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Asexual reproduction and Telomeres
Many eukaryotic organisms like yeasts, hydras , planarias, plants etc reproduce asexually.
Replication of End of linear DNA pose a limit to the number of cell divisions.
My question : Do asexually reproducing organisms have telomerase in all their cells ? Is the telomerase activated at specific times at specific places ?
If they don't, how can they reproduce infinitely ?

I'm not sure I can answer generically for all asexual organisms, but would an example of why this isn't an issue in E. Coli and yeast work?

@AtlLED Thanks! but I think I know why it works in Yeast and E.Coli - Isn't it because they have round chromosomes and so there is no telomeres.

E. coli is really a bacterium and has only a circular chromosomes. On the other hand, yeast like S. cerevisiae is an eukaryotic organism and has 16 chromosome pairs if it is diploid. The division in yeast is limited. It is done by budding, where there is a clear difference, which cell is a mother and which one is a daughter. Mother can have only certain number of daughters and stops budding afterwards. I do not know, if this is due to telomeres, or budding scars or both.

@AtlLED Ok, so I was wrong about the yeasts :) You could tell me about them.

Short answer:
No. Eukaryotes have more ways of maintaining telomere length than via telomerase alone and all organisms with circular genomes do not need to worry about telomere length anyway.
Long answer:
Firstly, the telomerase system is not the only observed mechanism in Eukaryotes that elongates telomeres. Other mechanisms such as the transposition of retrotransposons (e.g. Drosophila) or recombination (e.g. Yeast) can also be used in some species. Yeast  has been observed to use several of these mechanisms. So no, telomerase itself is not always necessary for immortality.
Ofcourse prokaryotes do not need to worry about shortening chromosome ends at all since their genome is circular - i.e. it has no ends to shorten with each cell division!

Here is a study of planarian worms, which are immortal in asexual reproduction and mortal in sexual reproduction.
Hydras also become mortal after they reproduce sexually.
Relevant to your question: Cells within planarian worm differ in expression of telomerase active subunit depending on body part. Immortal (asexual) worms have more expression in the area around the pharynx, those cells there are "the proliferative stem cells". There is a nice figure in the article.
I assume it is similar for hydra, that outer body coat has less expression than the cells inside. “Hydra is a bag of stem cells”
(Less relevant (a version of previous version of my answer. But does not answer the "every cell" inquiry well): In planarian worms "We demonstrate that this difference is reflected in the expression and alternate splicing of the protein subunit of the telomerase enzyme." The mentioned telomerase subunit was 1. comparatively more transcribed in immortal (asexual) worm and 2. within the resultant trancripts, there were possibilities of functional and non-functional isoforms due to alternate splicing. Immortal worms had higher ratio of functional isoforms. Summary: immortals have more transcripts and higher proportion of functional versions of them.)

Yeah, I know, I am offering 2 bounties myself. Watch my answer for edits, I might find more clear data when I have time.

I think the worm aspect of my answer is now correct. I must check later, whether really hydra cells have different telomerase expression in the coat versus inside the body. It interests me, but takes time to look at this thoroughly. If you are impatient, try to read the article "Hydra is the bag of stem cells" plus the original un-popularised reference.


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Could miniaturization be used to protect endangered large species?
In some animals (like dogs) size seems like it's controlled mostly by just a few genes (IGF1, and the genes that repress it). I'm curious:
(1) Does other miniaturization takes a similar route (for example, with pygmy hippos).
(2) Do we have the technology / knowledge to deliberately create "pygmy" animals?
(3) Is it possible that miniaturization could be a way to protect endangered large species? For example, we shrink them down so they need less room but they could still breed and preserve biodiversity. Also, later on there's always the possibility that we could gradually un-shrink the species if we get our act together and free up more habitat.
Note: I realize that they wouldn't be able to fill the same ecological niche at half the size.

Its not only the size - these animals fill an ecological niche. So if you shrink, lets say a rhino or an elephant, than they would show up on the "food plan" of big predators. And they would have to compete for food with other animals of that size which eat the same food.

I was thinking more of a zoo or some type of protected area (with predators fenced out). You're right - it would decrease their ability to protect themselves in the wild.  I still think it could work though (or at least help).

If zoos are the right place to maintain a species is disputable. And if you have the animal in a zoo anyways, why not keeping them at their normal size?

Asking 3 questions in one post is the best solution to never get a satisfying answer. I'd suggest you to narrow the focus of your post. You could edit your question (and title) and focus only on the two first points. Then, depending on the answer to this post, you may come up with a second post applying what you acquired through this question to conservation biology with an example maybe. Note: I also don't fully understand why miniaturization would be so helpful at saving endangered species.

Species are often also endangered by inbreeding or being outcompeted by similar species. The whole idea of preserving that species thus means "preserving exactly this species, without any changes". Otherwise, one might be able to change hunted species, so they breed more (and thus are less endangered by extinction), species whose environment has changed, so they adapt to the new environment and thus save them this way. Those would not be the original species though, which would still remain endangered.

If you bred an elephant to half its original size, could you still call it the same species? I suppose a mini-elephant could be easier to farm, and that would make it non-endangered, but it really wouldn't be same. But I still want those elephant burgers.

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Can you tell the sex of a white willow when it's not flowering?
Can you tell whether a salix alba tree will produce male flowers or female flowers by looking at it, touching it or generally using your unaided senses? If not, is there any way to do that without specialized equipment or lots of expertise?

Neat question. I wonder if there are any common trends / rules of thumb that hold true across many taxa for sexing dioecious plants?

DNA sequencing?

@shigeta If you know of a way of sequencing DNA by looking at trees, please post an answer. But do make sure that after applying your method I can actually tell what the flowers will be. I've never sequenced any DNA.

Not answering your question as written, but you can always try looking around the base of the tree to find fallen fruits/flowers from earlier in the year.

I wonder how many different senses people have tried to use. E.g., could the wood smell different? Could they sound different when you knock on them? Could the wood taste different when you lick it?

did you check for signs of old seed pods underneath the tree?

I remember overhearing a botanist some 10 years ago, that he cannot tell male poplar from female when they are not flowering or producing seeds. Poplars and willows are related, so it is a weak indication for you, you will likely not find any visible features in willow neither. But it is an old information, too.    (Are you interested in DNA sequencing evidence or not ? I can look it up for you, but it seems your statement in comment question was ironical.)
EDIT: have just found an article which says: "In Salix viminalis, the sex of plants cannot be confirmed until the first time they flower." At that time, 1997, there were no DNA markers for plant sex determination, but it is apparent, they did not know how to differentiate the sex of this willow just from morphology. This example is even closer to Salix alba than poplar. I find it even more likely now, that you will not find the morphological features.
I took the suggestion of Oreotrephes. This is what to look for under the tree - fruit and seeds:
.
Source.
( C. Alström-Rapaport, M. Lascoux, U. Gullberg. Sex determination and sex ratio in the dioecious shrub Salix viminalis L. Theoretical and Applied Genetics 1997, Volume 94, Issue 3-4, pp 493-497).

Thanks for your answer, Barbara. Well, I'm generally interested in knowledge, and it might be useful for somebody, so there's no harm in posting that, and I'd be glad to learn. I just asked the question because I wanted to know if I could impress people by telling them, "Look, this is a lady willow," with as much wisdom about my looks as I could summon.

Thanks for the edit too. This seems to answer my question completely. I will wait a bit with accepting, but I find it unlikely that a better answer could show up. :)

Data from year 2012: still unable to morphologically discriminate individuals before the reproduction age, plus no reliable DNA- based method, genetic basis for sex poorly understood. Source. The best is a DNA method, which predicts that Salix viminalis is a female with only 96 % accuracy.

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Prothrombin time when extrinsic pathway is turned off
I was searching for an answer that "why do we need intrinsic pathway when there is fast extrinsic pathway" and i found the answer in the following link:
http://www.pathologystudent.com/?p=3197
It says that the factor X produced in the extrinsic pathway turns off the extrinsic pathway and activates the intrinsic pathway. As the extrinsic pathway is turned off so, we need intrinsic pathway to continue the clotting process. But if the extrinsic pathway is stopped then how do we get prothormbin time because prothrombin time is for extrinsic pathway?

In order to understand the importance of both pathways, you first need to be clear about what is meant by them respectively. Clotting activation from tissue factor (TF) is known as the extrinsic pathway, so you've got that one right.
The intrinsic pathway doesn't involve FX
The intrinsic pathway does not (as often misunderstood) refer to the clotting cascade downstream of factor X (FX) which involves FV, FVIII and thrombin. Rather, the intrinsic pathway is a system which is able to initiate the clotting cascade without any tissue factor being present. It is triggered by the assembly of high molecular weight kininogen, prekallikrein and FXII on collagen. This is also known as contact activation, and sets off a small cascade producing active FIX (FIXa), which can then assemble with circulating FVIIa in order to produce FXa and thereby set off the rest of the clotting system.
The extrinsic and intrinsic pathway are separate ways towards a "common pathway"
So think of it this way: The extrinsic pathway produces FXa in one way (TF), the intrinsic pathway produces FXa in a different way (HMWK+prekallikrein+FXII). There isn't really any interaction between these two. Once FXa is produced from either of these two, it will start to set off what you could call the "common pathway", i.e. it will produce thrombin, which will activate co-factors that will then lead to more production of FXa and propel the entire thing forward faster and faster until it reaches what we know as the thrombin peak.
The intrinsic pathway is not important for haemostasis in humans
Aside from this, you should know that the intrinsic pathway exists, but it doesn't bear much significance in a living human. This is demonstrated by genetic FXII deficiency - you would expect it to produce haemophilia if FXII and therefore the intrinsic pathway was important (just like FVIII and FIX), but it doesn't (read here: http://en.wikipedia.org/wiki/Factor_XII#Role_in_disease).
The principle behind the initiation pathways and the common pathway
So to summarise: You fell victim to a misunderstanding and a bad explanation on that site you linked. The extrinsic pathway doesn't "turn itself off", and the intrinsic pathway doesn't "take over". What really happens in a human is that the intrisic pathway doesn't really do anything. Rather, the extrinsic pathway will produce a little bit of active FXa. But that is enough to produce a little bit of thrombin. And that bit of thrombin will then produce small amounts of FIXa and co-factors (FV and FVIII). These will start to produce more FXa, which will produce more thrombin, which will produce more FIXa and co-factors, and so on.
What the article you refer to is trying to mention are the inhibitory systems that will be set off alongside all of this. Think about it - if thrombin increases its own production perpetually, how does it know when to stop? These systems which ensure that clotting does stop are known as anticoagulation pathways. They are just as amazing as the coagulation pathways themselves, and they are extremely well-geared towards shutting off exactly the right clotting factors at exactly the right time, to ensure that a clot forms in the wound but only there and nowhere else.
Edit: It turns out people do use more complicated definitions of "intrinsic" and "extrinsic" - the problem being once again that everybody can define words as they like. This is rather based on the distinguishing of the two ten-ases, TF-FVII (extrinsic tenase) and FIX-FVIII (intrinsic tenase). In this understanding, the physiological process does indeed start off by the extrinsic pathway (i.e. mechanisms which generate extrinsic tenase), which will kick off the amplification cascade of the intrinsic pathway (i.e. which produces intrinsic tenase). It is true that this way, the contribution of the "extrinsic pathway" is minor once the "intrinsic pathway" is active, but even so, it does not "shut itself off". What turns the extrinsic pathway off is the layer of material which gets deposited on top of the exposed subendothelial surface, preventing access to TF!


