homozygous HERC2–OCA2 locus which is strongly associated with blue eyes.  In fact first link from google search gave me origin of blue eyes in Black Sea region (and guess which gene was correlated ? OCA2.

@Dexter Sorry about the wording "uninformative link" - I meant that the link text was uninformative, not necessarily the content. Your last link is the first one that seems to provide an answer to the question though. You should post it as an actual answer instead.

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Two different sized colonies from the same species of bacteria. What does it mean?
I have got two different sized colonies in a plate of Salmonella Paratyphi, identified by biochemical methods. What does two different sized colonies mean? What kind of question can I investigate in this regard?
Protocol followed:
Positivity of serum sample was checked in BacT/Alert blood culture system. Bacteria was subcultured from the positive result giving culture bottle from the BacT/Alert system and incubated overnight at 35 degree celsius. Two different sized colonies were found and they were subjected to biochemical and antisera tests and both identified as Salmonella Paratyphi.

Could you please add details about the protocol you followed ?

@MauroM Some details added

Do you happen to have an image of your plate?

Thanks @AhmedAbdullah ! Unfortunately i'm not expert enough to solve your doubts; the only thing that i can think is that the founders of the two colonies reacted to the culture environment differently e.g. the founder of the bigger colony was more rapid to adapt and divided more rapidly compared to the other... I would try to made another culture (exactly same conditions) to see if the size difference persists and then investigate the genomes of the two colonies even if i'm not sure wich technique to use since i'm not a microbiology expert.

@Chris Sorry I am away from lab for couple of days. When I return I'll try to manage a picture.

@MauroM thanks for you suggestion. I'll try along this line.

You're welcome @AhmedAbdullah !

It could be thousands of things, but only a few of them will persist if you keep subculturing both colonies. Happily those are the interesting things, so if you subculture both colonies and they're the same size it was probably something as boring as 'two bacteria stuck together, giving one colony an edge'. If they're still different sizes, report back! Something interesting has happened.

How different are the colonies in size? This could also be a result of human error while plating. You should repeat these experiments and measure the statistics and if the trend is consistent then consider looking for a reason.


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What are the molecular/cellular basis of pruritus ?
Could someone please explain the cells and molecules involved in the clinical phenomenon of pruritus ?
I'm interested in a general view about the subject, but detailed answers will be appreciated.

Molecular basis:  histamine.


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How to statistically test the predictability of evolution?
Can anyone recommend me an experimental study which tries to test the predictability of evolution? The closest works I found are the studies of fluctuation tests (f.e. classical study of Luria & Delbrück, 1943) which demonstrates that in bacteria, genetic mutations arise in the absence of selection, rather than being a response to selection. Is there any other point of view from which the predictability of evolution can be studied?

Luria & Delbrück (1943) Mutations of bacteria from virus
  sensitivity to virus resistance. Genetics 28: 491–511.

What does "intentionally occuring mutations" even mean?

Hi @fileunderwater! Thank you for your comment. My question has been rephrased for better clarity.

There are things we are good at predicting and things we are not good at. Predictability of evolution is too a vast subject. You should refine it to a specific evolutionary process.

Are you interested in determining our predicitve power of a given evolutionary process or in demonstrating that mutations don't occur in response but is a (mainly) independent process? I think I don't fully understand your question.

Thank you @Remi.b for your comments. The reason for this question is that laymens often ask whether the "evolution has some final goal" (and then stops). I was just wondering, if such question could be tested by some simple experiment (simple enough for approx. 12 years old kids).

The issue with this kind of statement is that it is poorly defined and it is hard to know what experience would be considered as a good contradiction. I suppose that if you consider any experimental evolution experiment that has some replicates, you can show that they all end up a little (or completely) different. A famous example is the one of citrate usage in E. col by Lenski. Among hundreds of lines only one evolved the ability to synthetize citrate (after more than 30,000 generations)

You can consider mutation accumulation experiment showing that different mutations accumulate in different lines that are subject to the same conditions. You also may want to consider short term evolution showing the effect of genetic drift on allele frequencies. There are hundreds of study who would more or less address but the statement is too uncear to understand which one is of interest.

Predictable Evolution Trumps Randomness of Mutations
http://www.scientificamerican.com/article/predictable-evolution-trumps-randomness-of-mutations/

I think Lenski's evolutionary long-term experiment should be a good example, without being familiar with Luria & Delbrück (1943). There they use replicated populations of E-coli to study (among other things) the "repeatability" (historical contingency) of evolutionary changes. Nice overviews of the project are given in Blount et al. (2008) and Philippe et al (2008), where they study to what extent certain mutations are repeated in replicate populations, in relation to citrate metabolism and size/shape.
References:

Blount, Borland & Lenski. 2008. Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli. PNAS vol. 105 no. 23
Philippe et al (2008). Evolution of Penicillin-Binding Protein 2 Concentration and Cell Shape during a Long-Term Experiment with Escherichia coli. Journal of Bacteriology 191(3):909-21

I second this.  I think with a Galaxy account, you could do the alignments and SNP calling yourself, if you so desired.


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what is the natural way of rose to propagate by its vegetative cells?
I have read that rose reproduces sexually. But I have also heard that it can propagate by its vegetative cells (vegetative cells in its root). Is this correct? If yes, can I know how does it propagate by its roots?


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How plasma cells switches secreting different Ig classes?
In Type 1 hypersensitivity how do B lymphocytes switch Ig classes, from synthesizing IgG to IgE? What is the mechanism? I studied multiple pathology books, it says the same as for IgG secreting pathway. So how does the body know how to change the Ig secretions in response to allergens?

The mechanism is called Class Switch Recombination and it is a form of error free NHEJ. Appropriate signals activate the recombinases.

In T-dependent antigen recognition, the B cell can switch the isotype by first altering the heavy chain gene. This is driven by Tfh cells. The specific cytokine stimulating the class switch determines the isotype of the heavy chain to be synthesized. For your example, interleukin 4 (IL-4) drives the class switch to IgE. You also need a costimulatory signal from the CD40/CD40L interaction between the B cell and the Tfh cell. This induces activation-induced deaminase (AID), see bottom paragraph on this.
There are switch regions (denoted S) in the introns between J and C segments at the 5' end of each CH locus, and upstream of that is an I exon (region denoted I) w/ it's own promoter. Induction by CD40 and whatever cytokine is present starts transcription of the I exon, switch region and CH chain of the H-chain the B cell is meant to switch to. This germline transcript facilitates dsDNA breaks at the switch regions Sµ for the IgM (switch region mu) and the switch region for the class to be switched to, Sε in our case for IgE. The intervening DNA is deleted and the coding region Cµ is replaced by Cε coding for the IgE heavy chain BUT, it ends up with the same V domain as the B cell originally had!
Some enzymes involved are AID, which deaminates cytosines and allows the germline transcript to hybridize in the switch region, Uracil N glycoylase UNG which removes uracils from the DNA, and APE I endonuclease that generates a nick at the abasic sites generated. These nicks lead to dsDNA breakages in the switch regions. Text shows that the switch region DNA is G-C rich and can form stable RNA:DNA hybrids with the coding strand of the switch region and the germline transcript. This is what frees up the noncoding strand for alteration by UNG and cutting by APE. The result is that the V region becomes associated w/ a new constant region.
I'd also be careful with the terminology plasma cell as used in the title because we aren't yet at the high-affinity secreting stage when we're talking about class switching. This is mediated at the activation of the actual B cell by Tfh cells.

All information above is summarized from Cellular and Molecular Immunology, 8th ED


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Is there an evolutionary advantage for coconut oils to be rich in saturated fats?
I know that coconut oil is composed of multiple saturated fatty acids, but is there a reason why this would have increased the fitness of the coconut plant?

Are you asking about coconut oil, the consumer product you can buy, or coconut oils, the fats found in coconuts that are pressed into coconut oil(the first kind)?

The product inside a brown coconut is called coconut milk and it is liquid.

I am referring to the unrefined consumer product(not coconut milk), but the first kind might also be interesting.

Possible duplicate of If a trait would be advantageous to an organism, why hasn't it evolved?

I think that's the converse of this question, isn't it? The generic form of questions like this is "given weird feature A in organism B, are there likely fitness advantages to weird feature A or is that coincidence?" not "given the fitness advantages to feature A, why doesn't it exist in organism B?". The first is sometimes answerable, even if the answer is sometimes 'dunno', but the second is always answerable with 'that's not how evolution works'. Furthermore questions like this are precisely how evolutionary adaptations are discovered.

