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Can you help me identify this "thing"?
I found these "things" by chance on my wild strawberries which I grow in my organic garden. Basically, some strawberries are completely covered with them.

They're transparent, they have dots equally aligned and they don't move. I've tried searching for transparent slugs and worms and also faeces but to no avail.

I don't know the answer, but the same thing appears in these two other questions which are unanswered: thing one thing two At this point given the variety of places they have been seen they must be some kind of egg, but surely someone with expertise will eventually tell us.

Alright, I searched for "gelatinous insect eggs", found a similar image, and encountered a 3-part discussion of these things that begins with part 1.   It's a fair amount to read but I think it is your "thing".

Where do you live and how big are these millipedes(just a hunch).Do they have legs because if they don't you can tell they're not millipedes and centipedes

@BryanHanson I don't think theyre the same thing these have a shape and look so much like millipedes but once OP replies it will become clear

@BryanHanson I did the same search as you and after looking at many images I guess I found the species (I am not sure, though). It appears like the egg mass of Chironomus.

@WYSIWYG I think you might actually got it right. I just google'd "chironomus egg mass" and I'm getting back images very similar to mine. Chironomus appears to be a non-biting version of mosquitoes (by how similar they look to an average Joe) and now when we're talking about it, in the area where I live there are mosquitoes but during summer time at night there might be hundreds if not thousands of mosquitoes/chironomuses attracted to lights nearby. I thought they're all mosquitoes but now I'm not so sure.

@WYSIWYG At the very end of the 3 part blog post I referenced above, it come down to caddisfly eggs vs chironomous eggs, with this important distinction, quoting now: "chironomid eggs are nearly always elongated or oval shaped. Caddisfly eggs, on the other hand, are nearly always spherical."  Not all the pictures on SO are clear, but in those that are it seems like the eggs are elongated, so I think you are correct about Chironomous.  I think you should post that as an answer, and also post a reference back to your answer here on the SO questions I linked to above.  Great work!

@BryanHanson I think you should post an answer. I believe you know about this topic better. I am not an expert on this field. My research was just some google searches :P

It appears like the egg mass of Chironomus.

First, I am no expert on this topic, I am simply synthesizing several different sources of information along with the very good work of others.  Since the "thing" featured in this question has appeared elsewhere, it deserves an answer.
These appear to be eggs of Chironomous midges (wikipedia).  This conclusion is based largely on reading the three-part blog by Tom of askanaturalist.com
Part 1, Part 2, Part 3 which is very thorough.  In the last part of that blog, it is stated "chironomid eggs are nearly always elongated or oval shaped. Caddisfly eggs, on the other hand, are nearly always spherical." Looking at the pictures here and on the other SO questions (here and here) it appears that the eggs are indeed elongated rather than spherical.  Hence they are apparently Chironomous midge eggs.

I doubt it can be Chironomidae eggs. These midges live aquatic, or at least in very wet conditions. "On wild strawberries" is way to dry i think.

This link supports that Chironomidae live in aquatic or in very wet conditions. https://www.google.com/url?sa=t&source=web&rct=j&url=https://www.eje.cz/pdfs/eje/2003/04/01.pdf&ved=2ahUKEwilj9-a_vLfAhVHaFAKHWpEC-EQFjACegQIBhAB&usg=AOvVaw0IYCx7tDciVnLlY6JT_ajV


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In percentage, how much is the human genome (DNA) similar to the mouse genome?
Some guy argued with me against evolution theory, and he claimed that human and mice share 98% just like human and chimpanzee.
I've tried to search online for a simple and accurate answer, but I couldn't yet.
In simple words, how much is the human genome (DNA) similar to the mouse genome?
Please use numbers as much as you can and provide references.

This question cannot be answered as simply as you put it, but it's not too much to elaborate on.
The order of the base pairs will be drastically different, but the same proteins and amino acids will be coded for in genes, just at different points along the DNA. For example, you may find the same sequence to code for a protein in a mouse as in a human, but they will not be found in the same place along the DNA code (although they will still be read and eventually produce the same protein).
http://www.nature.com/nature/journal/v420/n6915/full/nature01262.html
Additionally, this article shows that, if we take your question literally, "at the nucleotide level, approximately 40% of the human genome can be aligned to the mouse genome", that is, if human and mouse DNA was lined up side-by-side, and a percentage of identical match-ups was calculated.
However, taking a 'looser' approach, it is worth noting that about 5 percent of both of genomes consist of protein-coding genes (https://www.genome.gov/10001345), and the remaining 90%+ is non-coding. If we only count the protein-coding genes, the average similarity of genes between humans and mice in only protein-coding genes is 85%. The link above says that some are 99%, and some are 60% - there is a clear similarity here between humans and mice, albeit not 100% identical.
If you wish to know the explanation, simply it is because mice and humans both have a common ancestor (the last link also explains this) about 80 million years ago. Due to these similarities, and the striking similarities, scientists simulate genetic changes in mice that can occur to humans, and have used computers to analyse the similarities in mouse genome.
I hope this is understandable, if you need any clarification on terms, please ask :)

But what objective or rational reason does one have to only count the protein-coding genes? The other genes, as I understand it, are responsible for gene expression--in essence, the "program" running on top of the protein "building blocks". By that reasoning, Windows 3.11 is 90% the same as Windows 8, because they use almost the same underlying set of instructional building blocks in the processor, yes? Gene expression is an absolutely fundamental part of what makes up an organism, and it's absurd to just throw away some set of genes without a good reason to–I'm eager to hear such a reason!