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Is it possible for bacteria to acquire family-wide antibiotic resistance?
If there is bacteria, lets say Enterococci that is sensitive to:

Amoxycillin-Clavulinic acid
Ampicillin-Sulbactam
Ofloxacin
Ciprofloxacin

Is it possible to become resistance to Ampicillin-Sulbactam by using Amoxycillin-Clavulinic acid ?
Is it possible to become resistance to Ofloxacin by using Ciprofloxacin ?

It depends on the mechanism of resistance..

Yes, via point mutations, which can happen spontaneously and doesn't depend on anything.

The two amoxycillin formulations you mention pair the amoxycillin with a Beta lactamase inhibitor. This is because of the prevalence of resistance to beta lactam drugs including amoxycillin. If we were to invent a brand new never before seen beta lactam drug and started using it irresponsibly, there would probably be resistant bacteria within 5 years. The same beta lactam core structure that makes the drugs work against the peptidoglycan synthesis machinery make it susceptible to attack by beta lactamase. A new beta lactam could avoid the lactamase for a while, but the same evolutionary pressures that selected for resistant mutants against the other beta lactams would select for mutants resistant against the new one.
The same goes for the fluoroquinolines you mention. Their mechanism of action is different, they inhibit DNA synthesis by blocking topoisomerase II activity. But once a bacterial strain is selected for that has resistance against one member of a class of antibiotic it's relatively easy for it to acquire the mutations that confer resistance against other members of the class. Changing the structure of the drug enough so that cannot be defeated by the mechanism of resistance while retaining the drugs mechanism of action is probably impossible, or at least we haven't done it yet. Even vancomycin, one of our most powerful antibiotics, has some bacteria resistant to it.


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Can germs develop surfactant resistance in a harmful way?
Germs can develop antimicrobial resistance. It is a problem serious enough to deserve an FAQ page on the WHO website (http://www.who.int/mediacentre/factsheets/fs194/en/).
But how about surfactant resistance? We wash our body, our dishes, our clothes, and pretty much anything that is washable with soap/detergent, which means surfactants.
So can germs develop surfactant resistance in a way that is harmful to human health? If so, is there any recorded experiment about it? If not, why not?

Against detergents this is hardly possible (ok, never say never for bacteria but still), since detergents destroy the membranes of the cells. I don't think bacteria will have enough time to develop resistance mechanisms against it.

Never say never indeed!
a three part answer to the question:

Bacteria can develop resistance. These researchers did a screen for Staph and Pseudomonas which survived a detergent/soap treatment and indeed were able to select for many strains.  I'm not sure that their explanation of why they are resistant is a final answer, especially for the Pseudomonas strains which have no hypothesis at all.

Nearly all bacteria do this all the time #1  Most bacteria can go into spore or plaque forms which basically hibernate.  These plaque colonies are matrices of crosslinked bacteria and are resistant to extremes of conditions in the environment or lack of food.

Even Normal Resistance is a relative thing.  Alcohol sanitizers kill 99.9% of bacteria.  That sounds like a lot but that 0.1% can come back to full strength in a relatively short period of time.  0.1% is still millions of individuals surviving after a shower.  Resistant bacteria have a higher proportion of survivors and should improve the bounce back rate.  So resistance is a term which you need to define for a given situation.

Surfactant (soap) resistant bacteria can be nearly any sort of bacteria and a certain percentage of them are ready for a scrub down at any given time.  To get a surface completely free of bacteria takes a good deal of work.
As far as a danger to human health - resistance to being killed by soap is a real problem because the few of them which also have resistance to antibiotics and are pathogenic will be pretty much unstoppable.  Its not likely that surfactant resistance will itself make a bacteria pathogenic (never say never!) but if such a 'triple threat' emerges we'd all be in trouble.

I agree, I did a "death of kitchen bacteria" project and subjected pieces of sponge to different treatments. One of them was washing with lots of detergent and soap. When I grew the bacteria remaining on the sponge after the treatment, I found that it was not very effective.


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Chromosome 2 alternate explanation - apes gaining a set of chromosomes?
I'm preparing for a debate (just between friends) on evolution (I'm in support), and one of the points I plan to bring up is the Chromosome 2 evidence.  I'm now trying to predict their potential rebuttals.  The common statement I've seen is that since the apes have 48 chromosomes and humans have 46, then there are two possibilities: either we "lost" a chromosome, which would be fatal, or there was fusion.  This, I believe, was an actual prediction prior to the answer of Chromosome 2 being identified.  But couldn't there have been a third possibility - that the apes gained a pair of chromosomes, perhaps thru splitting of some kind?  This seems reasonable to me due to the other claim that we didn't evolve from apes but that we share a common ancestor, and so the ape lineage could have acquired the extra chromosome after the split.  (Note I'm a total biology noob, so if this doesn't even make sense, then please tell me.)  I understand that this isn't the way it turned out, that Chr 2 looks exactly as we would expect from fusion, but prior to this discovery, couldn't the apes gaining a chromosome have been a possible reason?  TIA.

does this help? http://biology.stackexchange.com/questions/5558/chromosome-2-fusion  What else might you need?

BTW splitting happens too.

shigeta, i saw that article and read it before I posted this question.  That page doesn't seem to answer my question directly - specifically, WAS IT PREDICTED or was it simply taken as evidence once it was discovered?  So ideally, someone could provide a reference to a paper or article that was published that says "we predict that...two chromosomes will appear fused", and which was subsequently confirmed by a later paper or article.  I've heard it was about 30 years, but I have no valid source.

I guess part of the question is...what exactly are you bring up Chromosome 2 as evidence of, exactly?  It's evidence of that chromosomal rearrangements are possible, but that isn't terribly helpful to you, so I'm not sure why you are bringing it up.
I think the fusion is a rebuttal to a claim that the disparate # of chromosome is a problem for the claims of common ancestry between humans and other apes, but if they don't mention it, I'm not sure why you would need to use that particular fact.
Have you consulted talkorigin's 29 evidences of macroevolution?  Lots of good stuff there.
http://www.talkorigins.org/faqs/comdesc/

It is useful, IF it was predicted.  This is one of the main differentiators between valuable theories and useless theories, and hence this is why I'm asking the question.  Creation, even if it allows fusion, doesn't predict it.  Given that apes have 48 and humans have 46, the "prediction" from creation would be "that's just the way god made it" and say nothing about fusion.  But evolution's prediction would be that we would see fusion (or other effects) and that's why it is useful.

Things don't have to be useful to happen in evolution. They have to (at the time they are happening) be no disadvantage for the organism. And no, you can not predict, what is going to happen in evolution as this doesn't follow a certain path. You can think about things that can happen (as is has with the chromosomal difference between human and ape) but it doesn't have to happen. It is a proof for a common ancestor to compare genome sequences and there where the differences are.


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How suddenly does lactose-intolerance onset?
How quickly can the loss of lactose tolerance onset in an adult?
Such as being able to process lactose normally to having notice symptoms associated with the inability to process lactose.
I am not asking how long it takes to digest food, but rather how long it takes for lactose intolerance to become noticeable (hours, days, weeks, months, years).

Disclaimer: I am not medically qualified, and this answer must not be construed as being medical advice of any kind.
Primary adult hypolactasia is the most common cause of lactose intolerance. The majority of the world's population have this phenotype.
In these individuals, at weaning, there is a reduction in the level of the enzyme lactase, which is responsible for digesting lactose to galactose and glucose in the small intestine. Undigested lactose can create symptoms via osmotic effects (causing diarrhoea) and because it is metabolised by bacteria in the colon, producing gas and thus abdominal bloating.
About 35% of adults have a genetic variant in an region upstream of the lactase gene which results in the expression of lactase continuing into adult life. These individuals are lactose tolerant. This trait is most common in Northern Europe.
According to references cited in

Ingram, CJE et al. (2009) Lactose digestion and the evolutionary genetics of lactase persistence Hum Genet (2009) 124:579–591

(I have removed citations from the passage for clarity.)

"most lactase non-persistent individuals can tolerate small amounts of lactose (as in tea or coffee), and some can consume a lot without ill effects. Variation in the composition of the gut flora between individuals, as well as a psychosomatic component may account for some of the interindividual variation in symptoms."