This is entirely speculation, but the part of seeds that is pressed for oil(the endocarp) is enriched in saturated fats and long fats in ocean-going fruits. The coconut is 91% saturated fats, the oil palm is about 50%, etc. The tamanu or 'ballfruit' produces monounsaturated long-chain fatty acids in the endocarp, about 75% C18 oils, mono- or di-unsaturated.The calabash is astonishingly 20% saturated and 78% C18 oils, and is also sea-distributed(these seeds are called disseminules).
It's not a totally straightforward correlation. Peanut oil is 75% C18+ and 15% saturated and the oil palm mesocarp is only 50% saturated, but the endocarp is 81% saturated fats.
There's an additional consideration here: longer chain fatty acids are slightly more energy efficient per unit mass than shorter chain ones.
Without better data on energy density or spoilage rates on different blends of long-chain fats I can't conclude conclusively that spoilage and energy density are why disseminules tend to have longer-chain oils and more heavily saturated fats, or even that they definitely do. But it looks like they do, and that would make sense.


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Why do teeth ache after fillings?
I had a filling which involved drilling the tooth, but the drilling did not touch the nerve. According to the x-ray taken at the same time, the nerve is in fact some distance from where the filling was taking place (lower right molar).
Now the local anesthetic has worn off, my tooth is aching. The gums do not hurt (so it is not caused by the dentist applying pressure to the area) and as far as I am aware there are no other nerves within the enamel of the tooth.
So, why does my tooth ache? Is it something to do with the nerve 'waking up' after being anesthetized?
Just to be clear it is not a severe ache or of any concern, only in the background, and I am curious as to the cause. The dentist did say it would ache, so it's obviously a normal thing, but I didn't think to ask why!

There can still be a pressure exerted on the nerve, the filling exerts a pressure on the tooth which then propagates through the entire tooth.

I didn't think of that - he did really seem to 'pack in' the filling and that could cause pressure inside the tooth.

See, since it was a simple drilling followed by restoration or filling, that means the infection was superficial, not involving the pulp where the nerves and blood vessels are situated.
Ok, so now to remove the superficial infection the dentist might have used an airotor. It's an instrument which rotates at high speed, has a hole for water spray to cool the fictional heat generated while it removes the caries or the infection from the tooth.High speed handpieces
Now as you may be knowing the crown portion of tooth has three layers- enamel, dentin and pulp. Only the pulp portion is innervated.
Now when the instrument is drilled into the tooth the infected enamel and superficial infected dentin must have been removed.
The dentin has numerous tubules known as dentinal tubules. These contain a fluid called dentinal fluid. Whenever there is any stimulus which has not yet reached the pulp, but may have reached the dentin, eg of stimulus in the form of pressure, temperature change, sweet food, sour food etc, cause the fluid to move or get displaced. The displacement of dentinal fluid stimulates nerve endings in the pulp and hence generates a pain/ sensitivity response to your brain.Hydrodynamic theory
Now the drilling causes heat generation, even though little, due to the coolant, plus pressure and hence causes the fluid to displace and hence pain. This pain usually ends after the treatment.
However the restoration placed, you should have specified which restoration- silver coloured (amalgam) or the tooth coloured. These again have chemicals. These chemicals can penetrate through the tubules to the pulp to elicit a painful response even after the treatment. To prevent this, a liquid known as varnish is applied which acts as an insulator. Also if the infection is deeper, a base or other material depending on the type of restoration is also applied to prevent other stimuli. Varnish and bases
So either there may be a failure in these insulating materials or your pulp may require some time to heal from the procedure. It may have got healed by third or fourth day, if it was due to procedural trauma. In either case you should contact your dentist.
Hope I have solved your question :)
References have been given in the parentheses

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Doubly-compound leaf examples?
I've got a project where we collect leaves, classify them, etc. There are some required classifications. One of the requirements is to get a doubly-compound leaf. What are some trees that are doubly-compound? Please help! I have Hickory, but that's just compound I think.
Edit: I did try googling, but it's hard for me to know what's available in my region.
From Comments: I live in Tennessee, U.S.

Where in the world are you? What kind of trees/plants do you have access to?

I live in Tennessee.

Hickories are not doubly compound (AKA bipinnate). They are just (once) compound leaves as you guessed.

For the future, you can try Weakley's flora app "FloraQuest". You can search for trees based on a dichotomous key and fortunately It'll automatically narrow your choices so you can only see local plants. Though this won't give you a list, it'll train you to use a valuable tool while searching for your own answers. (Note: it comes with a visual glossary of terms :D)

Albizia julibrissin (Persian silk tree) is doubly compound (AKA bipinnate) and has a conspicuous pink/white fluffy flower. This tree is an Asian native, but it's a commonly cultivated (and equally commonly escaped) plant in the U. S. You should be able to find it in numerous locations. Look in yards and along roads.

http://www.missouriplants.com/Pinkalt/Albizia_julibrissin_plant.jpg
For native species: Gleditsia triacanthos (honeylocust) is a fairly widespread (though uncommon) example of bipinnate leaves. Here is an image from Will Cook's wonderful website:

Many ferns have multiply-compound leaves
Take the one in this image, for instance:

That structure is one doubly-compound leaf.

Most plants of the caesalpinioideae subfamily of the leguminosae family are bipinnate, i.e., doubly compound. The best, and perhaps the most easily accesible one for you would have to be tamarind.

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What, if anything, would prevent flying fishes evolving to be capable of extended flight?
This extraordinary video documents a flying fish gliding above the surface of the sea for nearly two minutes. Occasionally it uses its tail for added impetus.
It is possible to imagine a fish gliding like this for longer and longer. However it would still be gliding. Is there any physiological reason that these animals couldn't evolve to flap their 'wings' and even learn to soar?
Another consideration is why this should happen. As I understand it, the behaviour is an adaption for escape from predators.  They do not fly in order to catch prey. What prey might they hunt in the air in the ocean?
Questions

Is there any physiological/anatomical dead-end that would prevent flapping/soaring from evolving?
Is there any adaptive reason that flapping/soaring should evolve?

The first problem is that they have gills and cannot filter oxygen out of the air... so they wouldn't get very far before suffocating. Second would be that  the mass to surface area of wings. Birds wing bones are very porous, so there is very little mass with a rather large surface area. Also they likely do not have the same type of muscle development. The flying fish generate most of there propulsion form their tails, not their side fins. Also birds tails are parallel to the ground which provides stability in flight while the fish are perpendicular, which helps with water propulsion.

I think this would be a better fit on World Building. The question is extremely broad and hypothetical, and is difficult to answer given the scope of this site.

Maybe I'll ask for it to be moved.


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Evolution of spider webs?
Web making seems like a fairly complex behavior built from a pretty strong material.  So how exactly did it evolve? Do we have any clues about what kind of features/behaviors preceded web making and made it possible? Are there any examples of convergent evolution?

All actually very interesting questions!

Some creator gods were involved. Spiders aren't creative enough to come up with this idea.

One of the comment to David's answer (which covers the history and reasons for spiderwebs in its two links) mentions a comparison between web patterns and molecular phylogeny. Not precisely that, but I found this article which opens up some interesting possibilities (I can delete this or turn it into a comment if you consider it too unrelated, please let me know).

Fernández, Hormiga & Giribet. 2014. Phylogenomic Analysis of Spiders Reveals Nonmonophyly of Orb Weavers. Current Biology.

Chopped summary:

Spiders constitute one of the most successful clades of terrestrial
  predators. Their extraordinary diversity, paralleled only by some
  insects and mites, is often attributed to the use of silk, and, in
  one of the largest lineages, to stereotyped behaviors for building
  foraging webs of remarkable biomechanical properties. (...) Prior molecular efforts have
  focused on a handful of genes but have provided little
  resolution to key questions such as the origin of the orb weavers.
  We apply a next-generation sequencing approach to resolve spider
  phylogeny, examining the relationships among its major lineages. (...)
  These results imply independent origins for the two types of orb webs
  (cribellate and ecribellate) or a much more ancestral origin of the
  orb web with subsequent loss in the so-called RTA clade.

When comparing molecular family trees, orb weaving araeonoids and deinopoids seem to be more distantly related than thought.
That discovery leaves two possible explanations for the evolution of the spider web: It either emerged much earlier than previously expected and was later abandoned by some species (most believe so). Or, web-spinning and the capacity to spin silk evolved multiple times. Both theories are viable, they just need to catch more spider families to prove which one fits better.

Maybe this answer to another post is helpful for you as well https://mathoverflow.net/a/372105/161287 . It gives interesting perspective on the various roles and purposes of spider webs (with interesting links), and it looks at spider webs from a conceptual point of view.


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Function of NaCl in yeast shuttle prep of plasmids
What is the role of NaCl in plasmid isolation from yeast cells using plasmid rescue solution? If the basic theory behind the method is alkaline lysis, then we is NaCl used and not NaOH?

High salt concentrations will cause the proteins and lipids to precipitate out, as in salting out. Free Na+ ions may also bind the negatively charged DNA backbone and give the molecules a neutral net charge, allowing them to concentrate as well.


