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Why does ear wax taste sour?
Why does ear wax taste sour?
I am interested in both the physiochemical mechanisms and the evolutionary reasons behind the sour taste of earwax.

Well, I am curious - How do you know ear wax tastes sour ?!

I know because... for science.

Earwax, also called cerumen, is slightly acidic (1), with a pH of about 6,  and acidic foods or substances taste sour. The composition of earwax, upon which its taste depends, is related to its functions. Earwax aids in cleaning and lubrication of the ear canal and has an antimicrobial effect. The antimicrobial effect is in part attributed to its acidity, which might give an evolutionary reason for the sour taste.
From Wikipedia:

Cerumen is produced in the outer third of the cartilaginous portion of
  the ear canal. It is a mixture of viscous secretions from sebaceous
  glands and less-viscous ones from modified apocrine sweat glands.[4]
  The primary components of earwax are shed layers of skin, with 60% of
  the earwax consisting of keratin, 12–20% saturated and unsaturated
  long-chain fatty acids, alcohols, squalene and 6–9% cholesterol.[5]
(...)
While studies conducted up until the 1960s found little evidence
  supporting antibacterial activity for cerumen,[15] more recent studies
  have found that cerumen has a bactericidal effect on some strains of
  bacteria. These antimicrobial properties are due principally to the
  presence of saturated fatty acids, lysozyme and, especially, to the
  slight acidity of cerumen.


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Functioning of EDTA
I know that EDTA chelates metal ions. It weakens bacterial cell wall and inactivates the DNases.
What is the reason why it can do so ? I guess it can inactivate DNases by altering the microenvironment. What exactly happens ?

The lipopolysaccharide layer of the Gram-negative bacterial cell wall is stabilised by divalent cations. Most recipes for disrupting E. coli cells include Tris-EDTA for this reason. I seem to just know this, so no reference at the moment.
All nucleases require Mg2+, which is why there is EDTA in the stop buffer added to restriction digests. Carry-over of EDTA in DNA pellets can sometimes inhibit digests.

A lot of enzymes need metal ion in their active center (it is actually the metal ion which is taking part in the catalyzed reaction). These are manganese, magnesium, copper and so on. For DNAses the metal in the active center is magnesium and EDTA simply chelates this ions, making them unavailable for the enzyme and thus hinders the enzyme from working.
Chelation is the process in which metal ions are coordinated in molecules and form coordinate bonds to the chelating agent. EDTA looks like this:

The 3d structure while chelating a metal ions like this:

You can see, that the metal ion is nicely located between the negatively charged oxygen atoms and the nitrogen atoms. These complexes are fairly stable and the metal ions do not escape.

Could you also tell me why it will disrupt bacterial cell wall ?

Who claims that, do you have a protocol for that (so I can have a look)? All buffers I know for this purpose also contain detergents which actually break up cell wall and membranes. EDTA has the function of inhibiting enzymes.

I read it in my textbook.

one might add that 'chelation' means: EDTA has two amines and four carbocylic acids which form a compact shell around metal ions, they bind so tightly that they cannot bind anywhere else.

Good point, i added this to the answer.

source: Stack Exchange

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Concentration of DNA by isopropanol
I have read that DNA can be concentrated by addition of isopropanol.
What does "concentrated" mean? What does isopropanol do on a molecular level to concentrate DNA?

What you are asking about is the precipitation of DNA (or any other nucleic acid) by isopropanol (or ethanol, which is more common). To do so, you add salt (usually slightly acidic sodium acetate) which makes sure that the phosphate backbone of the DNA is saturated with sodium ions to make it less soluble. Then you add the organic solvent, which precipitates the DNA from the solution by changing the polarity of the solution. This makes the ions form salts and the DNA precipites. The principle is explained in the Wikipedia article on ethanol precipitation. Finally the solution is centrifuged to collect the DNA at the bottom of your reaction tube and to be able to take off the supernatant.

Small addition: Isopropanol having a bigger alkyl group makes the solution more organic in nature compared to ethanol. Why isopropanol and not n-propanol is perhaps because it is easy to manufacture isopropanol. n-propanol is better at precipitating smaller nucleic acids.

It is because isopropanol is less toxic in the handling than n-propanol. n-propanol can cause severe eye damage and is generally more toxic than ethanol or isopropanol.

Point taken. but it is also easy to manufasture isopropanol :P

Not to mention every molecular bio lab has isopropanol on hand.

@Chris.. I am not sure why you say n-propanol is more toxic. It can be easily metabolized to propionic acid. This article says that isopropanol is more toxic in terms of longlasting effects.

This is mostly about potential eye damage though n-propanol (by splashes). This MSDS says for example "Eye contact with n-propanol may cause severe irritation with corneal injury, which may result
in permanent impairment of vision, even blindness."

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Consequence of touching Formaldehyde
I accidently touched formaldehyde some days ago. Skin on my hand got dehydrated as if I had placed it in salt solution. I washed it with water and it returned to normal state after 5 minutes.
But now whenever I wash my hands with water my skin gets dehydrated again, but returns to normal state after some time .
What's the reason behind it getting dehydrated again when exposed to water ? Will it return to normal state when new skin grows back ?
By dehydration, I mean something like this.

Formaldehyde is not something to play around with. If you touch it then you need to immediately run your skin under room temperature water.

Even my hands have bcom like that. I accidentaly was holdin a leaking formalin bottle. Which later lead to dehydration in my hand and also I'm not able to feel anything that I touch.

@biogirl did your fingers ever get back to normal?

cool pics!
Firstly, Formadahyde is a terribly toxic substance.

Skin Contact: CORROSIVE. Contact can cause pain, redness, burns, and blistering. Permanent scarring can result. Can be absorbed through the skin.

Formaldehyde causes organ failure and scarring if ingested.
In this case, since you don't have burning or blistering, it seems like a reasonably low exposure. You should nonetheless call your doctor to check in or drop by the campus infirmary or what you have.
A good experience to remind you to wear gloves when working with chemically active reagents or solvents (DMSO for instance!)
I'm not a doctor, but as a non professional and informal opinion, your finger will probably become normal again, eventually all the cells will do their best to repair themselves.

Those rnt my fingers. The pic is on google :) why do my finger dehydrate after washing with water again ?

You mean your fingers getting wrinkled after washing them (or keeping them in water for a longer time)?

not sure, but the docs do seem to indicate that your fingers would have chemical burns if you had had a more concentrated solution or longer contact, so a reaction that is not seen as often perhaps.

@Chris After washing them.

@biogirl, formaldehyde chemically denatures the proteins and some other biomolecules. The damage is not mainly because of dehydration (in case of $H_2SO_4$ it is the strong dehydrating effect that is one of the the primary reasons for the burn)

@WYSIWYG Thanks! Could you answer my second question - why would it lead to dehydration again after I wash my hands ?

It is not dehydration. The wrinkling is because of damaged skin, perhaps. And the wrinkling is because of hydration


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Bilayer synthesis?
If we want to design a bilayer from Myristic acid (14 carbon fatty acid). The average bond length between C-C is 1.5 A. What will be average thickness of the membrane?
Edited to include the OP attempt that was posted in a comment:
There are 13 C-C bonds in Myristic acid, 13*1.5=19.5A. 1A=o.1nm.. so 19.5A=1.95nm, so the average thickness would be 1.95nm. As membrane is bilayer it will be 3.9nm

Lewis & Engelman (1983) Lipid bilayer thickness varies linearly with acyl chain length in fluid phosphatidylcholine vesicles. J. Mol. Biol. 166: 211 - 217.
Table 1 and Figure 3 have the information that you need. For C14:0 the thickness of the hydrocarbon bilayer is given as 23 Å. Just in case this is homework, I'll leave you to convert that to nm.
added later
Just to follow up on the comments, as hinted at by Shigeta, if you wanted to calculate an estimated bilayer thickness you would have to take into account the C-C-C bond angle which for tetrahedral carbon is 109.46°.
Thus the distance between two C atoms in an extended C chain is 2 x 1.5 x sin(109.46/2) = 2.45 Å
For C14:0 the length is then 6.5 x 2.45 = 15.9 Å (from methyl C to carbonyl C).
Therefore, calculated bilayer thickness = 31.8 Å plus any distance between the two C chains in the centre of the bilayer. This is still a lot bigger than the reported 23 Å.
Clearly the bilayer does not consist of extended hydrocarbon chains. The chains are presumably partially collapsed (on average) and may also interdigitate to some extent.

I want to ask one thing that if we are not provided with the information about the thickness of membrane in any table or a graph then can we are capable to calculate the Membrane thickness according to some data that is provided in Question such as C-C bond length?                       As I have tried it tell me whether it is correct or not? :/  There are 13 C-C bonds in Myristic acid, 13*1.5=19.5A. 1A=o.1nm.. so 19.5A=1.95nm, so the average thickness would be 1.95nm. As membrane is bilayer it will be 3.9nm.

notice how your answer is ~70% longer than the actual answer?   Because the chains are flexible its not that simple. You might calculate the average length of the chain in the membrane given all the reasonable bond angles the chain might take, probably by molecular dynamics.  its not straightforward.  Even if you built a model of the molecule you'd find that the bond angles of the extended chain gave a length at least 30% shorter than your end to end number. The table cited here is the actual answer, from a measurement of membranes and so even better than that.


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Do people who have been blind all their lives dream?
Do the people who have been blind all their lives dream and do they experience or report "imagery" in the dreams?

Yes, they do. A blog post on the National Geographic website describes the results of a study about how blind people dream.(1) The participants who were born blind did not report any visual impressions. Among those who previously had sight, the number of visual impressions reported decreased with the time since loss of sight.