The clear implication is that there is a lot of variation in the tolerance of lactose amongst those lacking the lactase persistence trait. Given the contribution of the gut flora to the symptoms these could presumably vary as a result of, for example, antibiotic treatment. Also I imagine that the effects of undigested lactose could be synergistic with some other gut disturbance.
Added in response to comment from the OP:
In someone with the (common) genotype that corresponds to 'no persistence of lactase' the possibility of showing symptoms will be present from a young age. Apparently there is a lot of variation in the severity of symptoms. If an adult suddenly exhibits symptoms then I am suggesting that this could be due to an interaction of non-persistence with some other gut disturbance - I imagine this could happen quite quickly. Alternatively I suppose that a change in diet could trigger symptoms.

So are you saying the question isn't answerable because of such a wide variance in symptoms? If so, could you say that? Perhaps you are saying that it varies wildly person to person? If so, could you say that? Because I can't accept this until you produce an section of answer directly related to my question.


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Stay young by reinserting own DNA from years ago?
As far as I know, the DNA sequence becomes shorter every time a cell divides.
A shorter sequence results in information loss and aging characteristics.

As a countermeasure, shouldn't one stay young and healthy at least longer, if the DNA in a cell is changed with a "better" DNA (from years ago... let's say your DNA was extracted with the age of 20 and you reinsert it every 10 years or so)?

If this is true, then (as for today's technology)
- is it already possible to perfectly reproduce the DNA? (I only found articles about XNA)
- is it possible to easily replace the DNA in all human cells? (I found articles about bacteria inserting pieces of DNA into human cells)

The shortened DNA sequences are repaired by the telomerase enzyme. So, there is no actual loss of information.

I think this idea is being implemented for stem-cell therapy but not to control ageing. So, stem cells such as HSCs can be cryo-stored and used for therapy later. Umbilical cord cells can also be employed. With iPSC technique it is possible to convert a cell to any cell type. It might be theoretically possible to replace every old cell but we haven't completely understood the importance of ageing. So there is a possibility that it can have disastrous consequences (not social implications but biological ones such as cancers etc)

Lots of questions here. I recommend taking college level courses in Biochemistry, Molecular Biology, and Medical Physiology, and Geriatrics.
There are other issues than just DNA. Systemic failure is system-wide, and probably most of the issues are still yet undiscovered. Good news I guess if you want to be a researcher in this exciting field! As for DNA-ends, read up on Telomerase. As for DNA copying learn about PCR and sequencing methods. Generally speaking, reverse transcription can be dangerous. Please see many of diseases we are having a hard-time solving, which often use these pathways. Seriously avoid that one. Not everything in DNA is used by the organism at any given time, and some information is elsewhere. Moreover, what if we use DNA as DATA storage besides blueprint information? Hint: while the jury may be still out on Neurons, environmental factors may be passed as epigenetic traits by not just primary shape such as DNA methylation but by obstructing access via conformation and histone wrapping. Not even mentioning mitochondrial dna or prenatal development factors.
Instead: A good diet and exercise.

well, as I already am an engineer, taking college courses and focusing on that subject may be a little late. Because of a friend, I came across this strange idea, but it seems not to work. Thank you a lot for your explanation.

As far as I know, the DNA sequence becomes shorter every time a cell
  divides. A shorter sequence results in information loss and aging
  characteristics.

Neither telomeres nor aging are nearly that simple.

is it already possible to perfectly reproduce the DNA?

No.  Any method that would be used to replicate DNA requires using enzymes, and they always have a non zero failure rate.  You could use whole genome amplification to make a pile of DNA that was on average the right sequence, but each individual chromosome would have errors.  And forget copying over epigenetic modifications.
There are ways to get cells to incorporate new DNA, but every cell in an organ of a living organism?  And a whole mammalian genome's worth?  And to magically tell the cell that the new genome should replace the old one?
None of that is feasible.

(I found articles about bacteria inserting pieces of DNA into human
  cells)

Okay, let's get some scale here.  Most bacteria have a genome of 5-10 million bases.  Humans have a genome of 3 billion bases.  Even if a bacteria can transduce a small plasmid into a human cell, that doesn't scale up to bacteria replacing the whole genome of every cell in an organ.
And because there's always a relevant xkcd comic
http://xkcd.com/793/


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Why is the strength of genetic drift inversely proportional to the population size?
I saw a concept on the Internet that says "the strength of genetic drift is inversely proportional to the population size". I don't know why they are inversely proportional? Can somebody explain? Thank you all!

Both the answers are excellent but just to simplify - smaller the population larger is the probability of "chance events" having a profound impact.

Plane Crash Analogy
4 people in a plane crash
In a small aeroplane, there are 2 people that wear a blue shirt and 2 people that wear a green shirt. The plane crashes, half of the people died. The 2 survivors are those wearing the green shirt… well, nothing so surprising!
400 people in a plane crash
In a very big aeroplane, there are 200 people that wear a blue shirt and 200 people that wear a green shirt. The plane crashes, half of the people died. The 200 survivors are those wearing green shirt… This is quite surprising!
Genetic Drift
The same logic applies to genetic drift. Genetic drift is caused by events that modify the reproductive success of individuals in a random way (independently of their genotype). We usually referred to this as random sampling. At each generation, individuals are randomly chosen to reproduce and some genotypes might just happen to be chosen more often than others at a given draw (=at a given generation). Genetic drift pushes the frequency of allele slightly away from what would be predicted. According to the Wright-Fisher model, the frequency of alleles (of a bi-allelic gene) in a haploid population (to make it easier) in the next time step is given by:
$$p' = \frac{p \cdot WA}{p \cdot WA + (1-p) \cdot Wa}$$
where $p$ is there frequency of an allele at time = $t$ and $p'$ is the frequency at time = $t+1$. $WA$ is the fitness of the genotype which frequency is $p$ and $Wa$ is the fitness of the genotype which frequency is $1-p$. If the population is infinite, the predictions of this equation are exactly correct.
Now if we say that meteorites fall and half of the individual get killed. The probability of getting killed by a meteorite obviously does not depend on genetic predisposition, it is a question of chance! If you look at a population of 1 million individuals, half of them having the genotype $A$, the other half having the genotype $a$. It is very unlikely that more than 60% of all individuals that get killed are of the same genotype. Therefore, the meteorites won't change much the frequency of the genotypes. If you look at a population of 4 individuals 2 are $a$ and 2 are $A$, 2 of them get killed by a meteorite. Well, you have a probability of one half that the two survivors are of the same genotype and that the genotypes frequency would have changed drastically.
Genetic drift refers to these changes in allele frequency which are due to random events (such as meteorites) and the strength of genetic drift indeed depends on the population size for probabilistic reasons. The greatest the population size, the lowest is the strength (or the relative importance) of genetic drift.
How to model genetic drift
There are three famous models of genetic drift that all lead to very similar expectations. I shall just name them here but I will not develop the underlying mathematics.

Wright-Fisher model of genetic drift

Not to confuse with the Wright-Fisher model of selection written above
It models genetic drift as a random sample of the previous generation and hence uses a binomial distribution.

Moran model

It is based on a birth-death model (a type of Markov model).

Kimura's diffusion equation model

It is an extension of the above two models for a case of continuous time.

One comment; I think the statement "...random fluctuation in fitness..." can be misleading/cause confusion, since drift is usually defined in terms of selectively neutral alleles. Your statement could be read as implying fluctuating selection due to randomly varying fitness optima between years ("...fluctuation in fitness"), which would rather increase the genetic variation than decrease it. I'm sure this is not what you ment though. Sure, random deaths could be labelled as random fitness, but I find this slightly misleading and it is better to leave fitness out of it.

Indeed this sentence might be a bit misleading. I did not want to restrict genetic drift to "sampling" effects as it rather highlight the Fisher's mathematical model rather than the conceptual reality of biological populations. And I did not want to restrict drift on neutral allele as it does also applies on alleles that are (weakly) selected.

Yes sure, drift acts both with and without selection. And I agree that it's useful to think about the actual processes that cause the sampling. However, my main objection to using fitness in relation to drift is that the (expected) fitness of e.g. a genotype is unchanged under drift. That different individuals with the same genotype contribute differentially to the next generation is a property of the probabilistic process, but it does not modify the fitness of the genotype.

Yes, I totally understood the issue. I'd like to keep the fisher's thing. If you think you can make my answer more protected against missunderstandings and confusion between predisposed fitness and what is achieved at a given generation due to random events, you're welcome to edit.

My comment was only regarding the phrasing at the beginning of the paragraph (which you've edited - now referring to "...the fitness of individuals") - I didn't mean to imply that you should remove the wright-fisher equation. Fitness is tricky, since it's used in so many ways by different people.

Genetic drift refers to changes in allele frequencies that are due to random sampling effects, and not selection. If you sample alleles from a finite population (e.g. caused by the fact that only some individuals in the population reproduce each year), the resulting frequencies will deviate from the original frequencies due to random chance. If your sample is large (a large population) this deviation will be small, and if your sample is small the effect will be substantial.
This is exactly the same process as flipping a coin. If you flip a coin 10 times there is a large probability that the outcome will deviate a lot from 50% heads/tails (the outcome will follow the binomial distribution). This is analogous to the deviation in allele frequency due to genetic drift. If you flip the coin 10000 times the outcome will deviate little from the expected 50% distribution of heads/tail. Therefore the effect is described as inversely proportional.
There exist several models of genetic drift, but one way to look at it is as for how the variance in allele frequency changes over time, which can be described by:
$$ V_t \approx p*q(1-e^{-t/2N_e}) $$
where $p$ and $q$ are the allele frequencies and $N_e$ is the effective population size. Alternatively, the change in heterozygozity ($H$) over time due to drift is described by (Crow & Kimura, 1970):
$$ H_t = H_{t0}\left( 1-\frac{1}{2N_e} \right)^t$$
In both these functions, the inverse relationship between genetic drift and population size is seen clearly (population size is found in the denominator in both equations).
The concept of genetic drift is closely related to the founder effect, but in that case, the sampling is only done once, when a small subpopulation of individuals establishes a new population.