Fair point, it's just that OP's said that he wanted to know "in simple words". I did add about how 40%~ similarity can be aligned, but considering when you align only protein-coding parts of the genome, the percentage shoots up to an average of 85%.Considering these are found within all animals of nature, just like how Windows is all built upon the same, original code, then it can be seen as subjectively more important to focus on those ones, rather than including "junk DNA". I'm sorry for not fulfilling everything in my answer, but OP did want it to be 'simple'. I am only a student, after all

The idea that "junk" DNA is actually junk is greatly disputed. Also, your answer lacks any references. Without that, it's just a random opinion.

Well it was my first answer of this website, so I was limited to two links. I only use the term 'junk' DNA since it is widely used, and is only 'junk' from the perspective of "non-protein coding" and "protein-coding" DNA. I absolutely agree that 'junk' DNA is not 'junk' by definition, but in accordance to OP's question, I thought it was worth referring to it as such to further understanding of the difference in percentages being so drastic as a result of whether they code for proteins or not. I'm sorry if the answer was inadequate to you, but please add your own if you feel you can do better.

I don't have time to post an answer, but I have already balanced comment.

Fair enough, thank you for your criticism of my answer. I will try to improve upon it the next time I decide to post one :)

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What are the known natural biochemical reasons for a dead human's body not fully decaying?
What are the known natural biochemical reasons for a dead human's body not fully decaying (decomposing)?
EDIT:
I am interested in a scientific explanation of those cases, in which human body would not fully decay, for example, some parts of skin and hair would still be there, and I am not talking about such cases like hand-made mummification (like, say, those Pharaoh's mummies in Egypt).

Please clarify your question a bit. Are you asking under what circumstances a body might not decay, and the biochemical reasons thereof? Or do you have a specific circumstance in mind?

@jarlemag - "Please clarify your question a bit" - Sure. I am interested in a scientific explanation of those cases, in which human body would not fully decay, for example, some parts of skin and hair would still be there, and I am not talking about such cases like hand-made mummification (like, say, those Pharaoh's mummies in Egypt).

@brillant You can edit your question to add your clarifications. Additionally you should add some research you already did. For example try checking about a relation of humidity and temperature to decay.

related posts- 1 and 2

@brilliant are you talking about bodies preserved in bogs and ice.

@potterbond007: "are you talking about bodies preserved in bogs and ice" - Not really. I'm talking about those cases when a body in a coffin for some reason is not fully decomposed while all the surrounding natural conditions apparently should bring it the state of full decomposition (except, perhaps, for the bones).

question requires case study reference and clarification!

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In what sense is the "histone code" a code?
Since I started learning about molecular cell biology, I have witnessed an increasing amount of attention to this thing called a "histone code." However, unlike the central dogma of molecular cell biology (i.e. DNA RNA Protein), I still feel very confused about what exactly constitutes the histone code. Is this term code being used rigorously like it is for the central dogma? That is,  is there an actual code? If so, what is its alphabet (e.g. GTAC for DNA, GUAC for RNA, the amino acids for  proteins)? What kind of words does it encode (e.g. codons for RNA to protein)?
If these things are not known, how do we know it's actually a code then?
Thanks!

Here is a good resource I found on what all the known histone modifications are, their proposed functions, and literature references.

Yes that was helpful. Grazie.

As already mentioned by Stefan, the "histone" code is not really a universal code; it is restricted to eukaryotic systems and even then, not unambiguous. It is, at present related to two kinds of histone modifications and their correlation with the transcriptional activity at that locus:

Methylation
Acetylation

Other modifications such as phosphorylation and ubiquitylation also exist but they are not generally considered in this "code".
Acetylation masks the histone's positive charge and thereby loosens the chromatin (DNA wrapped around the histones), which in turn facilitates transcription. Therefore acetylation is almost always activating in the sense of gene expression.
Methylation, on the other hand has different effects. Methylation on Histone-3 at 4th lysine (H3K4) and H3K36 causes activation whereas H3K9 and H3K27 are repressive. There is also some difference between different extent of methylation i.e monomethylation, dimethylation and trimethylation. The effect of methylation is executed by proteins that have domains such as chromodomain and PHD fingers, that identify these modified histones. Sometimes the histone can carry both kinds of methylation marks H3K4me3 and H3K27me3 and these are called bivalents.
Other histones of the octameric nucleosome can also be modified. However as with other kinds of modifications that I mentioned previously they do not seem to be very common and are therefore not generally considered in this "code".

Is it known that only two kinds of modifications exist or do researchers expect more to be discovered?

@StanShunpike as I mentioned that there are other modifications as well but they are either transient (phosphorylation) or used only under specialized conditions (ubiquitylation). Arginine can also be methylated but it is perhaps not as common as lysine methylations.