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Microinjection method in C. elegans
I have a question about the experiment that using microinjection to inject RNAi into the C. elegans. To prepare the dsRNA for injection, fist have to clone the gene of interest from the worm genome DNA and insert into a plasmid that has either T3 or T7 promotors. To clone the gene of interests, one has to design the primers. There is a paper descripting the protocol of the microinjection. Here is the link to the paper: http://labs.bio.unc.edu/goldstein/dudleygoldsteinmmb05.pdf
It is said that the primer for clone need to add sequence of T7 Promotor, but why? and why just add partial not complete sequence? why is it in the second step of PCR? Is it required to add the restriction enzyme site to both primers? Why?
Also in the feeding experiment, the plasmid(insert) is transformed into the HT115 strain and use IPTG to induce the expression of dsRNA. However, the microinjection is using dsRNA to inject the worm. So after cloning the gene of interest and insert into the plasmid, is the dsRNA expressed in the vitro before injection? And how? Thank you!

What they're doing is called two-step PCR. In step one, some gene-specific primers with tags amplify genomic DNA, but the product has adapter regions now added to each end. In the second step, you add primers that complement the tag/adapter region and have T7 promoter sequences at the ends. Your second product will have the adapter region, and the T7 promoters on the outside. The paper you provided shows they just modified the process: the first product is the gene of interest flanked by part of the T7 promoter, and the second product is the gene of interest, the T7 promoters, and restriction sites for cloning.

Design and implementation of high-throughput RNAi screens in cultured Drosophila cells
It looks like from what they know, adding the partial T7 in the first step is just optimization for their procedure. You want to add those restriction sites to wherever you can imagine you want your insert cut by the endonuclease. In a ligation step for inserting the gene fragment, you'll have cut your plasmid open with the same restriction enzyme you use to cut the insert, so that it ligates in nicely.
The HT115 strain has some nice properties you can read about here like a lack of RNase III that would degrade dsRNA, so it's suitable to produce the actual dsRNA inside of, and for the feeding experiment this is fine. For microinjection, they're using in vitro transcription kits to get dsRNA from the PCR product, which should be a gene of interest flanked by T7 promoters and restriction sites. T7 polymerase will simply transcribe everything downstream of it's promoter, so we don't have to worry about the restriction sites except for the feeding experiment.
MEGAscript® T7 Kit
The above kit comes with a T7 enzyme mix, NTPs, DNase, reaction buffer, a stop solution, precipitation solution, etc. You should be able to follow the manufacturer's direction and get 100 µg RNA per reaction, according to the webpage. Then you purify the dsRNA. It's literally just T7 polymerases transcribing whatever is between the two promoters into dsRNA -and for that kit, linear DNA does work- and then you degrade any DNA, leaving you with the dsRNA.


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Can body temperature affect the quality of sleep?
If so, how does it influence our sleep? And what can we do to improve the quality of sleep by adjesting our body tempurature?

This question is way too broad. If your question is on the last three examples, and on those examples only, it is quite answerable, but rather poorly researched. They look like assumptions - where did you read it?

@AliceD Our tutor asked us to make a presentation on it. Having searched on the internet, we think these factors may have influence on people's quality of sleep, but we are not sure.

Try sleeping in a noisy floodlit insecure environment, with people stumbling upon you all the time.

If you can make your question more specific, please do. As of now it would need a uni library to answer. Then a better question would likely be "What does not affect sleep?" :)

@AliceD Like this?

Awesome. Much better +1

Might be more on-topic on health.SE.


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How can birds keep their eyes moist during flight?
Mammals have an upper lid and small mass  of tissue in the upper corner known as nictitating membrane. This helps keep the eyes clean; birds can moisten their eyes in flight using this membrane without blinking. How does this work?

Because the nictitating membrane secretes a fluid that is resistant to evaporation. Therefore, birds need not blink their eyes during flight.

Please do add some solid references.


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how to solve gap reactions in genome scale metabolic reconstruction
I'm making a project about modeling of nannochloropsis metabolism. My model is in the refinement stage. However, it is not running in the FBA test. Then i found there are 87 reactions that did not run. But the reactant/metabolites for those reactions to run are there in the model.
Is there any one know what is the possible reason for this, and how to solve this problem?
Really looking forward to see your answer.
Thanks,

I'm not exactly sure what you're asking I'm afraid. Could you provide some more information?

Hi Good Gravy, it is about the result of FBA optimizeCbModel when i apply for my metabolic model. it gives f=0, no flux through my model. I think the problem is what @ Roland said.

It is common that reactions in stoichiometric models cannot carry flux because there is a "dead end" metabolite somewhere. The problem may not be in the immediate reactants / products, but can be several steps away, and is not always easy to find.
If you have a network visualization tool, one option is to highlight all reactions that cannot carry flux; often this reveals an entire blocked pathway ending in the isolated metabolites.
A more systematic method is to examine the dual solution of the linear program for maximizing flux through a blocked reaction; this shows the active constraints, which are precisely the metabolites that are lacking for the blocked reaction to be able to run.

Hi Roland, Thanks for your answer. Do you know which visualization tool that i can use in this case? I'm trying to make with cytoscape but it is quite a bit messy for me.

Cytoscape should work well, provided you have a graph layout you can just export the graph with node labels reflecting blocked reactions.  If you don't have a graph layout it's much more work --- this is not trivial to do automatically, I have always done manual layout. The LP dual method might be easier.


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Thermoregulation Question
I had the following question on an exam of mine and I got it wrong, so I was wondering if someone could help explain the reasoning to me. Below I list my explanation.

An overheated and sick dog in a hot environment will have an impaired thermoregulatory response when its
(A) evaporative heat loss increases
(B) metabolic heat production decreases
(C) body temperature increases to match the environmental temperature
(D) blood vessels near its skin increase vasoconstriction

So here's how I approached this: A and B are clearly incorrect, as they aid the thermoregulatory response of the animal by allowing it to lose excess heat.
Thus, it comes down to C and D. I chose D because I thought that since vasoconstriction traps more of the heat inside the body, it would be counterproductive to what the dog actually needs (vasodilation). I'm assuming that the correct answer choice is C, but could someone please explain it to me?
Thanks in advance to all who reply :)

You're right, A and B both are normal thermoregulatory responses, so those can't be the right answer.
I'm guessing the rationale for C is that, if the dog's body temperature is increasing to match that of the hot environment, it must mean the dog has an impaired thermoregulatory response. It's kind of tautological.
But D also seems correct to me. If a dog is in a hot environment, and its blood vessels near the skin are constricting (say, because it's sick), that's counterproductive to the normal thermoregulatory response. If the dog isn't dilating its blood vessels near the skin, that's an impairment to the normal thermoregulatory response.
Perhaps the question is written wrong? Maybe D was supposed to say "vasodilation" instead of "vasoconstriction"? If this is a question written by a teacher I'd say you have a case for arguing it.

This is a question from Ch40 of Campbell's Biology, they seem to be getting at the fact that C is right because the dog is endothermic and only operates properly within a certain range of temperatures. For D, the argument is that since the environment is already hot, vasoconstriction to decrease heat interface is beneficial.

@Kendall - Such a helpful comment! Might you want to turn it into an answer?

Thank you everyone. I asked my teacher (since she's technically not the one who designs these questions) and she said that D is correct, so she rewarded me the points.

Heyy
Like you said, A and B are actually not the answers. However, C could be in this case the answer. The dog is already overheated meaning the core temperature is very high. The environment stated also has a very high temperature. The body is not supposed to match the environments temperature, instead, its (hypothalamus) supposed to set a lower temperature to be matched. Therefore, the dog body matching the environments temperature indicates an impairment in thermoregulatory response. In addition, since the dog is already overheated and trying to match the high temperature of the environment, it can lead to tissue deterioration or damage which is a huge problem


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Affinity Column of membrane bound receptors
I understand affinity columns can be used to study the ligand/enzyme affinity. But is an affinity column able to be used for membrane bound receptors? I

This is a classic reference where Stanley Cohen and Graham Carpenter used an affinity column made out of the epidermal growth factor (EGF), and used it to purify the EGF receptor: JBC 1980

Purifying Challenging Proteins
So this is definitely something you can do, but first you need to express proteins that have a tag the affinity column is going to recognize. You can engineer a 6x his tag pretty standardly, but the procedure I'm looking at says a long 8-10 his tag might be better for insoluble proteins. You also want to be careful to place the tag at the C-terminus to avoid messing with the membrane anchoring signal at the N-terminus.
You can express these in bacteria, for example, and you'll disrupt the membrane and solubilize the proteins of interest using detergents. You have to be careful here because while some of the solubilized proteins can retain their native conformation in solution, harsh treatment with detergent can remove critical lipids affecting stability.
The purification step for his tags involves an affinity column of immobilized nickel, which binds to imidazole on histidine. After pushing the associated binding, wash and elution buffers through the column containing the sample, you should in theory have your purified protein product. You elute by washing imidazole through the column, which should competitively displace the his tag and wash the protein of interest out.
Should you lack tagged protein to begin with, you'll need to use a number of purification steps like gel filtration, ion-exchange, etc., and a little knowledge about your target protein to get a good purification though, like it's ligand for affinity binding. Give that presentation a read through!