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Could below zero decibel environment cause arrhythmia?
While this topic has virtually no real life application and has never been examined due to obvious reasons, it is quite intriguing to me.
I've read a lot of speculations and claims about the world's quietest room (-8.7 decibel at Orfield Laboratories in South Mineapolis) including loss/deterioration of hearing, hallucinations etc. What I was wondering about is if any of the human self-preservance reflexes would kick in once an individual hears his own bodily fluids and organs expanding/retracting? Since, as far as I know, there aren't any scientific proofs or thesis on this subject, what are your thoughts based on your knowledge on regular body functions and reflexes?
Third-party links: TheDailySwarm's post, CBC's post, Quora's post

Can you include a reference to the speculations and claims that you've read? This makes it easier for others to fill in.

What are you referring to when you say "self-preservance reflexes"?

@MCM I was thinking of the involuntary actions a body makes when it detects a danger (e.g. removing extremities from a heated surface, increasing blood circulation to preserve BT in cold environment) so I was wondering if hearing your own heart-beat would cause your body to classify it as endangered state and try to adjust the pulse which could cause arrhythmia.

This question is better suited for skeptics SE.. As far as I understand, lack of auditory stimulus shouldn't interfere with any visceral function. People might feel depressed and heart may react to the psychological state but there cannot be any reflex here

@WYSIWYG I think its on-topic here as well - if there are potential effects and mechanisms they are clearly within the field of biology.

But the problem is, like I wrote in the question, that there exists no research on this topic, so any discussion would be pure speculation.

Since we are used to hearing sound it would not be very pleasant to be in complete silence. Hearing has not evolved to report the somatic state, but to merely perceive the environment. So my best guess is that this effect (if it exists) is purely psychological.

What makes you think that ".. an individual can hear his own bodily fluids and organs expanding/retracting"? in silence?


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How can Southern blotting be used to establish gene copy number?
I am reading a paper on a certain marine microorganism that can eat alkanes and therefore might be useful for cleaning up oil spills, etc. This sentence struck me as odd (although I am sure that the answer is pretty simple):

Using the same probe, Southern blotting analysis showed that there was only one copy of alkB1 in the B-5 chromosome.

I realized that I don't know how Southern blotting can tell you about copy number. Can someone help me on this?

please [edit] your question to include a link to the paper, so we can see everything in context.

This method is commonly practiced. Atleast I see the people working with zebrafish transgenics using it.
When you shear the genomic DNA or do a restriction digestion, you are likely to get fragments of different sizes.
It is highly probable that the two (or more) locations harboring a copy of the DNA element are a part of fragments with different sizes. So on the blot you'll get two bands.
But as I said this test relies on probability that the two fragments are dissimilar in length. Therefore, southern blot should not be considered as an absolute test to determine copy number. Inverse PCR, FISH, etc can be used to determine copy number.


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H₂S as a source of electrons for plants
The first electron source for plants was H2S, but now most modern plants use H2O as an electron source.
What is the advantage of using H2O instead of H2S?

Water can dissolve minerals and nutrients what H2S not can as a gas.

I would guess the abundance of them is relevant to this. Also toxicity/corrosiveness of hydrogen sulphide.

You can look at some articles which hypothesize about early evolution. It is hypothesized that some of these habitats were rich in sulphide (early enzymes also had Fe-S catalytic centres. Some enzymes still do) . So I concur with @GriffinEvo that it is all a matter of abundance.

The major reason for this is because H20 can cause hydrogen bonding. Hydrogen bonding is what allows for plants to transport "this electron source" from their roots through their stems an further.
The stronger polarity of H20 also allows for stronger interactions. Such as ionic interactions (not fully bound but 2 polar atoms interacting). This kind of ionic interaction also allows for other types of material interactions such as cohesion and adhesion.
Overall, aside from the discussion of abundance as mentioned above (which is a very good point), it also allowed the plants to grow in directions that were more advantageous (darwinian) for their survival.


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Can cerebrospinal fluid deliver nutrients/drugs to neurons during sleep?
I'm looking at this article on the possible mechanism of detoxifying brain during sleep using cerebrospinal fluid. It states that at night, the space between neurons may allow better (up to 20x) circulation of cerebrospinal fluid within the brain to clean out metabolic by products of daytime activity.
My question is if this may also work in reverse and allow to deliver drugs within the fluid to the brain.  If a person ingests a drug or nutrient before sleep, would the increase in circulation of cerebrospinal fluid deliver the drug to deep regions of the brain? Or does the blood-brain barrier prevent drugs from entering cerebrospinal fluid?

Certain drugs can cross blood-brain barrier. In such cases your hypothesis should be correct.

Only certain drugs can cross the blood brain barrier (BBB). However, there exist techniques to deliver drugs to the brain that otherwise cannot permeate through the BBB.
One such technique is called intrathecal delivery that injects drugs directly into the cerebrospinal fluid, avoiding the BBB problem and allowing the drug to reach cells, including neurons, in the brain. It has been used for certain kinds of chemotherapy, pain management, treatment of spastic cerebral palsy, and more recently for enzyme replacement therapy.
However with intrathecal delivery there is a risk of infection.
Having said that, if a drug reaches the CSF then your hypothesis should be correct. There is no experimental evidence for it yet.


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Systematic anticoagulant injection after a CVA
Since most of the cerebrovascular accident are ischemic ones, would it be usefull to have anticoagulant everywhere (we already have  AEDs everywhere) so that everytime someone would have symptoms of a CVA we would be able to destroy the blood clot before any permanent damage to occur ?
On the other hand may it make the case of ruptured aneurysm getting worse ?
So what are the potential negative and positive effect of such a policy ?

I think it would be useful to rephrase this to ask for the potential positive and negative effects of anticoagulants. Right now the question is close to primarily opinion-based.


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Real-time PCR delay in Cq due to insertion SNP in primer
I am collecting evidence, even anecdotal, how does single nucleotide deletion or insertion in primer region affect the outcome of real-time PCR.
I am most interested in how much there is a delay in Cq (treshold cycle value) if compared to perfectly matched primer. But if you do not have Cq data, I also collect "Yes or No" answers, saying, whether there was amplification or no amplification.
I am interested specifically in insertion or deletion mismatches. (For substitution mismatches, there is a lot of data.)
I will appreciate any published or unpublished evidence.

where is the insertion from the 3'end ?
Primer efficiency will be affected if point indels are introduced. If there is a mismatch at 3'end then extension may not happen at all.. As for data, nobody will deliberately design an RT primer with mismatches unless they are doing a research on primer efficiency.. :P

The insertion is at position 9 from the 3'end and the primer length is 19. The primer was designed to distinguish 2 related plant species, one was supposed to be amplified, whereas the other should not be because of insertion mismatch. I think that authors are wrong and that one deletion at such position is not enough to discriminate species. But I am asking people for empirical data, possibly something I can quote.

This question is connected to my previous one (http://biology.stackexchange.com/questions/14357/effect-of-single-nucleotide-detetion-or-insertion-on-primer-annealing), but is a little different now. Before I asked about melting temperature, but now I know the Cq value delay is the parameter I am looking for (and is not correlated with Tm).

you cannot distinguish between species accurately if your point mismatch is within the primer. Sequencing is the best thing to do but you should use a primer that binds upstream of variable region. Primer efficiency will change with mismatch which in turn will affect Ct-value, but there is no straightforward correlation between no of mismatch and Ct.

@ WYSIWYG Example of discriminating walnut from pecan by 4 mismatches in reverse primer. Recent study about various correlations between number of mismatches and delta Ct (and other correlations of other parameters). I do not expect similarly deep study about deletion mismatches, I am just collecting anecdotal evidence.

As @WYSIWYG pointed out, having the indel difference in the 3' end can be informative, but I'm having a harder time finding evidence in the middle of the primer.  Putting the mutation/indel at the 3' end will change the ΔCT.  To do it well, you need wide coverage on your mutation site.
I think that it is possible that there could be a difference with a mismatch in the middle of a primer, but it wouldn't be as obvious as if it were closer to the 3' end.  Unless there was some serious reason why you couldn't put it there (ie Tm below 45 on the reference) that sounds like poor primer design.
I will note I am certainly not a qPCR expert, and I don't think the question has been directly researched (as you surmised).  Again when I've looked for Indels before (was doing some interesting stuff with HLA types...) we used larger primers for the qPCR.
If this doesn't answer your question satisfactory, is there an initial reference you would have us look at?  I imagine things like good quenching and other factors could pull out some significance when comparing two templates (one with indel one without), but again, it's kind of odd to put the mutation in the middle.
Edit to comments:
1: I think the Cq delay is going to depend on things like length, sequence, and mutation.  There may be a grand scheme formula/algorithm to predict the delay, but I don't know of one, and I couldn't find it if it does exist.  Most of the graphs and differences I've seen have been big enough that it convinced me that it was significant.  I don't know if this is like flow where you can sit and argue all day about the biological relevance of 40% to 30% of a particular group.
2: Sorry I didn't have time to come in and give an adequate summery of them.  They are, as you pointed out, tangential to what you're trying to do, but do in fact address the problem through their methods.  I will attempt a better summery as I have time (I've got a grant on I'm trying to get done by Tuesday, so probably after that).  If you have any clarifications to the question to add, please do.
3: This may have grown from the general perception that it was needed, and that I aim for the highest Tm I can generally manage without structure problems being introduced.  I also have the luxury of not needing to worry over the cost of ulta-mers.  It also could have come from history of working in BACs years ago.  Longer primers always increased my success rates when I was knocking out cassettes.

I just thught it must happen sometimes that the primer is designed, without knowing all possible variants of the target gene. And sometimes, I believe, it is accidentally discovered, that there is a single nucleotide deletion or insertion between primer and variant (allele) of template. I hoped somebody came across something like this during their work, and can tell me how much was Cq delayed. (Or, in classical PCR setup, whether there was amplification or not). The articles you pointed to me seem relevant, although not exactly answering my question.

You know, I do not have time to read all the articles before my bounty expires. They do not seem to answer my question exactly, but they are relevant, and I was not able to find them myself before. And I do not want to waste the bounty... So let it be yours, but you might see me asking the same question different way later. Which I should do anyway, because most people seem to be confused by it.

how did you know you need to use larger primers, when you are introducing indel-like point mutation ? Where does that original recommendation come from ?