The histone code isn't a sequence of letters like you see in DNA and RNA but rather refers to the pattern of post-translational modification of histones. This is then, by definition, an epigenetic control of gene expression.
Histones are basic DNA binding proteins around which DNA is wound to form chromatin. For transcription to occur, transcription factors and RNA polymerase must bind DNA, which generally cannot happen if DNA is wrapped tightly around histones. DNA must therefore be able to come off from and translocate relative to histones in order to expose bare regions. Based on the level of compaction, chromatin can be generally classified as two types:

euchromatin: loosely bound, transcriptionally active
heterochromatin: tightly bound, transcriptionally repressed

The state of chromatin compaction is determined by specific  post-translational modifications to the residues in the histones' amino-terminal tail. This is the histone code. One commonly talked about and perhaps easiest to understand modifications is acetylation of lysine residues: this is generally considered to activate transcription since it neutralizes the positive charge of the amino acid so the negatively charged DNA isn't attracted as tightly. Phosphorylation of serine or threonine can have a similar effect by introducing negative charges. Other modifications include mono-, di- and trimethylation of lysine and arginine, ubiquitinylation and others that I haven't memorised. Each histone monomer can be modified independently and each has several residues that can be modified; this leads to staggeringly large number of ways in which just a single nucleosome can be modified. Importantly, these modifications can recruit proteins including transcription factors, histone modifiers and chromatin remodellers (which can condense or loosen the chromatin). All of these serve to tightly regulate gene expression. This is an active field of research and what all discovered combinations of modifications do is largely unknown, but certain modifications are often characteristic of active and repressed transcription.
There is a standard convention for conveying histone modifications. For example, if lysine 23 of histone H3 was acetylated, you would write H3K23Ac. For trimethylation of arginine 3 on histone H4, you would write H4R3Me3.

It's not a code in the strict sense of the word. With proteins and nucleic acids you have a strictly defined set of letters and strict rules for them to match one another (note that in some cases atypical base pairing occurs in nucleic acids). The "code" part in histone code is meant to convey the notion that modifications in the histone proteins influence the expression of genetic information. The main mechanisms of histone modification are methylation, acetylation, and ubiquitilation. In a very rough analogy, these would be the "letters" of the histone code (NOTE that this is a very imprecise analogy).

So it's not a true code in the math-cs sense, but a code in the loose sense of the word code. As in, it stores information that can be likely accessed, recalled and copied.

Yes, a "code" in a loose sense. Don't forget to up-vote ;)


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What is the role of Aspartate Transaminase in gluconeogenesis?
I know that oxaloacetate cannot cross the mitochondrial membrane, but can instead be converted to aspartate, shuttled out, and then re-converted back to oxaloacetate.  What does this have to do with gluconeogenesis?
The traditional route is to convert pyruvate to OAA to malate in the mitochondria, shuttle the malate out, and then convert malate back to OAA in the cytosol.  If lactate is the precursor, then the conversion of lactate to pyruvate in the cytosol can generate an NADH, making the conversion to malate in the mitochondria unnecessary.  Thus, OAA is converted directly to PEP in the mitochondria by mitochondrial PEPCK and shuttled out to the cytosol to begin gluconeogenesis.
If we have these two pathways, what is the point of using aspartate?

I think it is the other way round. Aspartate is pushed into the gluconeogesis pathway via OAA

I may have approached this problem from the wrong direction, so here's my attempt at an answer:
For gluconeogenesis to function, glycolysis needs to be shut off.  Glycolysis feeds the TCA cycle with Acetyl-CoA through the decarboxylation of pyruvate, and without glucose as a source, we need to look to other methods of generating OAA to make into PEP.  We can make OAA through Aspartate Transaminase by reacting Aspartate with α-ketoglutarate.

Here's an excerpt from Oregon State. See the section titled "Spatial separation of gluconeogenesis metabolites."

Now, the answer to "Why is aspartate pervasive in cellular metabolism?" That's a particularly hard to answer, and my speculation, in part, is that this was simply how the system evolved. We see aspartate participate and act as a precursor to many pathways, esp. in amino acid metabolsim, but not much data exists yet as to the "why" of it all.


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About radiation therapy
With radiation therapy, could some of the radiation used cause new mutations in non-cancerous cells that are near the tumour that is being irradiated? If so could these new mutations lead to new cancerous cell colonies (which might later metastasize)?

Yes, this can happen, although the risk is low. The problem is that some tumors need to be irradiated since the cannot be operated (this is true for some brain tumors). Here the radiation therapy is the therapy of choice. The effect of the therapy is that the tumor cells get a high radiation dose which either kills them or drives them into apoptosis.
The problem the irradiation is that you will always affect healthy cells, of which most will die. This causes some of the negative effects of the radiation therapy, but it is also possible that a healthy cell receives a dose which is "only" damaging and causes a secondary tumor. Here a benefit analysis needs to be done to see if the benefit from the therapy is woth taking the risk of acquiring more damages. See the references for some more background.
References:

Long term side effects of brain tumour radiotherapy
Second Cancers Caused by Cancer Treatment
Therapy-Related Secondary Cancers

I thought the apoptosis mechanisms in a cancerous cell have malfunctioned or are damaged ( that's why a cancer cell can't be shut down by its own 'self-destruct' mechanisms) so if a cancer cell is 'killed' by a high dosage of radiation how does this happen?