Just as there are many ways to take in the world, there are many ways
  to dream about it. Blind people dream, just as they live, with a rich
  mix of sensory information.
About 18 percent of the blind participants (both congenital and
  later-onset) reported tasting in at least one dream, compared with 7
  percent of controls. Nearly 30 percent of the blind reported smelling
  in at least one dream, compared with 15 percent of controls. Almost 70
  percent of the blind reported a touch sensation, compared to 45
  percent of controls. And 86 percent of the blind reported hearing,
  compared with 64 percent of controls.
(...)
Despite these sensory differences, the emotional and thematic content
  of dreams isn’t much different in the blind and the sighted. Both
  groups reported about the same number of social interactions,
  successes, and failures in their dreams. They had the same
  distribution of emotions, and the same level of bizarreness.


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Why do we find nature 'beautiful', from an evolutionary perspective?
Most people I know find nature beautiful and holidays generally involve a place that has 'natural beauty'.

I would say that beautiful is pretty subjective and has nothing to do with evolution. It is more something that humans find interesting, probably because of some romantic ideas.

there is an interesting TED talk about this, basically we don't find all nature beautiful, only certain aspects of nature have universal appeal, the ones that were advantagous for our ancestors like signs of water, food, and climbable trees. https://www.ted.com/talks/denis_dutton_a_darwinian_theory_of_beauty

Bright colors can attract a sexual partner as they are beautiful and are often a sign of good health. So, if you have bright and beautiful colors, you'll attract a partner to reproduce more easily than other and your genes will pass to the next generations. So, some animals are "beautiful" because of sexual selection.
For flowers, bright colors and perfume attract pollinators, so the brighter the better to reproduce.
Of course, as beauty is all relative, not all flowers or animals are "beautiful" according to humans' tastes. But they suit the environnement the organism lives in and whatever is needed to get to reproduce.
Sexual selection is not the answer to everything you find beautiful but it explains some.

We find valleys pretty. We find mountains pretty. We like sunshine and clouds.
I'd say all these have some advantages. Trees you can climb. In valleys you have protection. From mountains you have a good view across the landscape.
So yes it does make sense that we like nature. We like things that are good for us. Like fertile land and food.


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How does the creative process of Biological Evolution work?
In order for nature to go from microbes to man, there needs to be new information. Where does this new information come from?
It is understood that Evolution basically involves three elements. Natural selection, genetic mutation, and time. The problem for Evolution, is that none of those three elements are creative. Natural selection is basically just a pruning process. It selects from what is there and advantageous, and prunes off what is deleterious to the organism as far as its fitness.
Genetic mutation is just errors in replication. So it creates nothing. It simply degrades. We have no new information, just an erroneous replication, and degradation of what was there before.
That is still true of gene duplication. We have an error that repeats the same information/genes. So we have two copies of something but there is still no new information.
This brings us to the second problem. What mechanism or process of nature/Evolution, carries out the instructions. What I mean by this, is that it essentially has to work like a computer. If I want my computer to have a more advanced program, I need to input new information, and its often codified in the form of say a disk, or installation file.
What is the equivalent of this installation file for Evolution?
For example. Say I'm a cephalopod. And I'm getting environmental pressure from predators and I want, or need, to advance my defenses, so I want to built some spikes on a hard outer shell. Where does the cephalopod get the new information, or rather, instructions, to know how to do this new feature?

Please do not downvote questions because they disagree with our views. This is a fair question, despite being a little bit to close to a rant. The arguments presented are wrong, yes, but that is a reason to answer, and explain to the OP using arguments, not to downvote. We should welcome this type of question and do our best to answer it well.

The last comment was not directed at you, but to the regulars of the site. However, you might be interested in these: How does the modern theory of evolution solve these apparent problems?, How does evolution produce complex organs and Human evolution: Where *exactly* did the first human come from, whose parents were not? among other Q&As on the site.

But this question is not simply misconceived- it is not even wrong! I'd make the argument that this question is not well formed, nor do I see the possibility for a constructive outcome because OPs premise is wildly ignorant. Check OP's other questions- every one is a a variation on the same theme. None are useful and none are resolved. This is question is simply persistent noise.

@adamwong246 that's irrelevant. Remember that the SE sites are wikis and the information we give should not be aimed at the OP alone. The basic misconceptions here can be addressed, I've tried to do so in my answer. As I'm sure you know creationist and ID arguments tend to be ridiculously easy to shoot down, just like this one is. We should welcome the chance to do so in the hope that we might increase the understanding, if not of the OP, then of the next poor misguided soul who has fallen under the influence of pseudoscience.

Perhaps this should be moved to a meta-discussion but is there really a hope that OP will ever select one of the following answers as correct? I'm not optimistic.

@adamwong246 again, that's completely besides the point. The Q&As here are not only for the OP and this is the same for all sites on the SE network. We aim to be a repository of useful information.

@terdon I don't see a problem with downvoting this Q, but it should clearly not be done because of disagreement. However, this Q completely lacks background research (both from BioSE and basic biology), is mostly phrased as a personal trail-of-thought, and the poster has clearly not bothered to look up the basics of evolutionary theory - also see How do I ask a good question. I don't think the Q should be closed, but it is still not a good Q.

Creationism is off-topic on Biology SE.

@fileunderwater yes, that is a very good point. I commented when this question was at -2 with 1) no explanation of why people downvoted 2) no attempts to edit it into shape (I have now tried to do so) 3) no suggestions on how to improve. Had this been on another subject, we would have done all three. I just don't want us to downvote only because we disagree with the views expressed. I feel that one of the most important things this site can accomplish is to refute pseudoscience and any creationist/ID advocate who's willing to post here deserves a  good answer. Shoved down their throats.

opened chat for further comments/discussion: http://chat.stackexchange.com/rooms/13789/how-does-the-creative-process-of-biological-evolution-work

@JackAidley I'm not sure that it is and I'm very sure that it shouldn't be. There are conflicting views, see Creationist "canard" refutation type questions? and Are questions about creationism or intelligent design on-topic here? and Just how (un)welcome is creationism here?. Please weigh in on one of these meta posts, I don't think there's true consensus yet. I think we should welcome such questions (as long as they are Good Questions®) and just shoot the

@Jack Aidley "Creationism is off-topic on Biology SE" Your comment is very ignorant and troubling. It's ignorant because the question was ABOUT Evolution, not about Creationism. And your comment is troubling because it comes off as you treating Evolution as a religion, such that you get your defenses up if anyone questions or criticizes your religion of Evolution.

Adam Wong, reading your comments up there, you need to calm down. You're a little too aggressive and out of pocket over a biology question.

@TERDON "if not of the OP, then of the next poor misguided soul who has fallen under the influence of pseudoscience." Silly and unnecessary. Even more silly since I am an Evolutionist. This video is making me question that position: https://www.youtube.com/watch?v=Wf32BXMSN7A

@LotusBiology You may want to give details of the specific times in that video that are relevant. Its an hour long and has a lot of propaganda in it. It also has serious problems with the things it claims to accept. For example saying that "small mutations between generations is called breading and simply remixes existing genes" at 16:00. This is obviously wrong, twice, and brings into question how much research was done on this video. There are creationist arguments which are well reasoned (although they are rare), this is not one of them.

@LotusBiology Whatever your own positions are, the arguments you are presenting in this answer are based on several assumptions that are quite frankly wrong. Whether you believe them or not is another matter but they are classic examples of the type of question that arises when people have been influenced by the kind of pseudoscience of which the video you linked is an example. I'm not about to watch an hour of that drivel, but for example, evolution does not attempt to give an answer to how life originated, only to what happens after it has arisen.

@LotusBiology: When you rock up repeating a bunch of creationist misinformation using creationist language I'm going to assume you're a creationist. Trotting out "religion of evolution" in your response doesn't make me think this is any less likely.

@LotusBiology I recommend that you take some time and have a look at Understanding Evolution by UC Berkeley. It is fast and very introductory and you will learn a lot faster

Your basic problem is indeed a fundamental misunderstanding of how DNA and by extension its evolution works. First of all, there is no such thing as "correct" or "error", there are only changes, some of them are better for the individual and some are worse. You also have a basic misunderstanding of the concept of information. An error does not decrease the amount of information, it just alters that information. For example, consider this sentence:

The book is read

Say I make a simple error when I transcribe it:

The book is red

The two statements contain the same amount of information. Nothing has been lost, only changed. But that change created new information. Now what if I try a different change:

The book is rled

Now, this one is nonsensical, indeed, but how does that translate into DNA?
The computer analogy is a bad one. Programming languages have a very specific set of rules and anything outside those rules results in an error. For example, while this is a perfectly valid statement in many scripting languages:
print "Hello World"

This one is not:
priint "Hello World"

That, however, is not the way that DNA works. DNA is read in words of three characters, the codons. Every single possible
combination of those characters actually has a meaning. Therefore, a mutation like that above which would decrease the information content of the sentence (here, the gene) is not possible. Let's quantify. The DNA sequence consists of a long series of chemicals, commonly known as A, C, T and G. Since these are read in "words" of three "letters", this means you have:
$$4^{3} = 64$$
64 possible combinations. Of these 64, 61 are words with a specific meaning and 3, the STOP codons, are punctuation marks, full stops if you will. In other words, all possible combinations of letters have meaning in DNA.
Because all possible 3-letter combinations have meaning, no change will affect the information content of the "sentence". All it can do is change it. Now, changing the information can indeed result in "sentences" that make no sense. In the DNA world, this most often results in what are known as deleterious mutations. These happen all the time, but the result is usually a dead individual. Those with such mutations are not even born (speaking of mammals).
However, other mutations, such as the change from read to red that I mentioned before, can give rise to a change of meaning, this change, if it turns out that it makes the individual carrying it more likely to reproduce, will spread across the population and will be selected for. That is how new traits can arise.
In closing, another point that you have misunderstood is that evolution is not a path from the least to the most complex. In many ways it is the inverse. In fact, by any measure that counts, bacteria are far more "evolved" than humans for the very simple reason that the only way you can measure evolution is in terms of numbers of generations. Think of evolution as happening every time a species reproduces, this means that bacteria have had orders of magnitude more time to evolve than mammals have. Still, this is a useless comparison which is why nobody compares species by how "evolved" they are. For a discussion on that, have a look here.