@Barbara sorry I just logged in and noticed your comments.  I tried to at least address your comments some what.  I will need to come back to address them further as I have time.

" I don't know if this is like flow where you can sit and argue all day about the biological relevance of 40% to 30% of a particular group." - I did not understand this sentence. 2. "Sorry I didn't have time to come in and give an adequate summery of them" - I did not mean to say it was your responsibility to summarize (should one do it on this site ?), summarizing surely helps, but I am very thankful for raw citations.

@Barbara re:1, let's say you have a repeatable 5-15% change in a population via flow cytometry.  You can certainly reach statistical significance by large acquisitions and many replicates, but depending on the biological background, this may or may not be biologically significant/relevant.

Ok, thanks for explanation. That is not the type of work I am doing. It is more like as if I needed to determine by qualitative real-time PCR, if chocolate contains traces of walnut or pecan.


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Where to obtain metabolic pathway datasets
I've been looking through the files available at www.reactome.org along with some others but I only find images/pdfs of metabolic pathway diagrams. Where is the actual data these pathways are drawn from? I imagine there should be some kind of directed graph representation. I'm limited to freely available datasets, so unfortunately I'm not able to check out those such as KEGG.

KEGG should be open for anyone, if I am not completely wrong.

According to their download page, access to the ftp files for KEGG require a paid academic subscription (through http://www.bioinformatics.jp/en/keggftp.html). I suppose the tools on their website are free, but I haven't found the pathway data I'm looking for (that is, I see where I'm only able to browse pathway diagrams).

Well, now I see that KEGG has a XML markup of their pathways, but it is only available from querying their API (http://www.kegg.jp/kegg/xml/). I wonder if there is an easy way to grab all pathway files.

KEGG is definitely your choice!
It is possible to get the whole list(s) of pathways: http://rest.kegg.jp/list/pathway (reference pathways) or http://rest.kegg.jp/list/pathway/hsa (for human).
Then you can use these IDs to retrieve information about individual pathways: http://rest.kegg.jp/get/hsa00053 (GeneBank-like format), http://rest.kegg.jp/get/hsa00053/image (image), http://rest.kegg.jp/get/hsa00053/kgml (KEGG xml). It will take a while, of course, and I'd recommend not to overload their server and make delays between queries. With the GeneBank-like format batch querying is also possible: http://rest.kegg.jp/get/hsa00053+hsa00061
This should likely be a one-time or at least rare operation, because of the load on their server (and I don't think they make big changes very often). You can retrieve info for new pathways, once they appear in http://rest.kegg.jp/list/pathway/...

Yes, this is actually precisely what I ended up doing. I wrote a python script which iterated through the human pathway file, sent a get request to their API and just saved each kgml file to hard disk. For the GeneBank-like format, those don't indicate any relationship among gene or compounds involved right? It looks like it is simply a list.

@Aaron: as far as I know, they are just listed. It's a pity, the API has no batching for the xml output, but KEGG is great any case!


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Physiological reason why leaves got twisted when treated with indole acetic acid
I want to know the physiological reasons of why the leaves of my study plant got twisted when treated for 10 days with spray of indole acetic acid. I want to treat seeds with IAA, and I'm thinking about testing what will happen when I treat the leaves.
Here is a picture of what the plant looks like:

thanks

Please add some images - ideally both treated and untreated leaves.

Add study species as well. Also give some background; why did you perform the experiment in the first place? Why indole acetic acid?

IAA induces growth. perhaps that is leading to twisting. But unless you upload a picture and provide more information about the methodology it will be difficult for people to answer this question

@legend I think you need 10 reputation before you can add images yourself. I've added the picture now.

Speculation on my part: since IAA can induce growth, spraying it mostly on one side of the leaf (by spraying from the top) might cause the upper part to growth faster, which would lead to the leaf twisting downwards. From the picture, this seems to be what is happening most of the time. +1

IAA seems to act partially through cell elongation (http://www.biosynth.com/index.asp?topic_id=139), so differential elongation due to uneven spraying seems a likely explanation

how can I measure cell elongation or compare with untreated plant? is there any method for measuring?

Disclaimer: Not my area of research

Since IAA (auxins) can induce growth, partially acting through cell elongation (http://www.biosynth.com/index.asp?topic_id=139), it seems likely that the explanation to your result is differential growth/elongation rates on the upper and lower side of the leaves. This could result from uneven spraying, e.g. by spraying the leaves from the top. Faster growth on the top part of the leaf would lead to downward twisting, which seems to be what is happening most of the time.
You could test if this is the case by doing a simple experiment where you carefully apply IAA with a brush on both sides of the leaves for some plants, while others are sprayed. If uneven application is the cause you should see twisting when spraying but not when applying with a brush.
However, auxin is toxic to plants at high concentrations, so you also need to consider the concentration you are using.

The concentration was 50 ppm.

@legend I have no idea if that is considered high or low.


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Different level of toxicity between smoke
Has there been studies on the difference between the smoke generated from:

cigarette or cigar manufactured by brands which are proven to contain more than a hundred of dangerous additional components
tobacco/marijuana (more or less pure?)/any-plant-dried-leaves made cigarettes.

Apart from the nicotine both contain naturally, are the latter safer to inhale? in which scale?
The other question Effects of smoking tobacco compared to inhaling other smoke, reminds the danger of all source of intoxication, wall paints are also to consider.. and outdoors gas pipes, etc... But I'm doing a fixation on smoked drugs. I've been living in residences, sharing corridors with flats with more or less important smoke concentration, and had developped fumiphobia (but this is out of topic).
This is probably psychological but I'd never stay in the same room than someone smoking, but if someone take some dried leaves out of a plant,.. roll them in paper, fire it and inspire it. It never happened but I wouldn't be as much scared by the generated smoke. But if a study would show that manufactured cigarettes are between 1.5 and 3 times more 'toxic' then I would consider both cases dangerous.

I am not sure, if any comparisions have been made with other plant leaves, but unless these contain some pharmacologic active substances, I doubt that they are smoked widely.
There are comparisions between normal smoking and the smoking of marijuana and the short version is: Both are harmful. It depends on the temperature at which they are burned, how they where grown and so on. For smoking marijuana it also depends if you mix it with tobacco...
This fact sheet from the University of Washington lists a number of points on marijuana together with proper references.
Then there are some articles about smoking and marijuana in comparision:

A Comparison of Mainstream and Sidestream Marijuana and Tobacco
Cigarette Smoke Produced under Two Machine Smoking Conditions
On the Carcinogenicity of Marijuana Smoke
A possible chemical basis for the higher mutagenicity of marijuana
smoke as compared to tobacco smoke
Is frequent marijuana smoking harmful to health?

Thanks a lot for those data, indeed I heard the temperature is what is most harmful to smokers (not passive smokers though) but both share second-hand smokes


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Are there enzymes found in nature or the man made world that can help break down metals?
The title says it all.
Do natural or human engineered enzymes exist that can speed up the break down kitchen utensils, aluminum cans, wires, etc. into small particles or powders?
To be clear I am not talking about chemical transformation (e.g. iron turning to rust).

what do you mean by breakdown of metals ?

Can you clarify your question - what do you mean by breakdown?

I've attempted to clarify my question. Sorry for not being clear enough.

there are no such enzymes..

So you are asking about physical breakdown into particles and not chemical transformation, e.g. iron to rust?

I would say transformation of iron to rust makes the things more fragile and so they more easily break into particles.

@Barbara Sure, but the poster seems to (?) be asking for breakdown of the original substance. Iron -> rust involves a transformation into a different substance.

@fileunderwater yes I am talking about the break down into particles.

+1 for inspiring me.. just think of the economic implications in e.g. recycling-industries.

There are bacteria, which can assist the proces of rust.
"Some sulfate-reducing bacteria produce hydrogen sulfide, which can cause sulfide stress cracking. Acidithiobacillus bacteria produce sulfuric acid; Acidothiobacillus thiooxidans frequently damages sewer pipes. Ferrobacillus ferrooxidans directly oxidizes iron to iron oxides and iron hydroxides; the rusticles forming on RMS Titanic wreck are caused by bacterial activity. Other bacteria produce various acids, both organic and mineral, or ammonia." (http://en.wikipedia.org/wiki/Microbial_corrosion)
As you see, many of these active ingredients, like hydrogen sulfide, sulfuric acid, other acids or ammonia are not enzymes per se, although they are produced by enzymatic processes in bacteria.
Closer to your specification is Ferrobacillus ferrooxidans (synonyms: Acidithiobacillus ferrooxidans, Thiobacillus ferrooxidans, Ferrobacillus sulfooxidans), which directly acts on iron by enzymes associated with the cell membrane:
Valid XHTML http://c431376.r76.cf2.rackcdn.com/18185/fmicb-03-00096-HTML/image_m/fmicb-03-00096-g001.jpg.
Figure 1. Schematic representation of ferrous iron oxidation by the Gram-negative autotrophic acidophile, At. ferrooxidans. Controlled influx of protons is used to generate ATP via the membrane-bound ATP synthetase complex (ATPase). Iron oxidation is mediated by a cytochrome located on the outer membrane and electrons transferred via periplasmic cytochromes and rusticyanin either to a terminal oxidase (“downhill pathway,” indicated in brown text and by **) where they are used to reduce oxygen, or used to reduce NAD+ (“uphill pathway,” indicated red text and by *) in a reaction also driven by the proton motive force across the inner membrane (Bonnefoy and Holmes, 2011). Source: Johnson et al. 2012.

I am actually speaking of just breaking a metal object down into finer particles (powder). Thank you though.

Non-oxidized metals are rarely substrates for enzymes, although they can be used as electron donors in some reactions.
But you are asking about enzymes capable of cleaving metallic bonds without oxidation, and neither can I recall something of this kind, nor can imagine a biological role for such a reaction.

Ok but is it theoretically possible? Could such an enzyme theoretically be engineered?