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Batch several sequences for absent restriction sites
I have a collection of about 120 7kB sequences I would like to check for ether a list of specific restriction sites, or what restriction sites might be absent in all of them.
Is there a app or library that can do this?
So far I've only found systems that can do 1 or 2 sequences at a time.
Possible workaround:
Right now I'm trying to concatenate all the sequences together (about 850Mb) and then using Bio.Restrictions methods of the Biopython libraries.  As I kept running into memory overflow problems, I'm refining the search make a new RestrictionBatch based on 4-5 enzymes that are absent and introduce-able into 3-4 test sequences.
Even then I'm running into crashes, which will probably mean that I take the complete set and test over five or so combined strings.
Before I completely go re-inventing the wheel, can anyone let me know of something that already does this?  I don't really care about the language, we have Python, .Net, Java, R, and MatLab "covered" across the lab.

Why can't you read in each sequence one at a time, and use regex's to see if the recognition sequences are in there?

@swbarnes2 I can, but that seems only practical so long as I keep the restrictionbatch small. Vs a real test of hundreds of enzymes is that practical?

How long do you think it takes to search for 100 regex sequences in one string?  I don't think it will take long.

@Swbarnes2 that's backing out of using Biopython, but something we're considering. The actual full library we have is about 1200 enzymes, many of which with wildcards. I wanted to make sure something like that didn't already exist before we build it


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what are the best books for the IIT-JAM biological sciences exam?
I'm from India and i'm preparing for a competitive exam called the Joint Admissions Test for a Masters admission.
I need help in finding books to read from for these chapters:
General Biology: Taxonomy and physiology, Pro-and eukaryotic organism; cell organelles and their function; multicellular Organization; energy transformations; internal transport systems of plants; respiration; regulation of body fluids and excretory mechanisms; cellular reproduction; Mendelian genetics and heredity; biology and populations and communities; evolution; genesis and diversity of organism; animal behaviour, plant and animal diseases.
Basics of Biochemistry, Biophysics, Molecular Biology: Buffers; trace elements in biological systems; enzymes and proteins; vitamins; biological oxidations, carbohydrates and lipids and their metabolisms; digestion and absorption; detoxifying mechanisms; plant and animal hormones and their action, nervous system, nucleic acids, nature of gene and its function, Genetic code, synthesis of nucleic acids and proteins. Enzyme mechanisms and kinetics, nucleic acid metabolism, photo synthesis.
Structure of Biomolecules: intra and intermolecular forces; thermodynamics and kinetics of biological systems, principles of x-ray diffraction, IR and UV spectroscopy and hydrodynamic techniques.
Microbiology, Cell Biology and Immunology: Classes of micro-organisms and their characterization, nutrient requirement for growth; laboratory techniques in microbiology, pathogenic micro-organisms and disease; applied microbiology; viruses, Microbial genetics. Innate and adaptive immunity, antigen antibodies.Cell theory; Cell architecture; methods of cell fractionation; cell division; types of chromosome structure; biochemical genetics- inborn errors of metabolisms; viruses and fungi; principles of processes of development.
PS. I've studied biology only until high school.

This question is just too broad. Also, asking for examination tips is tantamount to homework. Book recommendation questions should be precise else they would be considered opinion-based. I'm sure there are plenty of websites that provide reading materials and recommend references for examinations like this. Unfortunately, this site is not one of them.


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Is it easy to test human Flicker Fusion Threshold?
How would you go about testing human flicker fusion threshold? Is the testable rate consistent in humans over time or volatile?

Flicker-fusion rates are very easy to test in humans: you provide a flickering light-source, set it to flicker at different speeds, and get the people to tell you whether the light is flickering or constant. This paper (from 1952) achieved a flickering light by putting a rotating disc with holes in it in front of a projected light source. A more modern testing unit is demonstrated here.
The human flicker-fusion rate does not appear to be a constant. In addition to being influenced by attributes of the light source (such as its wavelength, how much the brightness changes, etc), it also appears to be influenced by factors such as stress and fatigue (pdf).

Great - thanks for the information. I'm mainly curious on how human flicker-fusion rate in athletes might correlate to size and/or performance. As in some players (possibly smaller) 'see' the game faster. But this seems tough to test in a non-biased way. It seems like testing reflexes/reaction times would be more appropriate.


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How do you create a .snp datafile?
I'm looking to use the software DIYABC 2.1.0 to apply approximate bayesian computing (ABC) to some resequenced data that I have.
The resequenced data is in FASTA format however, and the software requires an SNP datafile format (.snp). How do I generate such a file from FASTA formatted data? Is it possible?

I don't know either piece of software.  Hopefully, someone will have written a utility to do the conversion you need, or maybe there is a set of utilities, so that you can convert from format A, to B, to C, etc.  However, sometimes you have to write your own genetic data file conversion program (in Python, Perl, etc.--whatever you like).  It's probably conceptually easy--you're just rearranging or recoding the same data--although the routines can require some care.  If you know enough to get started, but get stuck along the way, Stackoverflow.com would be relevant.  Maybe none of this is news.

You will have to detect SNPs. You can get the vcf by aligning your resequenced fastA to the reference genome (or previously sequenced genome) and use a Variant Calling method of your liking. Then there is this tool to convert vcf to the required .snp file: https://github.com/loire/vcf2DIYABC.py

@Mars That's very helpful, thank you. I'm very much a novice, so any input is appreciated!

@skymningen Great, I shall try and produce that intermediate vcf file. I did try using PGDSpider to convert the files, but there was obviously something else that had to be done. Cheers!


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Anomalous base pairing of nucleotide tautomers
What tautomers base pair with what bases?
I know that adenine pairs with thymine and guanine pairs with cytosine normally. My question is what does the imino form of adenine base pair with? Regular cytosine? What does the enol form of guanine base pair with? Regular form of thymine?
I cannot find any books discussing this issue and Google is of no use. However, my professor wants us to know how tautomers base pair.
I tried base pairing cytosine with adenine but does the -NH2 group on cytosine really hydrogen bond with the imino -NH group on the adenine tautomer?

http://blc.arizona.edu/courses/181Lab/MoBiByMe/Tautomers.html

The tautomers are rare but they can form and it is suggested that tautomerization can lead to mutations because of non-cognate base pairing.
Khuu & Ho (2009), have inferred the presence of adenine and thymine tautomers from the crystal structure of an in-vitro assembled holliday junction. They infer that imino-Adenine base pairs with amino-cytosine (normal form) and enol-thymine base pairs with keto-guanine (normal form).

Reproduced from: Khuu & Ho (2009)

Khuu, P., & Ho, P. S. (2009). A rare nucleotide base tautomer in the structure of an asymmetric DNA junction. Biochemistry, 48(33), 7824-7832.


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Determining the osmolarity and tonicity of a cell
Consider a cell with urea concentration inside being 2mmol/L and outside being 2.5mmol/L. The cell itself is permeable to both urea and water. Ignoring the effect of other osmolytes,
A) Urea flows in, water flows out
B) Urea flows in, water flows in
C) Urea flows out, water flows out
D) Urea flows out, water flows in
I'm confused because I thought water would simply flow out of the cell to equate the concentrations inside and outside such that there is no net flow in urea.

If you consider the cell to float in a bucket of water you can quickly envision that the efflux of water from the cell will never equalize the concentrations.

The efflux of water isn't instantaneous. Since urea is free to move across the membrane, it will (and with a net movement from higher to lower concentration).


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To have a drug travel to a specific place in the body can you just coat the drug in extracellular signals recognized by target cells?
In a lecture of mine the professor was talking about the issue faced in regards to drug therapy when it comes to targeting lung cells in cystic fibrosis. It was said that if unless the drug gets targeted just for the lungs it could simply travel randomly throughout the body and thus not effectively treat the disease. My question is if cells internalize extracellular signals and travel/respond accordingly why can we simply not coat a drug for cystic fibrosis in extracellular signals that specifically bind to lung cell surface receptors?

Yes you can, in principle, coat the drug particle with ligands such that it will be targeted to specific cell types. This is being considered and actively worked upon for development of targeted drug delivery. However, you should also bear in mind that doing these kinds of coatings would be costly and it would greatly increase the cost of the drug.
At least, in the case of cystic fibrosis or any other disease of the lungs, an easy method of restricting the drug to lungs would be by taking the drug in the form of aerosol, using inhalers.

Mechanism of inhalers.   Picture source: http://www.globalasthmareport.org/management/inhalers.php


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If two different diseases have more than one common pathway, the relationship between their occurences?
I just wonder that are there any special relationship between the pathway and disease occurrence.
For example, there are cancer A and cancer B (and they have more than one common pathway). Then if one person was diagnosed with cancer A, does he have a high probability for getting cancer B? Could you recommend any researches for that?