The computer analogy might work better if you look at machine code. Every combination of zeros and ones means something. Change one bit, and maybe a bit of data changes, maybe something gets stored in a different register, or maybe a different instruction gets called. It might end up doing that makes no sense, it might throw an error, or, just maybe, it does something that means meaningful. Still not a perfect analogy by a long shot though, and it's certainly not how genetic programming is generally implemented.

Nice answer. I would like to add that the last remark "Say I'm a cephalopod..." contains two further erroneous assumptions. First, it seems assume that individuals evolve - only lineages/populations evolve. Second, it is implying "guided" evolution (I have this problem; with what instructions can that be solved?), ignoring that evolution is a trial and error process.

@TERDON "First of all, there is no such thing as "correct" or "error"," That's interesting you say this, cause MCV said below that Mutation introduces random errors. So  you say there is no such thing as error, and MCV is saying that mutations are errors, or at least introduces random errors.

@LotusBiology so? We are two different people giving different answers, what's your point? Anyway, while there are errors at the cellular level, where the copied DNA is not identical to the template, there are no "errors" in the evolutionary level. The term carries a certain implication and it was that implication I wanted to avoid. As far as evolution is concerned, there are no errors, only changes.

It is worth mentioning duplications are fairly common mutations, which can add quite a bit of code.

Your question, I'm afraid, betrays a deep misunderstanding of evolution.

Genetic mutation is just errors in replication. So it creates nothing. It simply degrades.

This is patently false. The vast majority of mutations are "errors", in that they produce a less fit organism. But once in a while, a mutation will confer an advantage, rather than an disadvantage. This, I suppose, is where "new information" comes from, though I would not use those terms. Your metaphor with software is not very accurate. If you want to "evolve" a piece of software through evolution, you do not insert new functionality into the source code. Instead, you would make a number of copies of the source code, each with a small, random alteration. Then you make the software available to all. The version that is most highly used on the market is then taken and the process is repeated. But good software is not developed in this way, for reasons that I hope are obvious.
I would highly recommend reading "The Selfish Gene" or "The Extended Phenotype" by Richard Dawkins.

The Blind Watchmaker would be a good book to read, probably better than The Selfish Gene.  In any case, skip The Extended Phenotype until you are well acquainted with biology and evolution.

"a mutation will confer an advantage, rather than an disadvantage." Sure. But it will only confer an advantage in a horizontal way. In other words, it's just a variation on what was already there, not a new trait or morphology that will advance us from microbes to man. Which is what I was looking for as far as explanation. Also, what is the physical process that reads, understands and implements these changes and additions of new abilities? What is evolution's central processing unit?

This is no such thing as a "horizontal" advantage. Every mutation is a subtle tweak which may or may not have benefits. The evolutionary process is a steady procession of such small changes. There is no single process which can be said to comprehend evolutionary changes, other than the ordinary processing of DNA within the cell. And evolution certainly has no CPU. Evolution is a distributed, emergent phenomenon. In no way is the process analogous to a computer.
I highly suggest you step back, do some real research and reevaluate your premises.

Consider also The Magic of Reality. It is an introduction to science itself. http://www.amazon.com/The-Magic-Reality-Whats-Really/dp/1451675046

@AdamWong Let me explain what horizontal means there. It's known as horizontal evolution, where you have evolution that happens with breeding. To get from microbes to man, we need vertical evolution. Where we advance up in complexity and changes in kinds of species, rather than variation within kinds.

"In no way is the process analogous to a computer". Well, I don't know how else to explain what I'm looking for. When you build something, it works like a computer. You have an input, processing, then output. To get our vertical evolution, you need an input of new instructions, physical mechanisms to understand the instruction and PHYSICALLY implement it, and output the new ability or morphology. How is that done in evolution? Where does the new information come from, and what in nature physically implements this new information?

@ADAMWONG Let me give you another example besides the computer. To build something you need an Input/Output system. Take ants. When they want to build an ant mound for the queen. They already have this knowledge of how to build it, its innate. They then set out physically implementing this knowledge by gathering dirt and transporting it to the mound site. Eventually the mound is build which is the finished output. How does Evolution do that with organisms? New information, what reads it, and tells the genes 10 spikes, 1 inch apart, 5 inches up, and physically implements this morphology?

To answer your first question, your notion of horizontal vs vertical evolution is unfounded. There is no such thing- mutations are small, though their effects may be outstanding. But very large changes, (ie microbes to men) are merely the accumulation of smaller changes.

To answer your second question, I suppose the new information could said to be in the form of mutations and I suppose evolution can be said to implement that information in DNA. But that is projecting agency into a system which has none, so I would not use those terms.

To answer your 3rd comment, the mapping of genotypes (information) to phenotypes (characteristics) is complicated. Genes are not instructions like "Make the flamingo this precise shade of pink." Genes are instructions for creating proteins which eventually define the characteristics of the organism. (This explanation of gene expression is greatly simplified) In the same way, ants do not "know" how to build ant hills. They are parts within a larger machine (the ant colony) from which complicated behavior (ant hill building) emerge.
Read this: emergence

@LotusBiology: I almost wrote the same as adamwong246 just now. But one very accessible area (and I think quite amazing/beautiful) to help understand your question is introductions to Hox genes: see http://en.wikipedia.org/wiki/Hox_gene

"Genes are not instructions like "Make the flamingo this precise shade of pink." What does do that then?

@LotusBiology The shade of pink or the ant hill is emergent behaviour; simple rules leading to a complex outcome. Much like evolution itself

It's seems to me you forget something pretty important about evolution : it has nothing to do with improvement. All living organisms have the exact same time of evolution as they all derive from a common ancestor. They simply evolved through different paths, that's what explain the biodiversity we can observe today and no organism is better than others, not even human.
New functions are not created just like that, because a species need it. To take your cephalopod's example : if there's pressure from predators, they won't simply grow spikes in order to protect themselves. However, if mutations (one or many) appear in the DNA sequence that make spikes instead of, say, skin, then this particular cephalopod will have better chances of surviving than others and so, better chances to reproduce and pass his new genes.
Mutations do not necessarily imply degradation -just as the los of one function is not necessarily a degradation. Every organs appeared thanks to mutations and / or duplications. For example, the humans' ability to see colors is due to 3 types of pigments (blue, red, green) named opsine S (blue), opsine M (green), opsine L (red). You add rhodopsine which is sensible to light to see clearly. If you study a mouse's eye, you'll only find 2 opsines + rhodophsine. Scientists have been able to recreate evolution's story : you start with an ancestral gene for opsine. The gene is duplicated and the copy is translocated on another chromosome. You now have 2 copies of the gene on 2 different chromosomes. They both mutate as mutations occur all of the time. You end up with 2 new genes. Then, duplication will happen again (no particular reason). You now have 4 genes, identical two by two. Three genes stay where they are, one of them is translocated on another chromosome and they'll all mutate. You finally get 4 genes on 3 different chromosomes (opsine M, L, S and rhodopsine). New genes and new ability appeared thanks to mutation, duplication and translocation. It just took millions of years of evolution and probably an impressive amount of tests.
As Shigeta wrote, everything potentially exists. Some of the possibilities have been discovered, some have not. Evolution applies on hundreds millions of years and billions of living organisms and it process accidents after accidents. If what appears is selected, it stays, if not, it disappears.

"and no organism is better thant others, not even human." Are you seriously trying to tell me that a human is no better than a virus? Are you serious? You are seriously trying to tell me there's no advance in complexity or ability between a bacteria and a lion?

By "better", evolutionist mean "well suited to their environment." Many very simple organisms can be very successful within a specific domain. For instance, the eyeless fish that live in completely dark caves. In this instance, eyes are a waste of the creatures resources. Thus, over time they adapt to their environment and lose their eyes, though most people would say that fish with eyes are "better." Crocodiles and sharks are another example of an organism so well-adapted, they have hardly changed at all in the past few million years.

She was still wrong. Clearly some organisms are better than others, even under that undrstanding of better. Which is why some organisms survive, and others go extinct. Because some are better than others. I.E. MORE FIT.

I'm not. Check history : most extinctions occured due to big climate changes or geological catastrophes and very important selection pressures. A simple example -the one with "dinosaurs" and mammals : the second ones survived not because they were better but because environmental pressures were way not as important as it was for dinosaurs. You really don't seem to get that evolution does not imply any notion of superiority. Being more complex does not mean being better in a superior way. It means being different.

@LotusBiology while it is true that some organisms outcompete their peers, the word better is a moral construct and has no bearing here. More efficient is the best you can say.

"Being more complex does not mean being better in a superior way"  Oh, absolutely it does. That way you are higher on the food chain. The superiority in evolution is at the very least, the one that survives. Survival of the fittest. So clearly, complex animals that are high on the food chain, like SHARKS, are much superior in evolutionary terms, than say the plankton or fish they feed off of. Humans are WAY MORE superior than bison or cows.

I still havent gotten my questions answered. Where does the new information come from since natural selection and mutations are not creative, and what are the physical mechanisms that implement these new blueprints/information?

We cannot answer your question because it is not well-formed. The questions you have asked do not make sense in light of what is known about evolution. You might as well be asking "What is the square root of a purple?"

@LotusBiology doesn't your food chain analogy suggest that viruses/bacteria are "better" than humans?