No, I don't think it's even theoretically possible, because metallic bonds are very strong. Or, otherwise you need an oxidating enzyme to dissolve the metal (this step is difficult, if you want the metal to be direct substrate of the enzyme) and then a reducing enzyme. Such a system is potentially engineerable. May be, someone has a more realistic opinion.

@max, what do you really need to do with your metallic powder ? Or what was the exact argument which induced you to post this question ? The corrosion, even partial, would make metal easier to break into small pieces. That is the way nature will deal with your kitchen utensils, when they are disposed of as waste.

@Barbara I am just simply curious as to what is possible and what is not. The only way I have seen metal break down is via oxidization and I find that quite ugly. Metal powders can be used to create new metal objects. I guess I just want to see if a new technique can be developed to break metal down in a new more elegant way. Do you think it is possible to engineer a new set of enzymes that can achieve this?

I do not feel competent to predict what is possible in principle. I certainly never heard of such biotechnology you are looking for.

@har-wradim you need to think outside the box. Imagine a waste yard of cars.

Yes TMOTTM, exactly


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Allergic rhinitis vaccine
Note : Any answer to this question will not be (and should not be) taken as medical advice.
One of my friends has allergic rhinitis and has been prescribed an oral vaccine. He is allergic to 3 different classes of substances and so, has been given 3 different types of vaccines. He has to place them below his tongue.
I am curious about some of the procedures he has to follow.
1.How does a vaccine of this type work ?
2 He has been given 2 vials for each type of vaccine. First one is labeled SRS and other one as I understand is - it's allergen. So, What is SRS ? What's the requirement of it ?
3 It is written in the instructions that he should not eat anything one hour before and one hour after taking the vaccine. Why ?

SRS-A stands for slow-reacting substance of anaphylaxis. It is a leukotriene which causes eosinophil chemotaxis and thereby causes allergic reactions in rhinitis.
The described technique is called sublingual immunotherapy. I am not sure how it works (Cant find any article on that. Most articles are from medical journals which don't emphasize on mechanism). I shall find out and get back.

Rhinitis is irritation and inflammation of the mucous membrane inside the nose. Common symptoms of rhinitis are a stuffy nose, runny nose, and post-nasal drip. The most common kind of rhinitis is allergic rhinitis, which is usually triggered by airborne allergens such as pollen and dander [1].
Many questions regarding sublingual immunization still remain to be addressed, including the use of proper adjuvant and the optimization of vaccine formulation to further enhance the vaccine efficacy [2].
Sublingual immunization can induce both systemic and mucosal immune responses against a variety of antigens, including soluble proteins, inter particulate antigens, and live-attenuated viruses [2].
Sublingual immunization has been shown to be safe and highly effective in generating robust immune responses against the administered antigen. Moreover, it has been shown to confer protective immunity by simultaneously eliciting systemic IgG and mucosal IgA antibodies as well as cytotoxic T lymphocyte responses in the peripheral lymphoid organs and mucosal tissues. Studies also suggest that sublingual immunization could be a better alternative to the traditional parental route of vaccine delivery against both genital and respiratory pathogens [2].
Although the s.l. mucosa does not allow passage of macromolecules into blood, s.l. immunization with ovalbumin, a model soluble protein antigen, administered
alone or together with cholera toxin adjuvant, induces mucosal antibody responses as well as systemic immune responses in mice. The magnitude of serum antibody responses induced by s.l. immunization was in fact comparable to that seen after intranasal (i.n.) immunization and far superior to that after o.g. (oro-gastric) immunization [3].
Upon stimulation of mucosal surfaces by foreign antigens, dendritic cells among the antigen presenting cells are immediately processed and transport antigen via afferent lymph to draining lymph node for presentation to T cells. Subsequently they induce secretory IgA antibodies. This suggestive link between trafic pattern of dendritic cells and their functions led to the investigation of the chemokine responsiveness of dendritic cells during their development and maturation. It has been observed that type II mucosa tissues (e.g., skin, vaginal, and buccal), which are covered with stratiﬁed epithelia and devoid of
mucosa-associated lymphoid tissues, mainly express CCL20, CCL19/CCL21, or CCL27/CCL28 individually [4].
CCR7 (chemokine receptor) expressed CD8α-CD11c+ cells ferry antigens in the sublingual mucosa, migrate into the cervical lymph nodes, and share the antigen with resident CD8α+CD11c+ cells for the initiation of antigen-specific T and B cell responses following sublingual challenge. The sublingual mucosa is one of the effective mucosal inductive sites regulated by the CCR7-CCL19/CCL21 pathway [4].

References:

Wikipedia, Rhinitis
Byoung-Shik Shim, Youngjoo Choi, In Su Cheon, and Man Ki Song. Sublingual Delivery of Vaccines for the Induction of Mucosal Immunity.
Cecil Czerkinsky, Nicolas Çuburu, Mi-Na Kweon, Fabienne Anjuere and Jan Holmgren. Sublingual vaccination.
Joo-Hye Song, Jung-Im Kim, Hyung-Joon Kwon, Doo-Hee Shim, Nirmala Parajuli, Nicolas Cuburu, Cecil Czerkinsky and Mi-Na Kweon. CCR7-CCL19/CCL21-Regulated Dendritic Cells Are Responsible for Effectiveness of Sublingual Vaccination.


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Gel electrophoresis after RNAse treatment

I do not understand how to solve this question. I know that RNAse will cut smaller pieces of RNA.
The answer given is A

The question is a bit vague in some important parts, so I'll have to make a few assumptions about what the authors likely meant.
RNAses are enzymes that degrade RNA. There are a few different ones that lead to different kinds of degradation. The type that you would use in an experiment like this is an RNAse that completely degrades RNA. The purpose of this is to be able to distinguish RNA from DNA. So whatever is left after the RNAse treatment is DNA, and the bands that vanished are RNA.
If you isolate nucleic acids from liver, the major DNA part would be genomic DNA. The major RNA components would be mRNA and rRNA. Genomic DNA is huge compared to mRNA and rRNA. In gel electrophoresis of nucleic acids, the bands that move further are smaller nucleic acids, and the bands that move less far are larger nucleic acids. So the band on the left in your example is likely genomic DNA, and the band to the right is mRNA or rRNA. After RNAse digestion only the left band should remain, which is answer A.

RNA can fold and will therefore migrate faster than DNA. So it shows up as the band which is towards the positive front. After RNAse treatment you'll lose that band. So the answer is A

Adding to that: A lot of RNAs are relatively small and migrate faster than a genomic DNA prep.


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Recalling memories by electrical impulses?
I've read that in an experiment, a pair of stimulating electrodes were inserted into a blind man's visual cortex, and upon passing electricity, the phosphene phenomenon was produced. Is it the same with memory? Can each and every memory, of an individual be recalled by a similar method? And if so, in which region of the brain will the stimulating electrodes be inserted?

As far as I know, we do not know very much about the whole mechanism of memory. My guess is: no. You would be better off trying hypnosis.

You might be interested in reading the June 2013 issue of Scientific American which contained an interesting article on forming of memories..

it is important to first map the memories. Usually a memory involves a lot of different perceptions. So i guess it is not that easy. visual cortex is a specific anatomical location that is involved in a very specific task.

There have been quite a few studies on stimulating the brain with electrical pulses and it has been found to be successful too. Three papers of particular interest I found were:
1) In a study titled "Explaining How Brain Stimulation Can Evoke Memories", it was found that electrical stimulation in the temporal neocortex can cause neurosurgical patients to spontaneously experience memory retrieval. The subject's brain in the study when stimulated enabled him to recollect memories from the time that he was in high school. They concluded that there are patches of neurons encoding memories for differnt periods (in this case the high school). (reference)
2) In the second study titled "Memory Enhancement and Deep-Brain Stimulation of the Entorhinal Area", it was observed that

entorhinal stimulation applied while subjects learned the locations of
  landmarks enhanced their subsequent memory of these locations: and the
  subjects reached these landmarks more quickly and by shorter routes,
  as compared with locations learned without stimulation. (reference)

3) In a third study titled "Stimulation of Entorhinal Cortex Promotes Adult Neurogenesis and Facilitates Spatial Memory", it was found that stimulating a specific region of the brain leads to the production of new brain cells that enhance memory. (reference)
In two on these studies, memory is enhanced by stimulation to the entorhinal cortex and in the first study the neocortex was stimulated. So, in a broad sense the  cerebral cortex is generally used for these studies.
This is a continuous field of research as a treatment to diseases like Alzheimers (reference).

Gray-Brodman-Entorhinal Cortex (Wikipedia)

Neocortex location (reference)


text:
SNP genotyping using PCR
I read this wikipedia article on SNP genotyping and wasn't able to understand this part :

In examining the results, if a genomic sample is homozygous, then the
  PCR products that result will be from the primer which matches the SNP
  location to the outer, opposite strand primer as well from the two
  opposite, outer primers. If the genomic sample is heterozygous, then
  products will result from the primer of each allele to their
  respective outer primer counterparts as well as from the two opposite,
  outer primers.

Can anyone explain this ?

Valid XHTML http://nar.oxfordjournals.org/content/29/17/e88/F1.large.jpg.
Figure 1. Schematic presentation of the tetra-primer ARMS-PCR method. The single nucleotide polymorphism used here as an example is a G→A substitution, but the method can be used to type other types of single base substitutions. Two allele-specific amplicons are generated using two pairs of primers, one pair (indicated by pink and red arrows, respectively) producing an amplicon representing the G allele and the other pair (indicated by indigo and blue arrows, respectively) producing an amplicon representing the A allele. Allele specificity is conferred by a mismatch between the 3′-terminal base of an inner primer and the template. To enhance allelic specificity, a second deliberate mismatch (indicated by an asterisk) at position –2 from the 3′-terminus is also incorporated in the inner primers. The primers are 26 nt or longer, so as to minimize the difference in stability of primers annealed to the target and non-target alleles, ensuring that allele specificity results from differences in extension rate, rather than hybridisation rate. By positioning the two outer primers at different distances from the polymorphic nucleotide, the two allele-specific amplicons differ in length, allowing them to be discriminated by gel electrophoresis. (http://nar.oxfordjournals.org/content/29/17/e88/F1.expansion)


text:
What happens to our body when we undergo a sudden temperature change from 40℃ to 20℃?
We know that a glass gets cracked when it undergoes sudden change in temperature. But what will happen in the case of a human body if it changes from the maximum(>35℃) to the minimum temperature(<35℃) suddenly?