I think that a good point to start is a classic work in literature that i've seen cited many times in my courses: http://www.cell.com/abstract/S0092-8674(11)00127-9


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When did human ancestors learn to walk?
Where does our ancestor learn to walk from? How do we control our legs whenever we take a step?  I confuse every time whenever I take one step.

Are you asking about the evolution of upright walking in hominids or the physiology of human walking (balance etc)?

I think this questions should be better focused since as pointed out by @fileunderwater there are at least two broad issues here to develop.

Perhaps this previous question answers the evolutionary part of your question: http://biology.stackexchange.com/questions/27475/why-did-humans-become-bipedal. If you could elaborate on the issues you have with leg control (balance? neuromuscular system? ...) then this question may be answerable. As of now I vote to close because your question is too broad and unclearly stated.

It is unclear what you mean by "Where" in your first sentence. In addition to that you seem to be asking about the phsysiology of upright walking (which is too a broad question in itself) AND about its evolution. You should restrict your post to only one question.

In a sense, there's an easy answer to your question.  Humans became bipedal in Africa, since bipedality is well-established for the first species in the human lineage to leave Africa (Homo erectus/Homo ergaster).  This can be verified in many textbooks.  However if you ask the question when, in what species, or why, there's no easy answer to your question. The question comes down to (a) which fossils are specifically ancestral to humans (b) what fossils have evidence for bipedality, and (c) theories as to why those species became bipedal.
The narrow sense of humans, Homo sapiens, has been bipedal ancestrally.  Other closely related species were almost certainly bipedal (Homo neanderthalensis and Homo heidelbergensis for example).  In fact, the species or species complex from which humans likely arose, Homo erectus, was also likely bipedal (discussion below).  If we take the broadest sense of what "human" means, it could mean any species which split from the human lineage after the split with the extant great apes (specifically, post split with chimpanzees).  Here there's reasonable evidence for bipedality exists around the same time as this split, but not in all species.  Specifically, Orrorin tugenensis is a 6 million year old specimen with some (but not conclusive) evidence for bipedalism.
Question b, how do we know a fossil creature is bipedal, is a challenging question.  Homo sapiens, the only completely bipedal primate, have many adaptations which facilitate walking on two legs.  The shape of our pelvis facilitates the muscle attachments necessary for walking by flaring the ilium (the bone which forms the upper part of the pelvis).  This same flaring is found in Australopithecus afarensis (which includes the famous "Lucy" specimen), about 3 million years ago.  Australopithecus also has a fossil of footprints, which seems to indicate bipedal movement.  The human femur is bent inwards and the neck is thickened to support the weight of someone walking upright.  This same thickening is found in Orroin tugenensis and the angle in Homo erectus/Homo ergaster (these are two names which are either closely related species or the same species, depending on who you ask). The human big toe is also in line with the others in the foot, which likely allows us better motion on the ground.  This feature is also true of Ardipithecus ramidus, at about 4.5 million years ago.
The third part of your question, why humans became bipedal, is largely speculative.  Many theories exist for the process which lead to bipedalism.  A popular theory in the 1970s and 1980s was that humans became bipedal to enhance our abilities to see across tall grass, because many people thought Homo erectus/Homo ergaster was the first upright walking species, and grasslands dominated east Africa at the time.  However since earlier evidence for bipedality, many people have abandoned this hypothesis in favor of others.  These other hypotheses include that bipedalism arose after scaffolding on to arboreal (tree-living) adaptations.  If human ancestors lived in trees, they may have moved in a vertical posture, leading to many of the adaptations needed to move vertically on the ground.  Others include an increased reliance on meat, caught through endurance hunting, or even wading into tidal waters being the key feature (notably this is not the aquatic ape hypothesis, which is pseudoscience), and this reliance on key marine resources provided the essential stable food supply for brain enlargement.  The short answer is that there's a tremendous amount of speculation in this area, and few firm facts.
Whichever of these species you choose as the "first bipedal human," and how confident you want to be about that bipedality, they all evolved in Africa.


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Why do snakes not have eyelids?
Why is it that snakes do not have eyelids?
Is it due to that fact that they are not as evolved as we humans and other organisms that have eye lids, or is there any other significance behind it if any?

"the fact that they are not as evolved as we humans" - there is no such fact. Evolution is not a scale going from "less" to "more". All organisms are equally evolved. So, it can't be due to that "fact" by definition.

@Aneesh For more discussion on the concept of "more/less evolved", have a look at the post Are we “more evolved” than present-day bacteria?

Snakes have no eyelids. Each eye is covered with a single, transparent scale. These eye scales protect the eyes from mechanical damage, and prevent the eyes from drying out, just as an eye lid would do. In effect, snakes developed another solution to protect their eyes.
As a result, snakes cannot blink and they sleep with their eyes open.
A snake’s eye scales are part of its skin. This means that when a snake sheds its skin, it must also shed its eye scales. When it is time for shedding, the eye scale turns opaque, reducing vision (Fig. 1).

Fig. 1. Opaque snake eye before skin shedding. Figure source: Snakes are long blogspot
Source: Museum of Victoria

Good answer +1. It would be great (although that would probably take some work) to have some mapping of this trait on a phylogenetics tree (or just some information about their snakes and mammals sister species).

@Remi.b - thanks heaps. But the phylogenetics I leave up to you my friend. I'm in sensory systems you see :)


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Can specific B-cells be created in a lab?
Instead of creating protein sequences, could that stepped be skipped and just have B-cells created to manufacture a particular type of immunity?

Are you after clonal antibodies?

@AliceD That isn't what they are after. They want to gene edit B-cell receptors to recognize specific pathogens.

Please clarify your question with sufficient background information otherwise it is likely to get closed.

We aren't there yet.
There is a complex interplay between antigen recognition, presentation, and activation that would have to be worked out. You would also need to engineer the corresponding T-Cell which could recognize the antigen, become activated, which means you also need to develop a dendritic cell that can present to the T-cells, so that they could then go on to activate the B-Cells. Doing this in vitro would be a challenge.
You are actually asking to design highly specific receptors, and protein engineering then sequencing back to a genome would be difficult to do.
If you tried taking a known antibody, you would need to track down the actual B-Cell that produces it, due to somatic hypermutation creating a unique DNA sequence, which leads to the specificity that increases the affinity of antibodies for their ligands. I guess if you did it with germ free mice, you might have a shot at isolating their B-Cells and then finding out the gene sequence. Not impossible, in my opinion, but very difficult at this point.
The closest thing I have heard of so far is the work that is being done in Dr. Carl June's lab. They are working on taking cytotoxic T-Cells, and recombining their receptor DNA so that they can then recognize a patient's tumor and kill the cancer cells, but that is a bit different than what you are asking.


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Why do animal cells lack a contractile vacuole?
I was asked why animal cells do not have contractile vacuoles. Other than the lack of need, I don't know what else to say.

Lodish et al. (2000) explain that animal cells rely on the Na+,K+-ATPase to pump Na+ out of the cell. Exporting electrolytes decreases the hypertonicity of the cell, thereby preventing too much water from entering.
Plant, algal, fungal, and bacterial cells are surrounded by a rigid cell wall. Any osmotic influx of water in a hypotonic solution leads to an increase in intracellular pressure, but not in cell volume. hence, the cell wall effectively prevents the cells from lysis.
Protozoans do not have a rigid cell wall and these organisms sometimes contain a contractile vacuole that permits them to avoid osmotic lysis. A contractile vacuole takes up water from the cytosol and periodically discharges its contents through fusion with the plasma membrane. Thus, even though water continuously enters the protozoan cell by osmotic flow, the contractile vacuole prevents too much water from accumulating in the cell and swelling it to the bursting point.
Reference
- Lodish et al. Molecular Cell Biology. 4th ed. New York: W. H. Freeman (2000)


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If oxygen is such a good energy source, why do plants release it?
Why do plants release excess oxygen, rather than consuming it entirely given it is an excellent energy source?

I guess because plants don't walk around collecting food and it doesn't rain carbohydrates to burn oxygen with. But this gives me ideas for a sci-fi story involving farting trees.

One thing worth noting is that, at night, most plants 'breathe' oxygen and use it to metabolize stored sugars, just like animals.  However, they don't want to keep extra oxygen around during the day, when they're photosynthesizing, as oxygen actually competes with carbon dioxide during the photosynthetic process, slowing it down.

oxygen is not energy, its needed for energy, like when you want fire, you need oxygen.

As wonderful and abundant oxygen is, it is also highly reactive (consider rusted metal), and can contain ozone and oxygen singlets (a free radical). Free radicals are highly mutagenic and lead to double-stranded breaks in DNA. When cells die by programmed cell death they lyse their mitochondria, possibly to hasten the process. Finally, the enzyme super oxide dismutase exists to safely remove these free radicals from cells.