Whilst being higher on the food chain may make an organism "superior" in our eyes, evolution doesn't care about that. In fact, top predators are often more vulnerable to extinction (look at large predatory dinosaurs, or indeed modern examples like big cats), as their survival depends on what happens lower down in the food chain. Sabre-toothed cats may seem superior to algae, but algae is still here, and sabre-toothed cats are not.

@LotusBiology "Better because higher on the food chain" is a value judgement that you attach to a certain property. Humans like compexity, being high on the food chain, and generally feeling important, but from an evolutionary perspective, the only thing that matters is survival for you and your offspring. Bacteria are evolutionary unbelievably successful. They live everywhere (deep underground, in your gut), and there's far more of them than of more complex organisms. Fortunately for us, there's also a niche for more complex organisms.

"I still havent gotten my questions answered. Where does the new information come from since natural selection and mutations are not creative" : we answered that part of your question at least.

@LotusBiology I think a key issue here is that you are assuming that evolution has some "plan", or is going from less complex to more complex. It isn't, it's going in random directions; more complex (as in more DNA, not necessarily better DNA), less complex, dead, better at surving, worse at surving. Natural selection then cuts off all the directions that make an animal "less fit" - by killing it. You are saying "more information" but what I think you mean is "more useful-information", more information is ridiculusly easy; just tack some noise on the end

"doesn't your food chain analogy suggest that viruses/bacteria are "better" than humans" No. Because viruss and bacteria are not higher on the food chain than us. They also generally do not eat us, but rather, in the cause of viruses, use our machinery to help their replication, and in the case of bacteria, make us sick, but many times, it's a symbiotic relationship. Also, unlike plankton and fish, we can fight back and kill bacteria and viruses in return.

@Richard Tingle "it's going in random directions;" Yeah, and that's the problem. To think that a random process can create so much complexity, variation and purposeful looking design, make me doubt Evolution. Take a look at this video. This is where i got the crux of this question from: https://www.youtube.com/watch?v=Wf32BXMSN7A

@LotusBiology You accept that random mutation can create small amounts of new information and that natural selection can remove those changes that are in some sense "bad"? Having accepted that it is simply a matter of time, huge huge amounts of time. Remember if we represented the entirity of human civilisation (12,000 years) on a 24 hour clock reprensing the entire history of life (3.5 billion years) then our civilisation has existed for 1/5th of a second. Huge amounts of time are involved here

Where does the information come from?
From the environment, and the previous history of interactions in that environment. The process of evolution can be viewed as an undirected search for "good" solutions (i.e. those that better support replication) to problems presented by the environment.
There is a large amount of information (in the information-theory sense) in a differentiated environment.
Note that information content of the whole system is preserved when this happens. Partly the misunderstanding of "information is being created" is not seeing what a huge resource of information (in the same sense used with information theory that says it may not be created or destroyed) is available from the environment. It is many many orders of magnitude greater than anything stored in genetic codes.

+1 Short and to the point.  The other answers does a decent job of explaining evolution, but this answers OP's question.

So what in the environment, tells the organism to make a new innovation like compound eyes, or superposition eyes? And again, what is Evolution's central processing unit. I.E. what physically deploys these new adaptations and abilities into the organism or population as a whole? Also, if you have the time, can you answer this video if you have a Youtube account. This is where I got these objections: https://www.youtube.com/watch?v=Wf32BXMSN7A

@LotusBiology: The pattern of light distribution is the information that "tells" the organism to create eyes (or more accurately rewards organisms that better sense light). The feasible and likely process from no eyes to complex eyes is well-studied, and indications are that this process has happened multiple times in the history of creatures. As for "central processing unit" there is no need for such a thing. Genes and proteins do not need a "CPU"

@NEIL SLATER Cool. If you have the time and a Youtube account, can you answer this video by Mark Champneys. This is where I got the crux of these questions: https://www.youtube.com/watch?v=Wf32BXMSN7A

@LotusBiology: In my opinion, the "scientific objections" raised in the video are actually a thin veil over desire for the end result (evolution being "wrong"). That is because it protects a cherished world view, and not due to any rigour in the arguments raised. Which means debating with someone who has published a video and has a lot of face to lose (and a lot of like-minded followers) is a waste of time. That's probably how you feel logging into biology.stackexchange and trying to challenge scientific consensus. But I have no desire to reciprocate.

It is understood that Evolution basically involves three elements. Natural selection, genetic mutation, and time. The problem for Evolution, is that none of those three elements are creative.

They absolutely are creative in that they create something new. Mutation introduces random errors, some of which may never have existed before in that combination of genes. Now usually errors are bad, and natural selection prunes the result, but every once in a while, you accidentally stumble upon something new that provides an advantage, and now natural selection means it gets kept and passed on to the next generation.
So on their own, it might seem that mutation doesn't add information and natural selection doesn't create anything new, but together, natural selection adds information to the randomness of mutation: it selects what works and what doesn't.
Imagine you're rolling a die (warning! simplified analogies don't accurately reflect the complexities of evolution). What are the chances of you rolling 10 sixes in a row? Vanishingly small of course. But that's not what evolution does. What it does is in every phase (generation), it rolls 10 dice, and only keeps the sixes. What is the chance of getting a six in every phase now? Quite a lot bigger. All through randomness and selection.
(In fact, have you ever played Yahtzee? How can you get the right patterns there if you're just rolling dice and selecting some of them?)
Take your analogy with the sentence "Make an eye that is compound". A mutation might turn that into "Make an eyye that is compound" which is useless. But another mutation might turn it into "Bake an eye that is compound" which is grammatically correct though nonsensical. Yet another mutation might create "Make an eyr that is compound", and if that one happens to survive a generation, you might get "Make an ear that is compound".
Thing is, there are a lot of mutations. Really a lot. Most of them have no measurable effect. Of the remainder, the vast majority breaks something, which means they automatically get weeded out by natural selection. A tiny fraction accidentally adds something useful. If you look at any single mutation, it's impossible to imagine how that could ever result in anything useful, but there's a lot of them. Every generation again, over thousands and millions of years, and eventually, those very few positive mutations start to add up.
It's impossible to fully grasp how evolution can introduce totally new species without first grasping the enormous time scale on which evolution works. And we humans are limited beings and bad at truly understanding such enormous scales. But it clearly works. We can see the results all around us. We can run simulations on computers that show that the process really does work. I consider it one of God's greatest miracles (warning! personal opinion might not reflect those of others).

I think this is a little like writing a book.  The most common advice is for aspiring writers to write every day and write a decent amount.
Evolution creates by testing everything against its fitness - its ability to survive and reproduce.  If something is advantageous, it stays in the corpus of genes and genetic solutions to problems.  If something is not working well or even not as well, it may be lost and forgotten - dropped out of the gene pool.
So just as a writer may throw out 90% of their writing to get to their published novel, 90+% of biological experiments are thrown out and don't have long lasting repercussions in the biosphere.  its probably more like 99.9999999% really.
The creation of information you are talking about are all inherent in the physical universe.  Just as every computer program is potentially existant in the laws of logic and mathematics, all the potential mechanical and informational and configurational advantages of living things are embedded in the physical laws in which they operate.  It is not an event of creation, but an event of discovery when a new biological function appears.

evolution means unrolling http://www.etymonline.com/index.php?term=evolution
Now if you imagine a tree with one root then the stem rolls out, branches roll out twigs and leaves roll out etc. Same with the roots on the other and to balance it out.
And that's it. Evolution does not happen in a vacuum. It happens in and together with an environment. If the environment changes and you have unrolled something that helps you cope with that change then you can continue to procreate so that your offspring also have a chance to test any eventual new unrollings in the constantly changing environment. If they die then the branch or twig that was unrolled is cut off and might unroll again later and be cut off again until maybe, just maybe some sunlight will reach it and it can survive. Until night falls again.

Another important point about evolution is, that rhere are many, many small steps - not huge leaps.
E.g. going from a bacteria to something with four legs in one step will not happen - that is simply too much change at once, and it's probabillity is close to zero.
But small steps happen all the time - if we take your example with a cephalopod: Imagine that there are some individual cephalopods who have a harder skin. Without predatory pressure this is next to useless: the cephalopod are investing energy on something which brings no benefit. So they are less fit and will probably have fewer offspring than the original ones. Now a predator kill many soft-skinned cephalopods but sometimes fails to eat their harder skinned brethren. The hard-skin variant will producre more offspring and theier genes spread. Then the next round happens: cephalopods with the hard skin might have another mutation which hardens the shell even more - or the predators might get better teeth.
But be aware that this most not happen: maybe no variant with harder skin exists or the genetic error is not present at the time and the whole race simply dies - this happens a lot. Look at dinosaurs or the polar bear (is under pressure because the polar ice melts) etc.
Some fun fact: since each step is random and has a low probabillity, you willl never get the same reult twice. If you start the evoluation again, the world would look completely different because the steps would look different.

From bacteria to something with 4 legs probably close to zero? Just going from bacteria to single celled eukariotes took a billion years. That may have been the hardest and most fundamental step in our evolution. The chance of that happening in a single generation is as zero as quantum mechanics allows.

@mcv That should qualify as close to zero ;)
Acutally, the probabillity is even lower, because you need them twice (male and female), otherwise it will get lost at once.

@ChristianSauer Male and female is somewhat of a specialisation of sexual reproduction, things can be simultaneously male and female or it can be N/A. Even bacteria have sexual reproduction without the concept of gender. In the presence of individuals who are mixedgender becoming purely male isn't a disadvantage

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


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gene expression fold change threshold limit
When interpreting qRT-PCR results, which results are acceptable as fold changes, which are acceptable for housekeeping genes? e.j. a values of 0.8 raw fold changes for a "housekeeping" gene is acceptable as such? and conversely which is the threshold to say that there was "fold change"?