DNA double strand breaks, damage to proteins or the cell itself due to the high energy and so on.

How likely is a high dose of radiation going to cause DNA double strand breaks or damage to proteins or damage to the whole cell and so on regarding any type of cells in the high dosage 'path'? This sounds a lot like some sort of disintegration ray gun you here about in science fiction stories. How long has radiation therapy been used? 50 years?

Has anybody lived for 10 years after their last 'set' of radiation doses?

If radiation therapy can lead to new mutations but the risk is low..; how does anyone know if the risk is low as cancerous cells are hard to detect ,probably harder to detect when metastasizing. Even when a new colony of cancerous cells coalesce they.re hard to detect. So how is it determined if the risk is low?

@201044 It is clearly a trade-off between benefit and harm. Often cancers which are irradiated are the ones, that cannot be removed surgically (or completely). Then the tumor is immediately dangerous for the patient. From the dose the patient gets, you can calculate how likely additional damage is. And then you need to make a decision...

What kind of radiation is used in radiation therapy?

Since cancer cells are a lot more unstable than 'regular' cells couldn't a type and duration of radiation be found that would destabilize a cancerous cell and not harm a 'regular' cell?

A recent news item mentioned women who have had more than the usual amount of some type of scan ( Xray or C.T?) are more likely to develop further cancerous growths. Is this true? Using radiation to kill tumors is sort of like using a small amount of fire to 'get rid of' a big fire.

Are there ANY other types of radiation or radiant energy that could kill tumors. Like infrared radiation or microwaves?

@201044 Since the radiation therapy has to do harm in order to damage (to drive it into apoptosis) or kill the cancer cells, it is harmful. And thus it can cause cancer by itself. The question is the benefit of the patient and if it is ok to take this risk. As far as I know no other radiant energy sources are used, as these transport less energy into the tissue.

I don't think any others are used.

It should tell you something that they are not used, right? General rule for cancer therapy is: Everything what helps, does no harm and makes sense is used.

Radiation therapy has been used for 50 years at least; Marie Curie helped to start the practice. I was wondering if ANYBODY  has worked on the idea of using microwaves or infrared radiation or something else in all those 50 years??

In the last 50 years is cancer treatment JUST surgery or chemo therapy or radiation therapy and possible slight variations or combinations of these?

'Everything that helps, does no harm and makes sense is used..' ; yet radiation therapy can do harm and make a person feel sick ,right? Could narrow beans of intense microwave radiation kill tumors without doing much other damage? Microwave radiation wouldn't cause new tumors..

@201044 It is always the decision what is more harmful in the short and in the long term. Yes, radiation can be harmful, but cancers pose a much more immediate danger. I think microwave radiation is absorbed by the upper layers of the skin, so it won'T work in the lower parts.

Well if two narrow beams of microwave radiation that intersected where a tumor was it would be more intense  at the tumor site and have less energy elsewhere so it might not be absorbed by the skin. In a microwave oven the microwaves heat the food from the inside out ,( I don't know if that is because many of the beams of energy intersect at the 'insides' of the food).


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About the apoptosis mechanisms in a cell
The apoptosis mechanisms in a cell are like a type of 'self-destruction mechanism': is this correct?
As with any type of complex system with various necessary functions, if it has a set of self-destruction mechanisms for 'shutting down' the whole system, it would require some sort of 'internal programming' that can somehow 'target' each of the system's necessary functions and 'disrupt' each of them simultaneously or in some 'order'.
In other words a self-destruction system in order to be effective would have to be able to 'target' each necessary function in the system. And if a biological system has a mutation or a set of mutations that 'distort' some parts of the system then the self-destruct mechanisms might not be able to 'target' all of the functions.
So maybe the cellular mutation 'automatically' makes it hard or impossible for the self-destruct mechanisms to work. Is this possible??

Did you happen to look at any of the questions/answers tagged apoptosis? Why were they unhelpful?

I wrote some of those questions.

@201044 Your question was hard to understand. I took the liberty to edit it. Let me know if it is fine.

I am not sure if I understand your question right. Are you asking how and what kind of mutation is disabling apoptosis? What do you mean by "it would require some sort of 'internal programming' that can somehow 'target' each of the system's necessary functions and 'disrupt' each of them simultaneously or in some 'order'."?

Not at all. In order to self destruct, you don't need to disable all necessary functions, you just need to disable one. That's why the functions are called "essential". To take a very simple example, in every movie you've seen where the self destruct has been activated, that self destruct mechanism was almost certainly a bomb that blew the ship/installation/planet or whatever up. The self destruct did not go around disabling individual processes, it just activated a bomb and destroyed everything.
Apoptosis is quite similar. While there are many essential processes in a cell whose failure can activate apoptosis, the mechanism of apoptosis itself usually involves the straightforward destruction (lysis) of the cell. Simply put, the cell digests itself, breaking down its various constituent parts and, finally, destroying the cell membrane and breaking up the cell itself. For a summary see this Wikipedia page or here.
Briefly, when apoptosis is triggered, the caspase cascade is initialized which results in the breakdown of various proteins in the cell and, finally, in cell lysis. It really is analogous to setting of the bomb that destroys the facility of the bad guys.