Short answer
Plants release O2, because it is not an energy source. Instead, it is used to free energy from energy-rich organic compounds.
Background
Plants are solar powered. They release oxygen as a waste product during carbon fixation. Carbon fixation is basically the storage of solar power into carbon-bonds in glucose, a process referred to as photosynthesis or the Calvin Cycle.
To release the solar energy from glucose it has to be burned (oxidized). Oxidation of glucose can be realized via the the citric acid cycle (or Krebs cycle) and electron transport chain to generate ATP. O2 only comes in in the very last step by acting as the final electron acceptor to produce H2O (Fig. 1.)

Fig. 1. Electron transport chain in mitochondria. Electrons are sent through a chain of proteins that drive hydrogen transport out of the mitochondrial space. ATP-synthase uses the proton gradient to generate ATP. Source: Davis University College
Hence, O2 is not the source of energy, it is merely used to free it from energy rich compounds such as glucose. Because it is so abundant in the atmosphere, it doesn't make sense to store it.
Reference
- Berg et al., Biochemistry. 5th edition. New York: W H Freeman (2002)

"Because it is so abundant in the atmosphere, it doesn't make sense to store it." this makes only sense today, it made no sense when the first photosynthesis was done.

@plasma perhaps early plants (/weed/phytoplankton/...) did retain oxygen and released it when out of storage space. You could also drop evolution for intelligent design and be done with it.

@PlasmaHH - defintely true. But the fact that oxygen levels only increased when plant life became abundant still supports it being a waste product.

@AliceD: of course it is a waste product, but I do also throw away my waste because it is waste, not because it is abundant on the streets...

@PlasmaHH - the argument is that you don't have to store it because it is abundant. Not that you have to throw it away because it is abundant.

@AliceD: So why would I keep my waste products with me when they are not abundant in the environment? And why did the first organisms did not keep it, although it was not abundant?

@PlasmaHH - let's go to chat.

Another reason that oxygen is not stored could be that it would result in Warburg effect i.e, reduction in photosynthesis due to decreased functioning of RUBisCO due to increased O2 conc. and also due to photooxidation of chlorophyll due to same reasons.


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Photosynthesis Equation
The equation for photosynthesis is
$\ce{6CO2 + 6H2O + Energy -> C6H12O6 + 6O2}$
My confusion rests in the following: during the photolysis (water-splitting) step of the light reactions that occur in Photosystem II, water gets split into 2 H+ ions, 2 electrons (which enter the photosystem), and one Oxygen ion. But if Oxygen ($O_2$) is comprised of two oxygen ions covalently bonded to each other, doesn't this mean that
$\ce{6H2O -> 3O2}$  ?
Could someone please clarify this for me?

There are 12 oxygen atoms in CO2 and 6 in H2O giving you a total of 18 Oxygens on the reactants side of the equation. On the products side, you have 6 Oxygen atoms in glucose and 12 in gaseous oxygen for a total of 18. The reactants and products balance. You are forgetting about CO2.

These representative reactions are a bit misleading. CO₂ fixation is not directly coupled with production of oxygen. This may not be an answer to your question but my suggestion would be to just dump these oversimplified explanations in the trash can and have a look at the actual stoichiometries in the Hill reactions.

Equation you have mentioned is balanced chemical equation. In reality these are series of Redox reactions, major two as follows,
Oxidation of oxygen from water in presence of light (energy from photon),
$ 2H_2O  \xrightarrow{Photons} O_2 + 4H^*$
Ions produced from above reaction reduces carbon dioxide ,
$4H^* + CO_2 \rightarrow (CH_2O) + H_2O$
So both equations combined, we can write general form as
$nCO_2 + nH_2O \xrightarrow{Photons} (CH_2O)n + nO_2$
In simple words to answer your doubt, in final equation 2 oxygen molecule coming from per 2 $H_2O$ molecules and 1 coming from per $CO_2$ molecule. Hence final balanced equation is
$6CO_2 + 6H_2O \xrightarrow{Photons} 6(CH_2O) + 6O_2$

Reactions 3 and 4 do not use photons. It is a crude representation of the Calvin-Benson cycle.

Reaction 3 is general form to represent complete reaction (1+2)

But it is as misleading as the OP's reaction. It is an extreme oversimplification as you know very well. These reactions are not even directly coupled. I think you should address this point.

Are you sure we should add that detail here ? It might confuse OP more, considering OP is concern about where is extra oxygen coming from. If so, you can convert this to community wiki and edit answer.

I think the "representative reaction" is the source of all confusion. People have to realize that it is incorrect. In reality these are not coupled reactions and therefore the stoichiometry cannot be exactly balanced. The approximate stoichiometries can be obtained from analysis of the metabolic flux.

It's still a bit confusing, but that's okay (this is only for an AP Bio course and I just wanted to get things straight in my mind). Thank you Dexter and WYSIWYG


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Is it possible to grow E. coli K12 with algal amino acids as the sole carbon source?
Instead of glucose or glycerol, is it possible for E coli to grow on an amino acid mixture as the sole carbon source and, if so, what should the concentration be?

Why specifically algal amino acids though?

E.coli can do that and in fact does this a lot in a commonly used bacterial medium: The popular LB Medium. This is composed of three components:

Tryptone, a peptide mix made by digesting milk casein with the peptidase Trypsin (10g/l)
Yeast extract, made by autolysis of the cells (5g/l)
Sodium chloride (10g/l)

The original formulation of Bertani from 1951 (see reference 1) also contains 1g/l Glucose, which was later discarded, since the handling is easier without it (glucose cannot be autoclaved as it degrades).
Since the medium does not contain any other utilizable sugars as a carbon source, the bacteria use free amino acids (and small peptides up to 650 Da in size) for their growth. The reason for this limit is the exclusion size of the bacterial porin channels which allows the uptake of the peptides and free amino acids (see reference 2 for details).
Once these are exhausted, the growth stops, which is the reason why LB Medium is actually not very good suited to get really high densities (that's why SOC media are used for some applications). Read the excellent paper in reference 3 and the also excellent article in reference 4 if you want to know more about the topic.
I don't think it matters from which source your amino acids are coming. Regarding the concentration I haven't found any data, but in reference 4 it is estimated that only about 25% can be used by the bacteria. Since the mixture contains about 15 grams of protein lysate, this would roughly mean about 4 grams of free amino acids or more.
References:

Studies on Lysogenesis I.
Size Restriction on Peptide Utilization in Escherichia coli
Escherichia coli Physiology in Luria-Bertani Broth
The Limitations of LB Medium


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Can epiphyte share nutrient to host plant?
Sometimes plant share their nutrient with underground root network
But if there are plant that grow on other tree. Is it possible that it would merge into another tree and sharing resource. I mean opposite to parasite that it not steal resource but give the leftover to the host? Any plant do that?
I heard some plant like Coast Redwood or Banyan could grow their child on their branch as epiphyte. Can them sharing resource between each other?

No, per definition there is no connection between the epiphyte's and the host's vascular system. If there was, it would make the species a parasite.

Then are there any parasite specie that will give nutrient to host?

I doubt that and it wouldn't make much sense from an evolutionary perspective. What mechanism can you think of that would make it advantageous to waste your own nutrients to another, unrelated, plant species?

@Hav0k First, as I mention that some large tree could have their own specie grow on itself so if they could share nutrient it could benefit species as a whole. And second I think it could be like a relationship of market and landowner. When host get benefit to get stronger then the things rely on would be more secure

In the future, if you wish to change your question please edit it to do so rather than asking followup questions in the comments. Comments are impermanent and should not contain information essential to understanding the question. Thanks!


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Aloe species identification
I am trying to find out which species these are.  Someone claimed they were Aloe Vera, but I am skeptical as I have never seen Aloe Vera with that kind of growth. These look more like Aloe Juvenna to me.
What do you think?

Definitely not Aloe vera.

Try here: http://www.succulentguide.com/cactus/?genus=Aloe

Also please update if they decide to flower :)


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Why are cancer rates low in large animals?
Large animals generally have more cells and live longer than smaller animals. For example, bowhead whales live up to 200 years and weigh up to 100 tonnes, as opposed to humans (living ~71 years and weigh ~75 kg) and mice (10–25 g, <1 year in the wild). Hence, whales have an immense number of cells and those cells are subjected to environmental carcinogenic influences (chemicals, UV) for a longer period of time.
Cancer is caused by random mutations and those random mutations are basically stochastic processes. Given their long life span and larger number of cells, shouldn't larger animals have a substantially higher chance to develop cancer? In fact, story goes that bowhead whales in fact only very rarely contract cancer, and less so compared to humans?

Can you please provide a peer reviewed source backing up your claim that they do not, in fact develop cancer.