That depends entirely on the range of temperatures you're talking about. Please [edit] your question and add some additional details, because as it stands now your question is unclear.

The edit is not an improvement of the question. (>35 C) and (<35 C) is not a range.

Disclaimer: the answer is very broad and covers both the situations I am confident about, as well as those I understand only superficially.
The outcome depends on particular temperatures.
Example - cold shock response: "Cold shock response is the physiological response of organisms to sudden cold, especially cold water. In humans, cold shock response is perhaps the most common cause of death from immersion in very cold water, such as by falling through thin ice. The cold water can cause heart attack due to vasoconstriction, the heart has to work harder to pump the same volume of blood throughout the body. For people with heart disease, this additional workload can cause the heart to go into arrest. Inhalation of water (and thus drowning) may result from hyperventilation. Some people, due to body type or mental conditioning, are much better able to survive swimming in very cold water." But: " A person who survives the initial minute of trauma (after falling into icy water), can survive for at least thirty minutes provided they don't drown."
Sudden heat at entering sauna - I am not sure, but probably it also may cause heart attacks. Recent heart attack is a contraindication for sauna visits. Healthy individuals do O.K. due to thermoregulation mechanisms in the body.
As we move to more extreme temperatures, where the thermoregulation of human body simply has no chance at all to keep up, you can percieve the human body as a chunk of meat. The proteins denature, the water in the body gets boiled. The meat gets cooked, turns coal like, burns to ashes... Or by freezing, the water forms crystals, damages and breaks the cells. Eventually the meat freezes to be stone hard and does not change for a long time if kept at such temperature.

Blood vessels  tighten as the diferencial between the body temperature and the external temperature start to even out and the excess heat/energy disperses from the body to the environment. There should be a slowdown of heartbeat rate as less effort is applied to regain homeostasis.On the negative side, the sudden tightening of the blood vessels will add strain on the blood pressure until the heart starts pumping blood at a regular rate again, causing pains like muscle spasms and headaches. This can be minimizes if u got to a temperature of 25ºC instead of 20ºC and do a gradual decrease in temperature.
Reference
Alexiou. The effect of water temperature on the human body
and the swimming effort. JBE – VOL. 10.2, 2014


text:
Significance of having goosebumps?
What help does goosebumps do to us? I don't think it helps us noticeably when we are scared or shivering.

As a general rule, you might want to check wikipedia before posting here. On the other hand, I am glad you made me look the answer up.
Goose-bumps warm you up a little. "During the formation of goose bumps, the body is warmed from the muscle tension in piloerection."
There are other reasons, which do not directly serve humans, but may be a remnant from evolution. In animals with fur, the erected hair makes thicker insulation and further protection from cold. "Goose bumps can also be a response to anger or fear: the erect hairs make the animal appear larger, in order to intimidate enemies."
More on wikipedia: http://en.wikipedia.org/wiki/Goose_bumps

Hairs (with their nerve rich follicles) are sense organs, extending our sense of touch beyond the skin. When things disturb our hairs we feel them; bugs, breezes, close encounters. During fright or arousal goosebumps cause the hairs to stand on end, extending our sense of touch to it's furthest distance. In the process the hair shafts that are otherwise laid against each other are separated, reducing the dampening of vibration and movement from shaft to follicle - which increases fine sensitivity. Also during goosebumps the smallest disturbance of hairs causes a reaction in surrounding hairs, amplifying distinguishable sensations into hard to ignore. Goosebumps are sensory enhancers.
This goosbumps response predated hairs as fur for insulation and probably mammals as a group. Raising fur to increase insulation, as well as raising hackles to look intimidating almost certainly piggy backed on this pre-existing response.  It is a function that has never been lost and should not be considered vestigial.

"The formation of goose bumps in humans under stress is a vestigial
  reflex; a possible function in human evolutionary ancestors was to
  raise the body's hair, making the ancestor appear larger and scaring
  off predators. Raising the hair is also used to trap an extra layer of
  air, keeping an animal warm. Due to the diminished amount of hair in
  humans, the reflex formation of goose bumps when cold is also
  vestigial."

This is from the wikipedia article on human vestigiality under Behavioural category.

My guess was that it was used in the past as a technique to scare predators, seeing as our ancestors had a lot of hair, this could've been a lot of use.


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DNA ligase mechanism

I am unable to understand what happens to the phosphates from  ATP. What are they used for ?Charging 3' end or 5'end ?

When you ligate two strands of DNA you build up a phosphodiester bond. To do so, you need energy, and this energy for the DNA ligase comes from the ATP (in bacteria this energy can also come from NAD+.
The enzyme metabolizes ATP to AMP + PPi and binds the AMP in its active center. Then the AMP is involved in the reaction itself and released afterwards. This page has a few illustrations on this process.
If you want to dive really deep into the topic, have a look at this review:

Eukaryotic DNA Ligases: Structural and Functional Insights


text:
what is the difference between early blight of potato and late blight of potato?
apart from different fungus causing these diseases in potato, how are Early Blight of potato and Late blight of potato different?

Some Differences are listed here

Please consider reading these articles (article 1, article 2)


text:
What determines the thickness of Cornea?
In eye-operations such as Lasik and Femto, the thickness of cornea is key decision factor whether the operation is feasible. A normal thickness is between 500-600 µm. Cornea consists of a very special tissue having no blood supply and no vessels so it gets nutrients through diffusion of tear fluid and oxygen directly from air (hence in a way, it has its own respiration system not dependent on lungs).
Now I started to think the following questions:

I. What determines the thickness of cornea?

Helper questions

II. Is the thickness of cornea determined genetically so twins have the same cornea thickness?
III. Is the thickness determined by the environment and psychological things? Eg. how does diving affect cornea? Look it cannot get oxygen anymore through the air with the mask. What about drying? Does cornea gets too much nutrients all of a sudden from eye fluids?
IV. Does Homo Sapiens have more this kind of independent tissues? What about other animials? What determines the thickness of Cornea there?

"What determines the thickness of cornea? " - As you mentioned the efficiency of diffusion is the main size limitation factor here. I don't know much about the topic btw.

The corneal thickness is genetically programmed. There are multiple genes that induce the final corneal thickness:
USP37, Chromosome 2;
GPR15, 3;
TIPARP, 3;
CWC27-ADAMTS6, 5;
RXRACOL5A1, 9;
LCN12-PTGDS, 9;
FGF9-SGCG, 13;
and at least 6 other genes.
source
other questions had to be asked as separate ones


text:
Reference sequence for defining single nucleotide polymorphisms
Single nucleotide polymorphism (SNP) or genetic variation in general, by definition are relative to a reference sequence. When we talk about databases of SNP as in ("dbSNP—Database for Single Nucleotide Polymorphisms and Other Classes of Minor Genetic Variation", or "A map of human genome sequence variation containing 1.42 million single nucleotide polymorphisms" -- titles of well known research papers), what is the reference genome? Similarly for defining a "SNP Map/Profile" of a person (in medical genomics), what is the reference genome sequence? Is there a de facto reference, or is it context dependent? There is a sentence "Scientists are trying to identify all the different SNPs in the human genome" at http://www.cancer.gov/cancertopics/understandingcancer/geneticvariation/page36 -
what is the reference genome here?

the reference genome used is usually the hg19 (UCSC) or GRCh38(NCBI). For population based studies involving something like an endemic population a context dependent reference can be used.

I don't see your point. If we take e.g. the definition from Wikipedia:
SNP "is a DNA sequence variation occurring when a Single Nucleotide ... in the genome ... differs between members of a biological species or paired chromosomes",
there is no place for reference genome. SNP is just a variable position with (commonly) two alternatives in individuals of the same species. In whole-genome sequencing projects some SNPs can be discovered (namely those which are in heterozygous state), but definitely not all.
One can investigate SNPs and/or use them as genetic markers irrespective of the availability of the reference genome. That's the way one does it for non-model organisms - e.g. utilizing RAD Seq: you discover SNPs simultaneously with genotyping.

How is the location/position of genome where we look for variability/alternative defined?

If you are talking about coordinates, than they are defined either by location on the reference genome, by the location on the genetic map or not defined at all.

dbSNP actually indexes itself against several reference genome builds including hg19.  you can see this in the ssID records  - we use the bulk downloads and you can see them there as well.
Any difference with respect to any two genome builds is really a variant.  You can see this in the case of tri- and quad- allelic variants. There are cases where entire sequences lengths are added or removed compared to a reference genome build.  These are called insert/delete variants, which can contain short or single nucleotide variants as well.
will try to fill this out a bit more later... quick response here.

SNPs are discovered not only in whole genome sequencing projects. It's just a type of molecular markers.

certainly this is so.


text:
What is "transcribed strand"
This is an excerpt from a paper:

T>C mutations at NpTpN trinucleotides, also found in hepatocellular carcinomas, shows strong transcriptional strand bias with more T>C mutations on the transcribed than untranscribed strands

What exactly is meant by "transcribed" strand: the sense strand or the template strand ?
I tried looking up for it but couldn't find any definition.

I think it should be the template strand .

i too guess that but am looking for a reference that defines so.

I also found this term being used in one of the leading A Level textbooks.

@biogirl which one?

In my opinion they should mean the template strand, and they probably do. Perhaps if we had a link to the paper we could have examined the language more closely.
Here is a paper which uses the term in that sense:

Mugal, CF et al. (2008) Transcription-Induced Mutational Strand Bias and Its Effect on Substitution Rates in Human Genes. Molecular Biology and Evolution 26,131-142

In the abstract (which I have linked to) the authors make a clear reference to the transcribed strand in contrast to the coding strand (i.e. the strand of DNA with the same sequence as the RNA transcript):

All three [mutational rates] considered are found to be on average higher on the coding strand and lower on the transcribed strand...