That's a great point about only having to destroy one essential function. So is it true first comes at least one essential function failure then the apoptosis mechanism is triggered? Could some functional mutation that creates some different 'demands' on the cell make it so even if one or two essential functions are on the brink of failing the mutation masks this or makes these functions not as essential or somehow distorts necessary cellular system information so the apoptosis is not triggered?

If a cell or group of cell is reproducing and dividing a lot more than 'they' usually would if 'their' 'situation' was 'healthier' (because of cellular damage caused by an 'unstable' digestive system for example); if they are dividing and reproducing a lot and random mutations can cause cancer is it more likely the cells will develop some mutations if they are reproducing and dividing a lot 'more than normal'. And as such some of these mutations might shut down some important cell functions thus disrupting any apoptosis mechanism?

If a 'group' of cells divide and reproduce a lot more than usual would this increase the likelihood of mutations that could disrupt maybe some important cellular functions?

The apoptosis mechanism involves the failure of just one essential process , straightforward lysis; this seems simple yet how come in a cancerous cell such a 'shutting down doesn't work or can't be 'activated'. Do cancerous cells have all the essential functions that are normally found in the ' normal' versions of the cell ,yet they are still 'functioning adequately' in this cancerous 'version'?


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Is it possible to have multiple stop codons in one exon?
I would be very happy if someone can help me to find the answers for the following related questions.

Can one exon have many stop codons?
Can protein synthesis happen, if the stop codon is at the beginning of the exon?

An exon can have multiple stop codons but the first codon will terminate the ORF. The remainder of the exon will be a part of the 3'UTR.
However, there are some cases in which stop codon readthrough happens [1]. In these cases an internal stop codon does not terminate the translation and the ribosome reads through it. During this process an aminoacyl-tRNA successfully competes with the release factor. This is quite evident in the case of selenocysteine and pyrollysine- tRNAs which bind to the UAG (amber) stop codon in certain organisms [2,3] (this is also referred to as amber suppression). The exact mechanisms that affect stop codon readthrough are not elucidated but features in the mRNAs are likely to play a role in this. In case of amber suppression, the relative rarity of the UAG stop codon and lower concentrations of release factor-1, can be major factors.

I don't know what you mean by "beginning of the exon" but there are short ORFs (< 100 codons) which can code for small peptides [4]. Small peptide as small as 6 amino acid residues has been reported but most of the known small peptides are ~30-100 residues long.

References:
[1] Loughran, Gary, et al. "Evidence of efficient stop codon readthrough in four mammalian genes." Nucleic acids research 42.14 (2014): 8928-8938.
[2] Agafonov, Dmitry E., et al. "Efficient suppression of the amber codon in E. coli in vitro translation system." FEBS letters 579.10 (2005): 2156-2160.
[3] Wikipedia: Expanded genetic code
[4] Andrews, Shea J., and Joseph A. Rothnagel. "Emerging evidence for functional peptides encoded by short open reading frames." Nature Reviews Genetics 15.3 (2014): 193-204.

Thank you for your answer. I have one more clarification. In one of the human protein, i am getting three stop codons (UAG, UAA, UGA). However, i am getting more than 80% of UGA in my transcripts. I appreciate if any one educate me, which is the most frequently present stop codon in human transcripts.

@Krithi.S I have not checked but this is fairly easy to do. Just download all human mRNA sequences from RefSeq/GTF file with CDS annotations and find the stop codons.

I'm tempted to link articles from the sixties with me being so old. Amber is the most commonly read through stop codon throughout nature.  http://www.sciencedirect.com/science/article/pii/S0014579305003224 for a modern example of how it's used

Right that appears to be the mechanism, but it should be noted that it's specific to the Amber stop codon. In bacteria and viruses you can often see doubling or even tripling up of stop codons to prevent Amber readthrough

@AtlLED Is there readthrough in mammalian/human genes?

@MattDMo I certainly know of cases in cancers and viruses using host machinery. Off the top of my head I don't know of any endogenous examples in mammals, but one could look. I note the OP makes no mention in the question.

@AtlLED yeah, I haven't heard of any endogenous examples either, I was just wondering if recent work had come up with anything. Of course, anything goes with tumors/viruses, so that's not surprising.

@MattDMo Quiet true. But given that when it happens, it's normally only a small portion of actual translation, that I don't think anyone is looking closely enough in the absence of some pathology. I suppose if a bioinforamtics PhD student wants to tackle this, you could look for cases in the human genome where there is an amber followed by another stop codon and see if you find read through on that gene (with 2nd stop oblated). I think it would be hard to get funding on it though. Checking PubMed, I'm pretty sure nobody is looking.