What do you mean by "raw fold"? Values not normalized to the normalization gene?

yes, values not normalised to any housekeeping

Why not? This will make comparisions hard to impossible.

please clarify, what are you answering to

Why didn't you normalize your genes?

because my housekeeping gene got a 20% fold reduction under the experimental treatment

What is the difference in your gene of interest between treated and untreated? Fluctuations in housekeeping genes can (and do) happen and are not necessarily due to the experiment. Thats why I usually test two stable genes if possible.

as i already wrote i got a 20% reduction = 0.8 fold change treatment/control

Ahh, I thought this was only for the housekeeping gene. If both are reduced by the same amount, this will be difficult.

sorry i misread before. well i had 3 genes of interest and the results varied: 2 got upregulation of %20, other %100. the housekeeping nevertheless was downregulated at %20 under treatment

So now you have two possibilities to choose from: First it is very possible that your housekeeping gene varies a bit because of slightly different experimental conditions (cells a bit more dense, slightly more metabolism and so on). In this case you can correct for this and your values can be used. Second it can be, that your treatment also affected the housekeeping gene. If this happens you need to choose another housekeeping gene for normalization which is not affected. If the first is true (and I tend to think so) this correction can be done in a software like REST2009.

As I mentioned in your previous post. If your reference gene undergoes changes then replace it with another reference and if even that doesn't work out then use a spike in. You must normalize. Interpreting the raw values can be erroneous- there could be a loading bias. Don't think much- repeating RNA isolation and/or qPCR is not a very hard job. And as Chris said, use two references if you can.
BTW, if you are fine with it then can you tell what is the gene that you are studying and what is the treatment
w.r.t what is a significant fold change.
There is no hard and fast rule to determine what is an acceptable fold change. In some robust systems a minor perturbation in the gene expression will not translate to any great biological outcome whereas there can be sensitive systems in which minor changes can affect the cell state. These things depend on how the gene is integrated in the regulatory network.


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What's the fastest legal way for the nutrients in a dead body to re-enter the ecosystem?
Apologies for weirdness.
Of the various legal methods of disposing of a human corpse, which one ensures the nutrients which compose the body get back into the wider ecosystem the fastest?
Unless I've overlooked something (which is likely) the answer would seem to boil down to:

Burial, in which case soil microbes have relatively free access to the body but will initially restrict their nutrients to the sub-soil ecosystem.
Cremation, in which case most of the nutrients are converted into heat and light energy by the furnace, although this energy, and the remaining nutrients, are then made available to the wider environment much more rapidly.

In terms of cremation: Which remaining nutrients?

No idea. I presumed that not everything in the human body was easily oxidized?

Well, we are talking about 60-90 min (if I remember correctly) at temperatures of 900°C. There nothing carbon based will survive. The remains are basically the mineral parts of the body.

Perhaps you can remove the word "legal" from the question. I think there is no law on how to deal with a corpse. Even if there is one it will not be universal.

The Parsis and other Zoroastrians dispose of their dead in a so-called Tower of Silence, where the body is left on a raised platform to be eaten by scavengers, particularly birds such as vultures.
This is possibly (probably?) the quickest way for nutrients to re-enter the wider ecosystem, as scavengers usually work a whole lot quicker than microbes.
Tibetan tradition also contains a ritual known as the Sky Burial, which achieves the same sort of thing. The Tibetan version may be even quicker, as once the scavengers have stripped the body, the bones are ground into a paste along with flour and yak's milk/butter to be fed to a second round of scavenging birds.

Well, with cremation comes also a lot of harmful gasses entering the atmosphere as well, and from your question, I'm assuming you're interested in eco-friendly alternatives.
I've heard of organic embalming fluids, so it might be interesting to you to look into that. Also a lot of steel and cement go into a traditional burial; if you were to be buried in a plain pine box with no fancy coatings or finishings, that would certainly speed up decomposition. If you look at traditional Jewish burial customs, you may find a bit of what you're looking for.


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DNA of the human body?
If our DNA determines certain patterns within the human body such as hair color and eye color, if scientists were able to "turn off" such as the gene for eye color after the pattern was established, what would happen?

The classic analogy here is that of a blueprint. For example this one I found here which is kind of relevant:

If you use the blueprint above to make yourself a little sister and later change the blueprint, the sister you built will not be affected.
That is only part of the story though, the analogy can only go so far. DNA is constantly "read", what this means is that genes are transcribed to RNA which in turn is translated into proteins. To use a horrible simplification, genes are the blueprints for proteins. Therefore, if you change the gene, and the cell then reads from it to create a protein, it will indeed create a different protein than what the original gene would have coded for.
The point I am trying to make is that depending on which genes are changed, you can either have no effect or a huge one. Some genes are only read once when the cells are reproducing, others are read constantly as the proteins they code for are used up and then produced anew. So, if the gene you change is one that will be read again during the cell's lifetime, then you will see a change. A classic example of this is cancer. If, on the other hand, it is a gene that will not be read again, then the changes will not have any effect.

That was a very good answer and easy to understand.  You transcribed it to laymen's terms basically. Thanks!

@Jody I kind of figured that's what you were after :). You're very welcome.

I'll just extend terdon's answer into more concrete terms.
An example of a gene that is constantly read would probably be the one that determines hair colour. If you were able wave a wand over the head of someone with blonde hair, replacing all their DNA with a different version of the gene, say, the one for brown hair, then chances are that as their hair grows, you would see that it was now brown at the roots! Something like this:

Note that this picture is evidence of hair dye, not my magic wand. ;)
Every time the cells try to produce a pigment, they read that particular gene. But now, they find the "brown version", and produce a brown pigment instead of a blonde one.
On the other hand, if you replace the gene affecting the length of a person's fingers, they may not just sprout a couple of extra centimetres over the next few months. Those genes may only be read at a particular time of life, such as during puberty or as a child, so they have to be in place at that moment to have much of an effect.
By the way, that idea of replacing all the copies of your DNA with a different version is roughly called "gene therapy", and we're still really in the investigation stage of research (to my knowledge).
Hopefully that helps to solidify your understanding. :)
(And just to add yet another note for this, most traits in humans, like finger length and hair colour, are not the result of just one single gene. They tend to result from a number of factors, but the general idea still applies.)

+1 fingers are a very good example. By the way, for future reference, you can choose between the full size image, a medium one or a small one by adding m and s respectively before the .png in the URL of the image uploaded to imgur.


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If a gene altered causes cancer and creates a protein for cancer can the new protein be isolated in some way?
In the above title question, can the protein thats altered not be isolated (to separate out from other proteins) somehow?  Is there nothing that can bind to the specific cancer proteins that will not bind to other proteins?

I'm afraid your question is not very clear. What do you mean by isolated? There are many lab techniques scientists use for studying oncogenic ("cancer-causing") proteins, and individual proteins can be "isolated" or separated out from the cellular milieu quite easily by a variety of methods, including separation based on size, pH, hydrophobicity, affinity for other molecules, mobility in an electric field, etc. One can also use specific antibodies or other protein binding partners to bind proteins of interest. Please [edit] your question and clarify what exactly you're asking about.

Does this clarify it more?  I'm no biologist, I ask questions out of curiosity.

So are you asking if there is some way of inactivating the cancer proteins in the cell?

Your current edit just added several more questions. Please try to focus on one question at a time.

Still to much or good?

I would take the second paragraph and ask that as a separate question, as there is some interesting work being done now on the chemical signatures of various tumors, and specifically trying to catch them as early as possible via blood tests, and not invasive or semi-invasive procedures like colonoscopies, mammograms, biopsies, etc.

to matt - similar line of thought yes

From how I read your question, you're wondering if there is some technology to somehow isolate oncogenic proteins inside the cell so they don't do harm, is that correct?
The answer is somewhat complicated, as it depends on the protein. First, though, you need to understand that cancer is a very complex disease, and cancer is not caused by a single mutation alone. The "multiple-hit" or Knudson hypothesis essentially states that a cell progresses from a normal cell to a cancerous one, accumulating multiple mutations along the way. In pretty much all cases, at least two specific mutations are needed - the constitutive activation of a proto-oncogene, a group of proteins responsible for cell growth and proliferation, and the deletion or inactivation of one or more tumor suppressor genes, which are used to keep growth and proliferation under control. This way, you have a tumor driver (often this is a single protein, like a growth factor receptor) "driving" the oncogenic process, with no "brake" or regulation.
As I said, mutations in tumor suppressor genes generally result in loss-of-function changes, or complete deletion/inactivation of the gene altogether, so "isolating" these proteins in the cell wouldn't do much good. The focus of many tumor therapies is to down-regulate, inhibit, destroy, or otherwise remove the function of the protein that is driving the uncontrolled growth and proliferation of cells, forming tumors and metastases. If we're lucky, the tumor driver is an extracellular domain-containing protein (like a cell-surface receptor) that can be identified and targeted from outside the cell. Once this has occurred, scientists and doctors can use specially-derived monoclonal antibodies to target and kill the cells containing these proteins:

Monoclonal antibodies for cancer. ADEPT, antibody directed enzyme prodrug therapy; ADCC, antibody dependent cell-mediated cytotoxicity; CDC, complement dependent cytotoxicity; MAb, monoclonal antibody; scFv, single-chain variable fragment.
From WikiMedia Commons, released into the public domain.
There are a number of ways the cancer cells can be killed, from delivery of radiation or other cytotoxic compounds, to attracting killer cells from the immune system, to activating the complement system. However, all of these depend on the surface presence of biomarkers for the cancerous cells, so as to avoid non-specific killing or off-target effects.
The reason so much focus is put on killing the cancerous cells instead of trying to isolate the "bad guys" inside the cells is that by the time the cell has become cancerous, it already has accumulated so many mutations that a) the cell isn't really worth saving, and b) it would take an extraordinary amount of effort to corral all the mutated proteins together, and leave whatever unaffected or "wild-type" proteins were left to do their jobs.
You may recall that each gene we have (except for some on the X and Y chromosomes) is present in duplicate, one copy from our mother and one from our father. The initial mutations that begin the progression to the fully cancerous state may at first only affect one of those two copies of the gene, leaving a working version around for a while. However, as oncogenesis progresses, and more and more regulatory proteins are inactivated, chromosomal damage grows, and frequently the surviving "normal" copy is either mutated itself or completely destroyed. Once this occurs, even if you could isolate the misbehaving proteins, there would be no good proteins left to do the jobs of the cell. Therefore, killing is really the only option.
I hope I've covered what you were interested in. Please let me know if you don't understand any of it, or you can always ask a new question.