There are also definitions confirming this at this Wikipedia page.

Remember that DNA is double stranded and each strand has a chemical direction.  Genes are read by the ribosome in the 3' to 5' direction so that the DNA 'forward' direction is defined in this direction.  This is the direction of transcription.
Each segment of DNA can therefore be read in 2 directions.  In the direction of transcription each T will have an A on the other strand.  So each letter in the direction of transcription will not be the same if you read the other strand.
Transcription (that which is transcribed) refers to the ribosomal read strand.
Hope this helps.

I understand that.. But when the authors say "transcribed strand" do they mean the strand that RNAPol reads or the strand that is actually in sense with the transcript ?

transcription (that which is transcribed) is the ribosomal read strand.  i'll put that in the answer too...


text:
How did fish evolve the ability to breathe on land?
Doesn't make sense. It would be like a human evolving the ability to breathe on the moon without a spacesuit.
How would the organism be able to carry out such an evolutionary adaptation, when the evolution of it involves death to the organism, preventing it from ever being able to evolve it to begin with, because the variation cannot develop, or be passed along to the population due to it needing to be functional to survive at all.
Also, how does an organism gain the new information necessary to get those land breathing or moon breathing adaptions, from a genome that doesn't already have such an ability encoded in its genetic morphology in the first place?

Evolution doesnt happen suddenly.. Sudden changes in environment have caused mass extinctions several times in the earth's evolutionary history.
BTW, amphibians came before completely terrestrial animals.
You can edit the question to make it a more focused: e.g. ask about evolution of lungs.

Note: Reptiles and Amphibians are sister groups encompassed in the clade of Tetrapoda. See tolweb.org.

This assumes that it's either underwater breathing or air breathing.  The two could exist together in the same organism (and almost certainly did). The very first version would allow a "fish" to spend short amounts of time out of the water (I.e. be very inefficient). This would be a step up from a fish having to "hold its breath" out of the water.

Just out of interest, are you prepared in any circumstances to mark an answer correct? If not, then this is not a question according to the rules of SE and you should delete it. I will assume that failure to reply indicates an answer no. Please note this is a question and answer site, not a discussion site.

It would be like a human evolving the ability to breathe on the moon without a spacesuit.... strangely enough, the only thing preventing humans from just wearing a face mask and walking around in space is our skin is too flexible. It need a source of inward pressure..denser collagen.... or really super strong spandex clothes..a skin suit as it is called.. Human skin is already air tight enough that we do not need the skin suit to be air tight.

Air-filled, gut-tube-derived organs (i.e., air bladders, gas bladders, and lungs) have a very wide distribution among fish in general, so the most parsimonious explanation is that the first terrestrial tetrapods already had a lung-like structure.
The image below (from Kardong's Vertebrates) shows two major clades of fishes, Actinopterygii (ray-finned fishes) and Sarcopyerygii ("fleshy-finned" fishes, which include both lungfish and tetrapods). Given the wide distribution, a homologous organ was almost certainly present at the most recent common ancestor of these two groups. I don't know what the evidence is for lungs further down the tree, so I'm not certain about loss of lungs in Chondrichthyes (sharks, rays, skates).

You ask two question. it is always better to restrict a post to only one accurate and narrowed enough question. I will not provide a full review of how did the origin of tetrapods occur. I just give some critics on you question give some words about the evolution of lungs, discuss your comparison with "breathing on the moon" and answer your question concerning the origin of genetic variation.

How did fish evolve the ability to breathe on land?

This question is way too broad, you should narrow it down. You say that this evolution is impossible but you should provide some argument so that we can discuss them. For the moment there is not much to discuss about. The only thing one could si to review tons of article concerning the evolution of tetrapods. I bet you're interested in the evolution of lungs during at the origin of the lineage of the tetrapods. If so… In short, swim bladder and lungs are homologous organs. According to this that at the time tetrapods-like animals evolved, this organs was used to gulp air in oxygen-poor environment. This organs then evolved into various forms of lungs as we know them today in terrestrial and none terrestrial vertebrates. This organ also further evolved in order to control the buoyancy. Note: Several popular sources gives different informations. One would need to go into some articles in order to make sure of details such as "were this organ already used to control buoyancy before the speciation of the tetrapods?".
Here is a simple source that you may like
You say that evolving abilities to breath in the atmosphere for tetrapods is like evolving abilities to breath on the moon in humans. Well there are several differences that should be considered that make the moon really not a pleasant place to live! The temperature for example spans between 100K and 373K according to this wiki! But let's forget about these other ecological factors. One big difference is that humans do not live in an environment that offers a gradient from earth atmosphere to moon atmosphere while first tetrapods-like animals lived in such a gradient. Also, when you talk about human, it feels like you consider the wrong time-scale. It probably took quite a lot of time to evolve from fish-like to totally terrestrial tetrapods.
You might want to have a look to this interesting post. Life apparently independently emerged out of water at least 9 times.

"How does an organism gain the new information necessary to get those land breathing or moon breathing adaptions, from a genome that doesn't already have such an ability encoded in its genetic morphology in the first place?"

If I understand your point correctly one could rephrase your question into:

"I understand the process of Natural Selection (NS). It selects for some already existing variants but what process creates the variation from which NS makes its selection?

And the answer is: Mutations. In the narrow sense (in order to keep it easy), a mutation is a change in a genetic sequence. Such change typically occur during the meiosis, process that occurs in all sexual reproductions but it also occur during any mitosis (standard cell division) or other phases of the cell cycle.
In short, mutations create genetic variations and differential reproductive abilities between individuals in a population results in a selection (called Natural Selection) for variants that are the best at reproducing.

According to the WP entry on amphibious fish (http://en.wikipedia.org/wiki/Amphibious_fish) the swim bladder evolved from a lung-like organ, and in tetrapods this was the basis of air breathing. There are modern lungfish too (http://en.wikipedia.org/wiki/Lungfish).

@AlanBoyd Indeed it seems there is a contradiction between wiki and Berkeley's website! There are quite a lot of literature on the subjet but I don't feel going through it for the moment (and not for this post!). Here is a review that might be of interest. I updated my answer.


text:
Vesicular and non vesicular transport

I have to classify them either as transported in vesicles or without vesicles.
What I think -

Non-vesicular

2.vesicular
3.vesicular
4.vesicular
5.non-vesicular
6.vesicular
7.vesicular
8.vesicular
9.vesicular
Am I right ? Is it true that a  protein transported by vesicles is made on ER ribosomes ?
How are proteins transported non-vesicular transport ?

Any protein which enters the secretory pathway will proceed via vesicular transport to some point on that pathway. That includes lysosomal proteins, integral plasma membrane proteins and secreted proteins (also, not on your list, resident proteins of the ER, Golgi proteins, some endosomal proteins).
Cytoskeletal proteins are cytoplasmic: I suppose you could argue they are 'transported' sometimes, e.g. tubulin treadmilling, motors etc., but no vesicles are involved. Nuclear proteins enter the nucleus from the cytoplasm through nuclear pores. They have nuclear localisation signals; vesicles aren't involved. Mitochondria, chloroplasts and peroxisomes all have their own protein import systems with associated unique signals; again no vesicles are involved.


text:
Are sulfates or nitrates common ions in biochemistry (specifically of the body)?
It's a rather broad question but something I'm curious about.
I know sulfates tend to be very soluble ions and so don't know nitrates.
I also know that phosphates are extremely common in biochemistry (e.g. ADP) but they're not very soluble unless they involve group 1 elements, same goes for carbonates.
I think Carbonates tend to be more common in crustacea, or chicken egg shells. I can't remember if it's found in the Krebb's cycle (don't think so, but maybe in other vitamins?).
Solubility isn't apart of this question, it was just one of the ways I was just trying to pursue an answer. I'm more of a chemist than a biologist...


text:
Are HeLa cells edible?
I'm curious if HeLa cells are intrinsically poisonous or dangerous to ingest.
My understanding is that some of the contamination in HeLa cells such as HPVs are not readily expressed.
I have no plans to do so, but I'm trying to understand why they might or might not be.

..they are cancer cells from a fatal case of cervical cancer and they are favored because they don't stop dividing.  I would not eat them.  I'm sure the experiment has not been done. They are not poisonous, though.  Cultured mammalian cells (not HeLa cells) are being proposed as a way of making meat substitutes.

HeLa can't be as contagious as this dog cancer, but it is transmissible by cells invading the soft tissue of dogs... http://www.sciencemag.org/content/343/6169/437

I think HELA cells are edible, although from moral point of view this would be cannibalism.
Despite they are cancer cells, they are safe for foreign organism, because any ate matter is destroyed. Even if these cells were implanted into another being by surgery, they will be safe since immunity will recognize them as foreign and kill. They are much less cancerous for recipient than just foreign.
Remember, then when we are eating meat, we don't care if cow or pig had cancer. Even if we avoid eating explicit tumors, we can still eat metastatic cells from sick animals. I think this happening all the time and has no consequences.
Simultaneously HELA cells are dangerous for other cell cultures in laboratory. There were several cases, when other cultures were infected by HELA cells and crowd out. HELA cells were traveled by air and on objects unexpectedly. Scientists were not ready for this phenomenon.

I guess I would like the answer to discuss some of the contamination in the line itself. The line itself appears to be contaminated by various pathogens, often mentioned is HPV - although I am not sure if it is actively expressed. For example, if I eat a bunch of HPV contaminated tissue, will I also get HPV? I am not sure if the digestive system is able to deal with all of these pathogens, for example, If I eat a bunch of BSE contaminated tissue I will get mad cow disease.

Of course some pathogens can infect us when eat. But the point is that HELA cells are nothing special in this case. You said it yourself: you can get BSE or HPV in everyday life, you need not eating HELA for this. So, I can get some pathogens from HELA, but unprobably and this definitely won't be a cancer Henrietta died of.

I guess the outstanding question is, if in raw form, they might contain sufficient pathogens to be considered dangerous. I don't consider something that will give you HPV "edible".