@AMR - just checked - at least for sharks it's a myth

Short answer
Large animals do get cancer. They may contract cancer with an incidence less than that estimated by absolute cell numbers, but there seems to be a lack of data on cancer rates in large animals to support this hypothesis conclusively.
Background
Whales contract cancer (Martineau et al, 2002). There does, however, seem to be a lack of correlation between body mass and cancer risk, which is counterintuitive since larger animals have more cells. This is known as Peto’s paradox (Caulin & Maley, 2011), after epidemiologist Richard Peto of Oxford University in the UK, who noted it in the 1970s. He reasoned that larger organisms have more potentially carcinogenic cells, tend to live longer and require more ontogenic cell divisions. Therefore, statistically, cancer incidence should scale with body size (Nagi et al., 2007).
It is thought that larger animals use protective mechanisms that many smaller animals do not. For example, blue whales have 1000 times more cells than us, if they would contract cancer at rates 1,000 times higher than humans, they would die before they were able to reproduce and the species would quickly go extinct. However, the paradox itself has been scrutinized, because there may simply be a lack of data on cancer rates in large animals (Source: Nature News, 2013). In addition, it is thought that malignant tumors are disadvantaged in larger hosts. In larger organisms, tumors may need more time to reach lethal size, so tumors have more time to evolve without becoming lethal. Hence, in large organisms, cancer may in fact be more common, but less lethal (Nagi et al., 2007).
The persistent myth that sharks don't get cancer seems to stem from clinical evidence that cartilage has antiangiogenic properties, i.e., it inhibits the development of blood vessels, which are crucial to the growth of many cancerous tumors. Since shark skeletons are made of cartilage, it was thought that they can't get cancer. Recent studies have found that while the incidence of cancer in sharks and related fishes such as rays does seem to be low, cancerous tumors, including chondromas (cancers of the cartilage), have in fact been found in sharks. The reasons for the apparently low incidence are not necessarily related to their high cartilage content, but may simply be a matter of lack of directed research on cancer in sharks and related fishes (Source: American Museum of Natural History). Indeed, tumors have been found in 23 species of sharks, measuring up to 30 cm in a Great White (Source: Scientific American, 2013).
References
- Caulin & Maley, Trends Ecol Evol (2011); 26(4): 175–82
- Martineau et al., Environ Health Perspect (2002); 110(3): 285–92
- Nagi et al., Integr Comp Biol (2007); 47(2): 317-28
P.S. All animals, including whales, age and die, otherwise the oceans would've been pretty crowded, at least before whaling started.

@AlekseyBelikov, no worries. This one question was particularly interesting, because I was also under the assumption that sharks could not contract cancer. I never really delved into the topic up until now :)

@AlekseyBelikov If the answer answers your question, you can check it so that future users know you received the answer you expected (I am not sure you can still accept an answer now that the post is being closed). Accepting an answer also reward the one who answers with extra reputation points and may eventually bring more effort answering your future questions.


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What is the reason for having an extra recognition site for a restriction enzyme?
Can the size of a supercoiled plasmid DNA be determined by using standard DNA size fragment electrophoresed in parallel? 2. An unknown DNA molecule was cleaved using several restriction enzymes individually and in various combinations. The DNA fragment sizes were determined by agarose gel electrophoresis and the restriction enzyme recognition sites were mapped. Subsequently, the DNA was sequenced and an extra recognition site was found for one of the enzymes. However, all the other mapping data was consistent, within experimental errors, with sequence data. What are the simplest explanations for this discrepancy? Assume the DNA sequence had no errors.
My answer:
the  extra enzyme recognition site was cut-off with the fragment due to partial digest that occurred because of insufficient enzyme was added or the rxn was stopped after a very short time.
Am i wrong? my logic here was such that they only found the extra recognition site after they sequenced the DNA thus it was not available during the rxn and thus it was either cut off unevenly in one of the fragments OR it could have had the complementary sequence to it that was methylated that hid it.
Detailed answers are appreciated!!

The scenario in your question can be explained if the "extra" recognition site mapped very close to another recognition site for the same enzyme.

you mean if say i had ECOR1___HindIII___ECOR1 the extra recognition site would be neglected?

Yes, exactly. Although I was envisioning, for example, 2 EcoRI sites separated by between 0-50 bp of plasmid DNA. Depending on the type of gel being used, the resulting tiny DNA fragment generated could be difficult to detect (either because they run off the bottom of the gel, or because they don't resolve). Similarly, depending on the size of the adjacent fragments in the various digests, and the assay's limit on estimating fragment sizes, you might not detect that an "extra" fragment was generated, and "missing".

thanks perry, could you copy your answer and post it under answers? I would love to list you as a the correct anwer owner

The scenario in your question can be explained if the "extra" recognition site mapped very close to another recognition site for the same enzyme.
For example, if there were 2 EcoRI sites separated by between 0-50 bp of plasmid DNA, then depending on the type of gel being used, the resulting tiny DNA fragment generated could be difficult to detect (either because small fragments run off the bottom of the gel, or because they don't resolve well unless the gel contains a higher percentage of agarose or acrylamide).
Similarly, depending on the size of the adjacent fragments in the various digests, and this assay's limitations on estimating fragment sizes, you might not detect that an "extra" fragment was generated, and "missing".


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What are some examples of undirected weighted networks in ecology?
I'm a math major with a current interest towards network theory. A network can be considered as a collection of nodes, and edges between these nodes signifying some relation between them. The most ubiquitous example would be a social network like Facebook with nodes representing people, and an edge connecting two nodes if they're friends.
A network is called directed if the edges have a direction. This means that if there's an edge directed from A to B, it's not the same as an edge from B to A. An example of this would be a food web network, where the nodes represent species and an edge from species A to B means that A eats B. Obviously, this does not necessarily mean that there's an edge from B to A (rarely does the prey eat the predator).
A network is called undirected if it is not directed, i.e. none of the edges have any direction; if there's an edge from A to B, it necessarily means that there's an edge from B to A.
Now, one can assign weights (numerical values) to the edges in a network to signify the relative importance of edges. In the Facebook example above, this can be considered akin to assigning values to edges which indicate the strength of friendship/distance between the residences of friends, etc.
I wish to study ecological networks to see if I can make interesting inferences from my study of weighted networks.
So can you give me some examples of undirected, weighted ecological networks?

Network theory finds wide application in trophic ecology (food webs) and genetics (gene regulatory networks). Have a look at that.

Interaction/foodweb networks where we only know the correlations between species (e.g. correlations between the abundances of species over time) would be one example of a undirected, weighted network.

Epidemiology, the spreading of diseases, is probably one of the most famous applications of network theory in biology, going all the way back to John Snow.
A more relevant example would maybe be something like graph models of habitat mosaics. Populations are often both spread out over landscapes and clumped together in smaller pockets of suitable habitats. While fragmented, these populations still have a certain amount of contact, resulting in gene flow and the creation of what is often called a meta-population. These things can happen on a vast range of scales, from your back yard to whole continents, but by modeling them like graphs they can all be studied comparatively and tested for resilience agains disturbances, habitat loss etc.
You mention social networks, but there is no reason why you can't study the same in animal populations. Say one individual learns something useful, maybe the location and route to a rich feeding ground. That information can then be shared with other individuals, either by show-and-tell, or maybe by some kind of abstract communication. The information spreads in familiar exponential fashion until everyone knows, then any one of those individuals can relay or be "eaves dropped" on by a neighbouring population, it doesn't even have to be the same species in some cases, and the information flows again. As with the habitat mosaics the benefit of these models is that very different systems can be compared and tested on an equal footing, anything from fish, to birds, mammals, even some social insects, lend themselves well to this.

Started working on an answer, then decided just to upvote this one. Some undirected, weighted networks for epidemiology can be found at http://ndssl.vbi.vt.edu/synthetic-data/ , or as component of the ergm R package, if one is so inclined.


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Was the dodo a dinosaur?
I've always believed that the dodo was a dinosaur, I don't know exactly why. I've done some searching on the internet, but except for toy stores selling "Dodo the Dinosaur's" I didn't find anything very useful of which I could conclude if the dodo was a dinosaur or not.
So, was the dodo a dinosaur or not? And if the dodo wasn't a dinosaur, why do people say it's a dinosaur?
(I couldn't find a related tag, I think 'palaeontology' was the closest to what I needed)

It was a bird, and is now extinct. Typing 'dodo' in the Google search engine yielded the Wikipedia entry as the number 1 hit.

I've read the wikipedia page, but it doesn't say anything about it being a dinosaur or not. Which could point to the direction that the dodo wasn't a dinosaur. But I'm wondering why stores say it's a dinosaur. Where does that come from?

Perhaps you would have more success posting your query in ToyStores StackExchange, or PeopleWhoSayThings StackExchange? In this forum for Biology StackExchange I don't think you will encounter anyone with the appropriate expertise.

Yes, dodos were dinosaurs, but that probably doesn't quite mean what you think it does.
Dodos were birds, closely related to pigeons. All birds are dinosaurs.