Another good answer today for little ol' dumboy. Thanks:)


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Quantitative Traits Genetics

Can someone please help with this question? I'm not so sure whether part A should be 11 inches or something else. Also, is part B correct

Question a

The only possible genotype that brings a phenotype of 12 inches is: $AABBCC$. Similarly the only possible genotype that bring a phenotype of 6 inches is: $aabbcc$. In consequence the offsprings can only be: $AaBbCc$ which measure $2+1+2+1+2+1 = 9$ inches.

Question b

Now the question is: if we breed two $AaBbCc$ how many offsprings measure 11 inches? Because there are three bi-allelic genotypes you have $2^3=8$ possible gametes and therefore you have to draw a 8x8 punnett square. Doing so, just count the proportion of offsprings that measure 11 inches. You can reason slightly more logically and get a faster answer. To measure 11 inches you need to have only capital letters in your genome except at one position. In consequence, if your father gives the gamete $ABC$, you mother should give the gamete $ABc$, $AbC$ or $aBC$. You can inverse the role of the father and the mother and it works as well. Therefore, you have 6 possible combinations that give rise to an offspring that measure 11 inches. Because there are $8 \cdot 8 = 64$ possible combinations, the proportion of offspring that are 11 inch-long is $\frac{6}{64} = \frac{3}{32} = 0.09375 ≈ 0.1$. About 10% of your F2 individuals are 11 inch long.


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Do cancer cells give off specific chemical signatures?
Do cancer cells give off specific chemical signatures?   Are these signatures different from normal cells?

The answer is it depends.  First, take a step back from the definitions of "cancer" versus "normal" cell and recognize that cells and tissues can undergo a variety of changes in their growth.  A solid cancer/tumor (as its usually defined) is something that grows and invades the surrounding tissue.   A spectrum of possible cell growth can be :
normal -> hypertrophy -> hyperplasia or dysplasia -> hamartoma -> benign tumor -> carcinoma in situ -> invasive cancer -> metastais
(this list is NOT suggesting these are the actual steps to cancer, but instead they are useful for the next paragraph):
The point of this list is that from a human perspective we can see something odd happening when we see a tumor, but the view from inside a cancer cell is basically "things are fine, I'm just doing my cell thing".
But, that said...when a tumor grows and cancer cells invade tissues a few things happen which can give rise to differences between cancer cells and normal tissues and which can be detected.
First, it needs energy, and cancer cells often switch to aerobic glycolysis (a phenomenon called the Warburg effect). As the link shows, a special form of labelled glucose can be used to detect this in the body.
Secondly, a tumor invades the surrounding tissue and generates new blood vessels, and so enzymes that break down extracellular matrix  are released.
Some tumors over-express and secrete markers (usually proteins) that can be detected.  The prostate specific antigen (PSA) and carcinoembryonic antigen are two examples.
Other things secreted by certain tumors may include volatiles that can be detected by dogs.
The challenge with any 'signature' detection is the sensitivity and specificity  which often limits the use of tests that show some early promise.
Cancer cells DO have specific changes to their DNA that can be used as very specific signatures for detection.  Tumor DNA is shed into the blood and possibly the urine.
Finally, tumor biology overlaps with many aspects of normal biology, including wound healing and pregnancy and this continues to make it challenging to identify tumor specific markers that have high sensitivity and specificity.


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Understanding DNA supercoiling
While trying to understand DNA supercoiling, I came across these lines in the book Genetics by Ursula Goodenough :

All natural DNA is superhelical. The axis of the duplex itself follows
  a helical path in space. For virtually all DNA, the sense of the
  superhelical turns is opposite to that of duplex, thereofer, they are
  negative supertwists.

I am unable to understand these lines. Specially, the second one.

It means that the direction in which the normal double-strand is wound up (which is also helical) and the direction on which the double helix itself is twited to reach the supercoils are opposite to each other. Have a look at this image from the Wikipedia, I think it makes this clearer:

The first show a DNA ring with the normal helix-coiling. The second show the supercoiling of the coiled ring molecule. Imagine a rubber band. This you can twist around its band axis to get the coiling and around its vertical axis to get the supercoiling.
For linear DNA molecules, this looks like this (taken from here):

The rubber band example was awesome !


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How does HBeAg change to Anti-HBe in acute hepatitis
I am thinking this figure

which can also be drawn like this

How does HBeAg change to Anti-HBe?
There are some triggers that stimulate Anti-HBe production after HBeAg level is done.
I think they can Anti-HBc.
There must be other mechanisms too.

Can you please introduce your abbreviations? This would be a good style so people can understand the figures better.

Alan answered the question. Just standard antigens and antibodies for HBV.

I'm not sure that I have understood the question but ...
HbeAg is a secreted variant of HbcAg (the core antigen of HBV). Unlike HbcAg, HbeAg is found in the blood. I believe that it is produced as a result of a splice variant of the corresponding RNA.
The phenomenon described in these Figures is an example of seroconversion. Before seroconversion the antigen is detectable in the blood but there is no antibody directed against it; after seroconversion there is antibody but no antigen.

Thank you for your clear answer! You understood what I mean. I missed the term seroconversion. I think there are actually two windows periods and two  seroconversions in the figure. First, for HBe and then for HBs. I would like to know how these two seroconversion stages and/or windows stages differ. It would be nice to use some analogous words like "isovolumetric contraction" and "isovolumetric relaxation" just to differentiate some property between the two window periods. I do not know which property that can be.


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Single channel micro arrays
What does single channel microarray mean?
When is it used?
 Thank you for your case in advance.

@PlaysDice - please avoid answering questions in comments - see the meta discussion here for more background. Thanks.

Single channel refers to the system used to detect the labelled probes.  A single channel array, as shown in this slidedeck (slides 6-8) uses one type of molecule for detection.  In the example, (slide 8) the optical label is phycoerythrin.   Contrast that to a double channel array (e.g slide 7) that uses a "green" or "red" molecule used to label probes.  Detecting two different labels requires two channels, one to detect red and one the the green.   The key to using two (or more) labeling molecules is to ensure that your detection system can discriminate between the light spectrum emitted by each of the labels.   Many modern microarray readers have designs that handle multiple labels.
When you see single channel results, they often have colors.  The color is a pseudo color representation of the intensity of the emission of single-color label, which is due to how much probe has bound to the array at that spot.

Adding to this: When using only one color to mark the sample, you can only use one sample (direct comparisions are not possible, since they can not be discriminated). The intensity of the signal here is used to measure the strength of expression, which can also cause some bias.


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Measuring reverse transcription yield?
Is there any measurement I could perform after RT that allows me to check the efficiency that the procedure had? Nanodrop cannot be used as remnants of RNA and poly T primers mask measure, or?

Nanodrop may be fine for the volumes but as you rightly guessed it is not so easy to distinguish DNA from RNA (and primers). Qubit (invitrogen) is a sensitive, dye based quantification assay. You can use that for estimating cDNA yield. The kit contains different dyes for DNA, RNA and protein estimation.

Treat with RNAse and spec at 260.
A spec can definitely be used. The extinction coefficient (Beers Lamberts Law) will not  be calculating measuring  NTPs, just intact dsDNA.


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Why don't we see new diseases more often? Or, ever?
It seems like every disease we ever hear about is something that's been around since ancient times, since thousands of years ago. Of course new diseases were catalogued over the course of the past couple hundred years, but they weren't actually new diseases-- they just hadn't been previously classified/identified.
Given that (in my understanding) viruses and microbial lifeforms can evolve and change considerably more rapidly than higher order organisms, why don't we often/ever hear about completely new diseases that have never been seen before? Diseases that may have only just been born.

You might find this interesting: http://royalsociety.org/events/2006/plagues-parasites/?gclid=CLD5yoOTs70CFedV4godnwUA1A#

Evolution doesn't really work like that, everything is a slightly different version of what we had last year, it's only on the very long term that you can see major change. New flu arrives every year, but we still call it flu because it's only a little different

HIV anyone? It's new in the sense that it only came to infect humans recently.

The terms about we are speaking are relatively long. There are a number of pathogens (mostly viruses) which are relatively new. Among them are SARS and MERS, HIV, Ebola, Marburg, Hendra and so on. These are mostly viruses which spill over from their reservoir hosts into humans. There is an excellent book on that topic, which I can really recommend. It is "Spillover" by David Quammen.

I think the answer is completely given in the comments. One could group these comments to make an answer and add some link to seasonal flu or to new pathogens.

Zoonosis is another term for spillover. BTW @Chris, I loved reading spillover :)

@WYSIWYG I know :-) Another interesting reading: http://stories.weather.com/virushunters

The first thing to note is that nothing is truly new, everything is a slightly different version of what existed previously, it's only on the very long term that you can see major change. Mutations occur continuously and new variants arise often. For example you need a new flu shot every year due to the high mutation rate of the influenza virus but we still call it flu because it's only a little different.
While disease causing organisms evolve at a relatively slow rate new diseases can appear suddenly when the effect on humans suddenly changes; the most obvious example of which is when a disease changes host species. For example the sudden appearance of HIV when Simian immunodeficiency virus (SIV) "jumped species" to infect human, most likely through the consumption and processing of Primate meat. While HIV appears new it is again ancient in the sense that it has caused a similar condition to HIV/AIDS in many African non-human primates for a significant period.