@AtlLED something for me to do at home in my spare time. Minus the wet work, of course :)

@MattDMo the linked article (ref#1) talks about readthrough in human genes

@WYSIWYG My point was that wasn't endogenous. I was thinking a Crisper exp. would be more convincing than transient expression.

@AtlLED As long as the entire cDNA is cloned and expressed there should not be a great difference, unless the plasmid expresses too many mRNA copies in which case there might be concentration dependent effects. I agree that working on an endogenous system is better. By CRISPR experiment you mean mutate one of the stop codons?

@WYSIWYG That's exactly what I mean.  The transfection experiment was a good 1st step, but I have a hard time imagining that cDNA under CMV or PGK promotion will not confound studying read-through (over expression or lenti incorporation as done in ref 1).  I think oblating the second stop codon in the genome would be the ideal way to look at this.  Also, we should probably move to chat after this, because I think we're diverging from the question.

@MattDMo absolutely. Not only is there "abnormal" readthrough, you also have selenoproteins where the amber codon codes for a bona fide aminoacid, Sec.


text:
How does electrolarynx work?
I have heard that this is an effective replacement for patients who have a dysfunctional larynx, partly due to cancer.
I am curious to know the inner working of this device and why such a robotic voice comes out?
What is the basic principle of this device. Does it simply captures vibrations and converts it to sound? Just like how a mic does?
Thank you.

Your vocal chords vibrate to produce a tone, but your mouth shapes that tone into the sounds that make up voice. If your vocal chords fail or are removed, the electrolarynx can be used to vibrate the throat for you, but your mouth still needs to shape that sound into words. Because the electrolarynx produces a mechanical buzzing vibration, you get mechanical buzzing words. This is similar to how the talkbox works with electric guitars, the guitar sound is piped through a tube into the musicians mouth, they have to shape that sound into words with their mouth. Go listen to Peter Frampton for a good example.


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Why do different pain killers have different effects on people?
I've noticed some pain killers working great for me, while others have no effect.
Works for me

Aspirin
APC †
Naproxen

Doesn't work for me

Paracetamol
Diclofenac
Tramadol

I doubt there is much of a placebo effect at work, since most of these either did or did not work when I first took them, without having expectations either way.
Whenever I have a head ache, I take an APC. I suspect it's actually the aspirin in there that does the job, since when I take just paracetamol, it doesn't do squat. As a kid I got children's aspirin, which worked.
I once had a severe back ache. I was prescribed diclofenac (a heavier variant than the over the counter one), which didn't work. I was then prescribed tramadol — same results. I then tried naproxen, which worked rightaway.
Why do some pain killers work while others don't?
Is there an underlying mechanism, that explains why some of these work while others don't? Does that predict if pain killers that I haven't used yet will work?
Please note that I'm not looking for medical advice on which pain killers to take; I'm just curious about how my body interacts with the various ones.

†: the one consisting of aspirin, paracetamol, and caffeine, not the one containing phenaticin. Think Excedrin.

Related: http://biology.stackexchange.com/questions/2922/how-do-the-pharmacodynamics-of-the-nsaids-differ-and-are-there-resistant-cox-p

@jonsca That's interesting. The weird thing is that diclofenac is an NSAID as well, but doesn't work for me. So it's not just a case of NSAID vs non-NSAID.

NSAIDs are a pretty diverse group of drugs. You might find http://en.wikipedia.org/wiki/Diclofenac#Mechanism_of_action interesting.

I've read that, and more, but I still don't have a clue. I don't even have a clue where to look.

Even if you're not looking for medical advice, I can't help but see this as a personal medical question.  If you wanted to re-write it as a general question, I would be more inclined to answer. Right now I'm questioning why it shouldn't be voted to close.

@AtlLED I understand your concerns, but other than writing in the third person about myself, I don't know how to make it more general, without losing any significance for me.

Well here are some pointers, and info that will give you insight. Not all pain is the same.  It can be from verious tissue (pain from muscle injury isn't the same as bone), with verious stemilius. If you think of a headache and back ache, there might be some drugs that are better for one of the other.  The effectiveness of verious pain relief mechanisms are well studied, so you might look at some to see how you can break down your types of pain, types of medication, and their applied efficacy for different types of pain. Don't forget stress and neuropathic pain when considering headaches.

Also, that comment solidfies my opnion that as written this is a personal medical question.  If you can not imagine how to extraplote it generally, the chances are it is personal.

NSAID is a very broad chemical category and the only similarity between different NSAIDs is that they are not steroids and act on Cycloxygenase-2 (?).
Mechanism of action for almost all of them is poorly understood. Even structures- paracetamol and aspirin are somewhat similar. Naproxen  is very different. When you say some drug acts/doesn't act you have to note that both are delivered to the body in equal doses. Properties like solubility can also affect the pharmacokinetics of a drug.

Bounty will be auto-awarded. My question hasn't been answered fully, although I have learned some valuable insights.