Thanks! Now I get it. Never knew I've seen so many living dinosaurs ;)

@snake This post will probably help to understand the possible confusion with the term dinosaur.


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Why would a bacterial population show initial growth when it is in unfavorable growth conditions?

This figure shows the anaerobe E. faecalis grown in aerobic conditions, E. coli grown in restricted conditions that are not specified. Why do they show an increase in abundance initially? The black line is growth rate and to me I would think neither would grow at all.

E. faecalis is an aerotolerant anaerobe. It can't use oxygen but it doesn't harm it.

E. faecalis is an aerotolerant anaerobe, while E. coli is a facultative anaerobe therefore if in a non-aerobic environment it can switch to anaerobic respiration. E.coli is also capable of fermentation.
Here is an article for on the various respiratory pathways of E.coli: http://www.sciencedirect.com/science/article/pii/S0005272897000340
One other reasons why cells may grow in a nutrient poor medium is that many types of bacteria have programmed cell death that ultimately is for the better of the entire bacterial population. When nutrients get low some cells commit "suicide" and release nutrients to surrounding bacteria. Just an extra thought.


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Where can I find a global life expectancy table?
I've found good information on specific countries and demographics, but I can't seem to find global numbers.  I know that the world life expectancy is around 71.0, but I'm trying to get a percentile breakdown in the form of something like an actuarial life table.

Not surprisingly, the WHO has a lot of data, I think especially interesting for you is this interactive figure, which you can find here:

Other data on this topic can be found on the WHO website here, in the Wikipedia or from the Worldbank.


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Are there antibiotics for all bacteria somewhere in the earth?
When I read about Penicillin, I found that it came from a green mold to protect itself.
If all bacteria and/or molds in competition to survive,
can we believe that there is an antibiotic for each bacterium somewhere in the earth?
In other words, just like bad bacteria change themselves to resist against the existing antibiotics, could good bacteria/molds produce antibiotics against the bad bacteria?
If so, can we use them like Penicillin, or should we still develop most of them?

Life is a constant arms race between organisms and their pathogens, each pushing the other to adapt ways to survive. Humans with competent immune systems are able to make their own bactericides, the only issue is the time it takes to mount this response, days to weeks, versus the replicative power of the bacteria and the virulence of their exotoxins. Vaccines against the most potent of toxins provide steady levels of antibodies to neutralize proteins that make snake venoms seem wimpy. Many antibiotics just keep bacterial populations in check until the host immune system can respond.

One other point is that you would have to do extensive testing to see what the toxicity of a bactericidal compound is on mammals. Penicillin goes after bacterial ability to produce a Lipopolysaccharide cell wall, something we don't have. Others take advantage of blocking ribosomal subunits that are different than ours, so we can use them without blocking our own ability to produce proteins. If the compounds we discover have specificity for a receptor that we make as well, then we can't use it.

The number of antibiotics that remain undiscovered is huge, but is estimated to be tens of thousands of compounds.
The number of bacteria that remain undiscovered is also huge, but is estimated to be perhaps millions of species.
Resistance to antibiotics is developed by bacteria in response to other bacteria and human antibiotic use, but in theory all antibiotics should work on previously unexposed bacteria. In practice there are resistance mechanisms that operate on whole classes of antibiotics at once(drug exporters, for instance). So there might be a bacterium that happens to be actively or passively resistant to every antibiotic on the planet, but it's a question of statistics. I think it's pretty unlikely but there are a lot of bacteria, so it's theoretically possible. (It wouldn't be a dangerous pathogen, that amount of drug-resistance genes would 'weigh down' the genome and make it slow to divide, and all those transporters would be great immune system targets. The human immune system would eat it for breakfast.)
What is true is for every bacteria, there are at least some antibiotics it's already resistant to. Furthermore, some antibiotics aren't useful because they aren't selective enough and they are simply poisons. (We use them for chemotherapy agents sometimes, but they're not useful antibiotics).
Some fun examples: Vancomycin-resistant S. aureus is completely immune to nearly every antibiotic, including the last line of defense(methicillin) and the toxic really really last line of defense (vancomycin). It's susceptible to trimethoprim-sulfamethoxazole, one of the oldest antibiotics out there(~80 years old). On the other hand, the organism that causes tularemia is naturally immune to trimethoprim-sulfamethoxazole and always has been. It, in turn, is susceptible to nearly all other antibiotics.


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Discrete vs Continuous Replicator Dynamics
The replicator eqn in the case of discrete non-overlapping generations and asexual reproduction is given by the discrete replicator eqn:
$$x_i(t+1) = x_i (t)\frac{f_i(t)}{\bar f (t)}$$
where $x_i$ is the frequency of the strategy $i$ and each individual playing strategy $i$ produces $f_i$ copies of itself in the next generation. $\bar f$ is the average fitness. Thus
\begin{equation}
\Delta x_i = x_i(t) \frac{(f_i(t) - \bar f (t))}{\bar f (t)}
\end{equation}
In the case in which $x_i$ is a continuous variable, we have the continuous replicator eqn given by
$$\dot x_i = x_i (f_i - \bar f)$$
Question: I suppose we should be able to derive the continuous replicator eqn from the discrete replicator eqn by evaluating the discrete replicator eqn for $\lim_{\Delta t \to 0}$. How can I do this derivation?

To make this derivation, it is better to focus on the population size of a strategy as opposed to the frequency of a strategy. Let $N_i$ be the population size of the strategy $i$. Strategies in the replicator dynamics change exponentially. The equation for continuous exponential growth is $\dot N_i = f_i N_i$. Since $x_i=N_i/N$ and $\dot N = \bar f N$, calculating $\dot x_i$ by using the quotient rule gives us the continuous replicator eqn.


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Do adult humans exchange beneficial bacteria? If so, how?
Recently there has been increasing interest and research into symbiotic bacteria present in humans and human gut. I'm aware of two new discoveries:

humans are surrounded by a unique cloud of bacteria, similar to fingerprint, useful in forensics
human brain and cognition could be influenced by gut bacteria that produces up to 90% of serotonin and dopamine in the human body (not sure how, vagus nerve is implicated)

I've also heard that mothers pass a lot of beneficial bacteria to children during childbirth to jump start intestinal flora. Apparently this happens as the baby travels through the birth canal.
This makes me ask - do adult humans share/ pass along symbiotic or beneficial bacteria or other micro organisms?
I'm aware of viruses and diseases that can be passed via blood or be transmitted sexually, but does anything beneficial get transmitted this way?

It comes down to a question of whether or not they are able to colonize the surfaces, skin, lungs, gut epithelium, not if they are exchanged. A large majority of gut microbiota are anaerobes and their ability to be passed in any medium other than direct contact with feces (how baby's born vaginally get their sampling of most of the maternal gut microbiome) is limited.

Also as an adult your own microbiome is part of your innate immune defenses and they keep out other organisms by taking up space on the exposed surfaces of the body. Pathogens have an advantage over commensals as they have virulence factors to let them gain the upper hand.

Nonpathological bacteria Staphylococcus epidermidis on the human skin are part of normal bacterial flora that help to protect against pathogenic bacteria, such as Staphylococcus aureus. You can get "infected" by Staphylococcus epidermidis the same way as by other skin bacteria and you get a potential benefit from them.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2807625/
You can get beneficial effects from pathological bacteria passed from someone, if you you develop antibodies to them, so you can become more or less resistant to them. For example, if you are from US or Europe and travel to South Asia, you at high risk to get food poisoning from either bacteria or viruses, bot local people are at much lower risk, because they have "shared" microbes one from another.
You can get beneficial effects from probiotic supplements (live nonpathological bacteria), which prevent overgrowth of pathological bacteria in your large intestine. The bacteria in probiotics are similar than those in the human gut.

You forgot to add the most important bacteria when the baby passes through the birth canal.

@Muze, the question is strictly about adults.

Every human has it owns unique bacterial biome, and they acquire it the day they are born. Another interesting thing is that the bacteria that each individual acquires gets much of it from there family/parents. An analogy would be portions of bacterial biomes are passed down from generation to generation although each person does generally acquire a unique set of bacteria.
Bacteria is passed throughout the population all the time generally though you only hear about the negative transfers i.e pathogens. It is hard to track what gets transferred though as most bacteria is not culturable.
The Human Biome Project has been uncovering the variety of bacterial biomes among the human population in different demographics, etc. You would probably have a fun time looking through there and uncovering some cool information.
Here's the link: The Human Biome Project

Most exchanges, aside from neo-natal transfer, are fecal-oral. Some exchanges are pneumonic, but the study of those has been limited to pathogens. I am not aware of any studies of direct epithelial contact.
In humans, the preponderance of exchanges happen early in life (neo-natal). The current school of thought is that the microbiome is established by passing through the birth canal and through breast feeding. Only Archae and bacteria have been studied up to this point, and the study of the constellation of viruses is currently being proposed.