New diseases appear all the time. Some of them have been around for ages but are detected due to improved surveillance, while others appear due to shifts in host. Others are detected because they spread geographically into a region where they are either more conspicuous or just more highly reported/investigated, or because new hosts are introduced into their original range.
For example, in the last few years alone both the snappily-titled arthrogryposis hydranencephaly syndrome (caused by Schmallenberg virus, a previously unknown bunyavirus) and bovine neonatal pancytopenia (aka 'bleeding calf syndrome') have been discovered. Both were first detected in Europe, where veterinary surveillance is among the most intense in the world; Schmallenberg was detected because of syndromic surveillance in use in NL and DE. When bluetongue first emerged in Europe a slight difference in primer sets used in Switzerland detected a novel related virus that was called Toggenberg orbivirus (later classified as a new serotype of bluetongue virus). This may have been circulating in Europe undetected for many years and it's only by chance that it was detectable by the Swiss primer set (although it doesn't appear to cause clinical disease).
Incidentally, bluetongue and two other high-impact livestock diseases originating in sub-Saharan Africa (African swine fever and African horse sickness) appeared at the end of the C19th when European settlers introduced 'improved' breeds of livestock into the region; before that the pathogens were circulating subclinically in the natural hosts (warthogs for ASF virus, zebra for AHS virus and various ruminants for BT virus).

Whatever the perception, the reality is that there are many new diseases which have emerged over the last few decades alone.  There was one study mentioned by NPR in 2008, which found that the rate at which new infectious diseases appear has increased.  This is based on an analysis of 335 diseases that emerged between 1940 and 2004.  During that period the rate increased over time, with a spike in the 80s likely owing to HIV/AIDs spreading untreated and thus making more people susceptible to new pathogens.
I imagine if you followed organisations dedicated to monitoring diseases you'd hear about plenty.  But most of the time this sort of information won't appear in mainstream consciousness unless it's a really big event.  Most new diseases won't be capable of causing a pandemic, so the consequences will be localised and unreported outside of specialist literature.


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Initial population when I count backwards?
My question deals with the number of ancestors it took to produce me:

--> To produce me, it took 2 people (my parents) = ($2^1$) people = 2
--> One generation further included = ($2^1 + 2^2$) people = 6
--> In the past 500 years, my pedigree chart contains 15 generations, so $2^{16}$ people = 65.532 people to produce me (-2 to be completely correct)
--> When I calculate back to 35.000 year ago I get a larger number *)
--> When I calculate to all humans 2.400.000 ago I get a ridiculous large number *)
--> When I include up to all mammal grandfathers and grandmothers 60.000.000 years ago the total number takes pages to scroll *)

*) see: http://ed.je/2L6 for the actual numbers did not want to clutter here.
*) I took 3 generations per 100 years to let the numbers be small as possible.
So, I think I'm making a mistake somewhere. Only I don't know where: to create a child you need 2 parents. And to create a parent you need 2 further parents. But somehow calculating back to "all mammals" just related directly to me would mean $2^{1.800.001}$ mammals walking around 60 millions years ago being my direct predecessor back then.
So, where am I going wrong? Somehow, I can't figure out where my error lies (I've not studied Biology though).
I visualize a pedigree tree (reverse pyramid) starting with me and then logically each parent needs to be born out of 2 other parents just calculating my way up.

Your calculations are the following. Assuming non-overlapping generations, the number of ancestors you have in the last $t$ generation is given by:
$$\sum_{i=1}^t 2^t$$
This sounds correct. But there are some very strong assumptions:

Generations are non-overlapping. A more realistic model would need to consider $t$ as a continuous variable a give a probability of reproducing which depend on the age of the individual.
Never two related individuals mate together. Otherwise, you paternal grandfather might be your maternal grandfather. In reality we are all somehow related, we have a common ancestor (Hey Bro). For example if you consider that your parents are siblings and that their parents are siblings and so forth… then you don't need more than 2 great-great-great-great-grandparents. In order to keep track of such events (inbreeding), you need a stochastic model and you would need to know the population size $N(t)$ as a function of $t$.

Tracking the change of population size through time is part of a very big in biology which is called population biology. For example you will find in this post a model of population growth of two interacting species (prey-predator)

so the amount of non unique nodes in my pedigree chart will be this ridiculous large number. but the unique nodes will be less? (as the one i see in www.geni.com containing 65.532 people in 15 generations?)

@edelwater I didn't fully get your comment. What is (non-)unique node? Given that you checked the answer, I hope it means that you understood and agreed with my point Let me know if it is not the case.

if I draw a pedigree tree (genealogy) then i make a pyramid filling in the names of the grandparent etc... so each node in the tree is a uhm node. At some stage (probably longer than 500 years ago) some nodes will contain the same persons (or even mammels) as other nodes. So they are non unique nodes (and would have to draw a dotted line between the nodes). (while another representation would be a graph family tree where each unique individual occupies only one node).

thanks will dive more in population biology to make a follow-up. Will check population size as factor and other facors. Must have huge impact on the 2^1.800.001 direct forefathers I now have. Probably boils down to "the complete population" at a certain moment back in time.

@edelwater Ok, I understand the meaning of non-unique node. As I said, in order to compare the relative number of unique and non-unique nodes you need to know the population size. For example, if your population size is 2, then you are sure that you paternal grandparents are the same than your maternal grandparents. If the population size is very high, then you paternal grandmother is probably not the same person as your maternal grandfather. And if you want to assume different sexes, you will also need the sex-ratio

An easy way to visualize the mistake in your thought experiment is to consider a bottleneck event, when the ancestral population was very small, maybe just a few individuals. This would mean that the entire current population is descending from just a few individuals. Your thought experiment is assuming that the "pyramid" of your ancentors is expanding all the time, while the bottleneck event will essentially result in the opposite situation with an inversion of the pyramid, such as:
Your assumption:            Bottleneck:

 xx xx xx xx                     x
   xx xx                        x x
    x x                        xx xx
     x                      xx xx xx xx
           (present time)

The reason why the number of ancestors is smaller in the bottleneck event is naturally that the population is inbred (all individuals are related). In contrast, your thought experiment is assuming that all individuals forming the pyramid of your ancestors have completely unrelated ancestry. This is equivalent to assuming that the subpyramids for all ancestors never overlap.
Your assumption is unreasonable since human generations are overlapping, the fecundity distribution of individuals is skewed, inbreeding is common and reproduction between more distantly related individuals will happen by pure chance. We also know that humans have historically gone through several population bottlenecks, see e.g. Hawks et al. (2000) and Lui et al. (2006) for an overview. An realistic model of your ancestry is more likely to be (highly idealized and compacted):
       x
      x x
     xx xx
  xx xx xx xx
  xx xx xx xx
     xx xx
      x x
       x
     (you)

The issue we are discussing here is actually known as pedigree collapse, where you will eventually find overlap between your ancestors, which will mean that the pedigree collapses instead of growing exponentially.
Beside historical bottlenecks, there are also modern examples of extreme human inbreeding. Even if this is not directly related to your thought experiment, you might for instance want to look the pedigree of the Habsburg royal family. Here is the genealogy of Charles II - remember, narrow loops in pedigrees are seldom a good idea:

Here you can for instance see that Charles' father is also the uncle of his own wife. You can also see that only 5 persons enter in the family tree from the outside through marriages, which means that Charles only had 7 completely independent ancestors (ignoring relationships further back, outside of this tree). Going back 3 generations (sort of - hard to count with overlap), it is also apparent that Charles had a total of 8 ancestors instead of the 14 expected under your model. Another modern example of extreme human inbreeding is the Fundamentalist Church of Jesus Christ of Latter-Day Saints, where marriages between close relatives have been common along with high levels of rare birth defects. Both these examples definately show, in an extreme way, that you cannot assume that all your ancestors are unrelated.

Thanks, very interesting esp also the pedigree collapse. ALSO a great example since I'm in 19 steps related to Charles II of Spain :) (then again we are all related) : http://www.geni.com/path/Edward+de+Leau+is+related+to+Carlos+II+el+Hechizado+de+Habsburgo+rey+de+Espa%C3%B1a?from=6000000000569063853&to=6000000000840743803

Glad you found it useful, and cool that you have a Charles II connection  - hopefully with fewer loops in your part of the family tree thought ;)

Another way to demonstrate that the underlying reasoning in the calculation is not correct is to project into the future.
Given the assumptions, the approximately 7 billion people on Earth today could only produce 3.5 billion people (two parents per offspring). Projecting forward, after approximately 32 generations, there would be just one human in the world.
However, we know this is not accurate because a woman can have more than one offspring.

10 years later...

In addition: if you do not take into account uniqueness (of both individual and "2 individuals + unique child as unique) and draw a reverse pyramid starting from yourself it comes closer. But in that reverse pyramid the further you go upwards the more "patterns" you see of identical structures that you could replace with 1  reference block instead. This would however form the numbers above (if not unique). So if you would draw a genealogie tree of individuals but in that tree an individual can be represented more than once (e.g. by reference in the comments) then its a pyramid.

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


text:
Why don't birds in flocks fly into each other?
I've seen videos of hundreds of birds flying in the same general direction but creating incredible patterns in the sky seemingly instantaneously! How do they all know in what direction to turn at the same time? Is there a "Lead" bird dictating this somehow?

Not an answer because I've totally forgotten where to find the papers involved, but this is an active area of research in fields ranging from biology to machine learning to mathematics.