X-posted: https://medicalsciences.stackexchange.com/q/1696/12704

I don't know of any interesting mechanism that is specific to pain killers, so I will instead answer for drugs in general.
Drug action is a complex process consisting of many steps. Let's take a simple example: A systemic direct inhibitor of a kinase. This drug would need to*:

Be absorbed into your bloodstream
Remain in your bloodstream for sufficient time
Be absorbed into the tissue
Be able to bind the target protein

1 can fail due to interaction with other concurrently taken drugs or food, or simply genetic factors affecting the particular functioning of the gut mucosa. 2 can fail because the kidneys are too good at eliminating it, or the liver is metabolizing it too agressively (both also subject to modulation by other drugs, foods and genetic factors). 3 can fail because the transports in the cells aren't working as rapidly, or represent an allele less likely to take in the drug, or are modulated by other drugs/foods. The tissue can also have efflux pumps or enzymes that break down the drug. 4 can fail because the drug was designed for a specific allele of that kinase, but you happen to have a different allele, which has a slightly different structure that is no longer targeted by this drug.
Then you have a host of physiological variables, and addiction/tolerance.
Apparently the most common genetic reason by far for variable drug sensitivity is the specific set of CYP genes you have. CYP enzymes are abundant in the liver and chemically process various molecules (including drugs).
Besides this, an interesting set of specific examples used to be available from 23andme. I'm not sure if they still provide this after the FDA ban on health information.

Clopidogrel sensitivity - CYP2C19 variation
Proton Pump Inhibitor (stomach acid reduction) - CYP2C19 variation
Abacavir (HIV drug) - HLA-B*5701 SNP
Acetaldehyde (alcohol flush) - ALDH2 mutation
5-fluorouracil (chemotherapy) - DPYD mutation
PEG-IFN-alpha/RBV combination (Hepatitis C medicine) - IL28B SNP
Phenytoin (epilepsy drug) - CYP2C9 variants
Choline esters (class of muscle relaxants) - BCHE (CE degrader) variants
Sulfonylurea (used for type 2 diabetes) - CYP2C9 variants
Thiopurine (immune suppressant) -  TPMT (enzyme that degrades thiopurine) variation
Warfarin (anticoagulant) - CYP2C9 variants
Caffeine - CYP1A2 SNP
Metformin (diabetes drug) - SNP rs11212617, near the ATM gene
Antidepressant - SNPs in ABCB1 affect likelihood of sexual dysfunction (common side effect)
Beta-Blocker (heart disease) - Mutations in ADRB1 which is normally blocked by the drug
Floxacillin (drug for staphylococcal infections) - SNPs in the MHC region affect liver toxicity of this drug
Heroin - OPRM1 receptor (target of heroin) SNPs affect efficacy
Lumiracoxib (used to treat pain and symptoms of osteoarthritis) - SNPs in the MHC region affect liver toxicity
Naltrexone (alcohol and narcotic addiction drug) - SNPs in OPRM1 affect how much it can reduce pleasurable feeling from narcotics
Statins (cardiovascular disease) - SNPs in COQ2 (mitochondrial component) affect risk of myopathy

As you can see, our friends the CYP family enzymes come up frequently, and some are even repeat offenders like CYP2C9. Besides that, there is a fair number of cases where variation in the specific target of the drug are relevant.
Note that this list is not comprehensive: Many drugs have not been studied in sufficient detail, and some may have complicated mechanisms instead of just "bind and inhibit protein X".
I have omitted many details and links to literature, I am sure you can easily find them by searching on Google Scholar with the keywords I already gave. Let me know if that doesn't work, though.

*: Note that these aren't necessarily required for all drugs. For example, some drugs can be applied directly to the skin and hence do not need to pass through blood.

Drugs, even for the direct inhibition of a kinase, don't have to enter the blood.  Many do, but one could also, just as a quick example, apply a drug in a cream/skin permeable solution (to a skin tumor for the sake of argument for a kinase inhibitor). This is what defines a "local" treatment.

Out of curiosity: Are there any cancer treatments which are not systemic? Besides the tumor cells at the actual tumor site you always want to hit metastatic cells as well. At least for melanoma all kinase inhibitors (like vemurafenib) are given systemically as far as I know.

@Chris off the top of my head imiquimod, but when discussing pain management, there are far more. I find the phrasing "must: ..." to be incorect/misleading in this awnser.

Also, if you open yourself up to treatment and not drug, you had better hope your radiation treatment isn't systemic.

@AtlLED You definitely have a point with local treatment, but I can't figure out how to work it into my answer. To be sure, I was only giving an example of an inhibitor which happens to be delivered by blood, in order to illustrate how there may be several distinct families of factors at play.

@Superbest I don't think you have to work in local treatments, just adjust the phrase "Even in a very simple case, direct inhibition of a kinase, the drug must:" by noting items 1 and 2 are not actual requirements ("must"), given that a kinase inhibitor can be administered locally.  I get the point you were trying to make, I just think it's a little misleading as written.  You can probably just add the word systemic, and maybe add some info on step 3 related to targeting.