Is there somewhere you can point me where I may be able to gather a little more info on this research?

Searching scholar.google.com for swarm, swarm behaviour and the like should yield some results.

I'm sorry I can't be more help, but remembering references from a talk I heard 3 years ago is hard! You might have to experiment a bit to get the right search terms. If you have access to ISI Web of Knowledge, you may be able to search better there (narrow things down by field, etc).

The guy who gave the talk has probably published at least one paper on swarm behaviour, so this should give you a starting point if you can find the relevant paper. If you can get hold of the paper (or email him for a copy), the citations list is probably a good place to start. http://scholar.google.co.in/scholar?q=author%3A%22Shan+He%22&btnG=&hl=en&as_sdt=0%2C5

You might be interested in artificial life programm called "Boids".

Ive recently stared designing a similar program for some collision detection practice, it is in fact what led me to this question. Boids will not collide because of the code written but i'm 99% sure there's is no collision detection code written for birds:-)

This might be a good starting point....http://www.npr.org/2013/06/13/191348007/what-flocks-of-geese-and-fish-can-teach-us-about-the-future

Richard Dawkins discusses this in his book The Greatest Show on Earth: The Evidence for Evolution.
The birds, in the aforementioned example Starlings, 'know' which direction to fly and where to be by obeying simple local rules concerning the distance and spacing of other members of the flock in their immediate vicinity, without any global knowledge of the size or shape of the flock in its entirety.
The key to this behavior is that there is no choreographer and no leader.  Order, organization and structure all emerge as by-products of rules obeyed locally, many times over.
Dawkins equates this to 'bottom-up' design or 'self-assembly'.  This is also how embryology works.  Beautifully 'designed' bodies emerge as a result of single cells obeying local rules.  The idea of a blueprint is a misconception.
Dawkins mentions a man in the book named Craig Reynolds who wrote a program in 1986 called 'Boids' which models the flocking behavior of thousands of birds - http://en.wikipedia.org/wiki/Boids


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Can SIRS occur without Sepsis from Infection?
I am thinking this figure

It suggests me that there has to be Sepsis that infection can lead to SIRS.
I am thinking particularly the pathogenesis of Cryptococcus neoformans where

respiratory tract $\to$ pulmonary infection $\to$

asymptomatic and nonspecific pulmonary signs in normal patients
progressive systemic disease in immunocompromised patients

and the last row.
Can SIRS occur without preceding or simultaneous Sepsis?

According to the classification of sepsis, it is SIRS with a suspected or known source of infection. By definition therefore, sepsis without SIRS is not sepsis but SIRS can exist without sepsis. In all fairness though, SIRS can exist if you run for a while (elevated heart rate and respiratory rate by themselves qualify for a diagnosis of SIRS).
Sepsis is however not the same as a bacteraemia which may be caused even by brushing your teeth (although the bacteraemia in this case is transient).

Very clear explanation with good examples! Thank you!


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What can cause the bloating in high protein diet of Whey proteins?
I am thinking what can cause the swelling of gastrointestinal system i.e. bloating after high protein diet of Whey proteins.
Liver does breaks those proteins to branched chain amino acids (BCAA), which can cause this swelling.
However, I am not sure if this is the reason.
It may be the carbohydrates which are broken to enable this BCAA synthesis.
If you take the protein diet with carbohydrates, there seem to be less swelling.
So apparently easier energy for BCAA synthesis.
The combination of proteins, carbohydrates and lipids seem to be important.
Creatine should also be mentioned.
Fat burner thing is also important here, I think.
What can cause the swelling of gastrointestinal system after high protein diet of Whey proteins?

What do you mean by "swelling"?

@CaptainCodeman http://en.wikipedia.org/wiki/Swelling_(medical)

Yes but what do you mean by "swelling of high protein diet"?

swelling caused by ... Or Swelling in ...

Still doesn't make any sense.  You're saying the diet swells?  You mean the broccoli I'm eating gets fatter?  Or do you mean there is a part of the body that swells?  I think you're using the wrong terminology to explain something, and it's very unclear what you're trying to say.

There is a part of the body that swells i.e. included in the definition of the process Swelling. I use the question word "what" to ask what is the key factor that can lead to swelling. You can also ask the same by "how swelling in high protein diet ...".

With all due respect, I don't understand a word you're saying.  The definition of swelling means when a part of the body gets larger, but which part are you talking about?

@CaptainCodeman Gastrointestinal system.

Aha, thanks, now it makes sense! I could be wrong, but I think most people call that bloating, not swelling.  I think lactose intolerance has something to do with it as well.

@CaptainCodeman Thank you for the correction! Yes, lactose intolerance and many other diseases like celiac disease contribute to the ethiology of bloating i.e. swelling of abdominal area.

The cause of the swelling is lack of lymphatic carriage capability of proteins to the muscles, because of systemic conditions affecting the circulation of proteins through your lymphatic system.
There will be edema extracellularly because of insufficient carriage of proteins through lymphatic system.
My schematic drawing about the fluid movement between these spaces

I started to think why some people do not observe so much swelling.
I discussed with a few and come to conclusion that the main difference between those people who did not have noticeable swelling was that that they did lymphatic system massage by maximising abdominal breathing after taking whey proteins (before training and after training).
I think it sounds sensible to some extent.
Those people also included lymphatic system massage in their recovery after training.
One video here Lymphatic Drainage for Abdomen and Trunk.
So another reason what may cause the swelling is insufficient drainage of lymphatic system.
The swelling does not happen to the same extent in all people.
Some people swell much after one intake of protein drink.
Some people also do not have to do lymphatic massage.
My conjecture: The reason to this is most probably one glue-gene-group.
Those people who have this genome have other systemic diseases that causes the lymphatic drainage have high proportion of proteins already:

for instance, uncontrolled asthma patients, who are circulating lysed DNAs of lymphocytes from small bronchial tree through the lymphatic circulation

Lymphatic circulation is the system which circulates the proteins to the muscles.
After absorption from the digestive tract, lymphatic circulation carries proteins systemically.
However, since there is already a high proportion of proteins, lymphatic circulation cannot take much more proteins to carry.
Our body has to remove toxic wastes before it can build new materials.
Catabolism then conquers anabolism in some situations.


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Knockout Rat Phenotype Database?
Is there a database where I might list the phenotype of a certain rat knockout and/or search for other similar phenotypes?
There is a International Mouse Phenotyping Consortium, which has the goal of characterizing the phenotypical changes of homozygous knockouts for each of the 20,000 genes in the isogenic mouse line C57BL/6.  The International Knockout Mouse Consortium is responsible for creating the knockouts and the two consortiums work together closely.
There is also a Knockout Rat Consortium, but I haven't found a Phenotype Change database for rats.

Opinion:
the Jackson laboratory
http://jaxmice.jax.org/
Is the industry leader in transgenic mouse production. Their list of mouse strains is almost a db in itself but currently no db exists that I'm aware of. I take it your looking for something similar to what's available for c elegans:
http://www.celeganskoconsortium.omrf.org/


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Plastid and mitochondria
I am not a biologist, so please bear with me for this basic question. Although I tried googling, I am confused.

What is the difference between plastids, chloroplasts and mitochondria?
Are there any plant sequence databases for each of them (plastid, chloroplast and mitochondria)?
Can we separate chloroplast, mitochondria, plastid sequences from whole genome assemblies?

What is difference between plastid, chloroplast and mitochondira?

Plastid is a general term for an organelle which consists of Chloroplasts, Chromoplasts, Leukoplasts/Amyloplasts and Apicoplasts.
Chloroplasts (Chloro = green) are involved in photosynthesis; they express Chlorophylls and have the thylakoid structures which are involved in the electron transport chain that results in ATP formation during the light reactions of photosynthesis. As it is obvious chloroplasts are found in the green parts of the plants such as leaves. Chloroplasts also have the enzymes of biosynthetic pathways involved in carbon fixation.
Chromoplasts (Chromo = colored) express more of other pigments and less of chlorophyll. Neither do they have thylakoid structures. Therefore they are not involved in photosynthesis. When fruits ripen, the chloroplasts differentiate to chromoplasts. Flowers also contain a lot of chromoplasts.
Leukoplasts (Leuko = white) do not have any pigments and usually carry out biosynthetic processes. When they store starch they are called amyloplasts.
Apicoplasts are found in parasites like plasmodia (causes malaria) and are vital for their survival. The Apicoplast is involved in biosynthetic pathways but the precise importance of it remains unknown.
The mitochondrion is a very different organelle and has a different evolutionary origin. Mitochondria, like Chloroplasts, produce ATP from an electron transport chain but use chemical substrates (NADH, flavin etc) rather than light as a source of initial energy. Mitochondria are thought to be an outcome of an endosymbiosis between an ancestral eukaryotic cell and an $\alpha$-proteobacterium. Chloroplasts, on the other hand have descended from a Cyanobacterial endosymbiont. Therefore the structure of mitochondria is very different from that of chloroplasts.
Chromoplasts, leukoplasts, amyloplasts and apicoplasts have lost the photosynthetic ability. Similarly, there are variants of mitochondria which use different electron acceptors (other than oxygen) and some are just incapable of ATP synthesis.

Are there any plant sequence database for each of them (plastid,
  chloroplast and mitochondira)?

Chloroplast genome database: {link}
I don't know of a separate plant mitochondrial database but you can see this resource called MitBASE.
NCBI also has the organellar DNA sequences.

Can we separate as chloroplast, mitochondria, platid sequence from
  whole genome assembly?

Usually the organellar genomes will assemble as separate contigs when you sequence from the whole cell DNA prep. By homology it is possible to say if the contig is a mitochondrial or chloroplast DNA. But the best way would be to experimentally isolate the organelles and sequence their DNA.