Short answer: different people have different amount of active receptors.
In treatment, combination scores of Pharmacodynamics and Pharmacokinetics determine the final effect of the drug.
Receptors determine many effects of the drug in many pathways.
Different people also sense pains differently (Psychology).
Review answer
The purpose of treatment is to relieve pain and maintain function.
Your question is biased.
You cannot only concentrate on painkilling in maintaining health.
These both are the reasons for the complains of the patient, not only the pain.
For instance, in rheumatoid arthritis, response to therapy can be quantitated using many measures including American College of Rheumatology system values ACR20, ACR50 and ACR70, which denotes the percentage of patients showing an improvement of 20%, 50% or 70% in a global assessment of signs (maintaining function) and symptoms (pains).
Each patient has own health, different from one another.
Our body adapts to the environment and individual conditions of the body to maintain homeostasis.
Receptors adapt for instance.
They can be active or inactive - in short-run and long-run - again depending on the conditions at hand.
Painkillers i.e. analgesics have different properties:

anti-inflammatory effect - acute and chronic conditions (inflammation is the major mechanism under many pathologies) e.g. nonsteiroidal anti-inflammatory drugs (NSAIDs, please, see this answer about the particular mechanisms and how different people have different effects from NSAID painkillers) and glucocorticoids (most)
symptoms relieving specific drugs e.g. disease-modifying antirheumatic drugs (DMARDs)
anti-platelet effect - e.g. the older you get, the more platelets stick together.
anti-pyretic effect
...

which all can be toxic.
Note that many drugs alone or/and as combination can work as painkillers i.e. pain relievers.
Aspirin for instance has both anti-inflammatory and anti-platelet properties.
However, it is rarely anymore used as anti-inflammatory.
The anti-platelet property is dependent on the exact dosage of the administration.
Aspirin's mechanism of action is to inhibit platelet COX which antiplatelet effect lasts 8-10 days (life of the platelet).
In other tissues, synthesis of new COX replaces the inactivated enzyme so that ordinary doses have a duration of 6-12 hours.
Please, review any Pharmacology -textbook for more info about aspirin.
Each these drug has own Pharmacodynamics and Pharmacokinetics

Pharmacodynamics answers to the question What drug does to the body? It stimulates some receptors, activates some pathways, ...
Pharmacokinetics - What does body do to the drug? It metabolises it (enzymes, receptors). It distributes it. It excretes it (kidneys, feaces).

In treatment, you consider what is the target organ.
You need to think what is causing the dysfunction and the pain.
You try to restore the function and relieve pain.
The component of drug needs to reach the target tissue e.g. your pancreas' beta cells do no produce insulin so your blood glucose is high.
Complications of this are polyuria and eventually exodus if untreated.
Insulin is injected into the fatty tissue.
We do not have long-term acting insulin administered orally - our metabolism start to break the drug so it does not have wanted treatment.
If insulin administered to the muscle, the time of action is too times less, again because muscle is metabolising the insulin i.e. a chain of peptides (protein).
No all symptoms and diseases have painkillers.
For instance, prehemorrhoid and some types of itching related to  posthemorrhoids.
However, for both, there are some special salvas for proplylaxis but they are not complete.
Now, you can start to read something in SuperBest's answer about host's physiological variables and addiction/tolerance which alters the mechanisms (receptors) of pathways in Pharmacodynamics and Pharmacokinetics.
Sources

Basic and Clinical Pharmacology, 11th edition, 2009, Bertram Katzung.
My notes in Pharmacology classes during 2014.

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text:
How useful are vitamins and trace elements in E. coli culture medium?
In protocols for minimal media for growing bacteria, I often see that a vitamin mix or a mix of various trace metals is added. But at least for E. coli, I know that those are not strictly necessary, they also grow in minimal medium without any of this.
Does it make sense to add vitamins or trace elements when growing common E. coli for protein expression like BL21 (DE3) in minimal medium? Is there some literature data on how this can affect the growth of the bacteria?

Not sure that I have ever come across trace metals in recipes (I assume that you aren't referring to the Ca/Mg salts component of M9), but it is certainly the case that many K12 strains (e.g. C600, DH5α) require thiamine because they are thi mutants. This doesn't apply to BL21 since it is from a different lineage (it is a B strain). In a lab where several strains are being used it will always make sense to standardise on a universal recipe so that the medium available will suit all strains in use.
There is a useful list of E.coli genotypes here.

I co-authored some literature that partially addresses this.
Amongst others, we measured the growth rate and yield of E. coli (MG 1655, not BL21) with and without a typical trace-element supplement. Supplementing trace elements roughly tripled the yield, but only slightly affected the growth rate.
However, the focus of our work was another: If you don’t add trace elements, inevitable contaminations will do it for you, but unreliably. Since trace elements already take effect in, well, traces, these contaminations may make rather huge biological difference. By supplementing trace elements, you make the entire setup less sensitive and get more reproducible results.
For E. coli and our conditions, we found that supplementing trace elements significantly reduces the variability of growth (from 5% to 3%) but not of yield. Beware that this is specific to our benign experimental conditions, and will probably be worse for typical experiments. If you rely on a metabolic pathway that didn’t matter in our conditions and requires some trace element, the impact of contaminations may be considerable. The same applies if your trace-element contaminations vary with different batches of medium – some standard ingredients were shown to have considerable trace-element impurities.
I don’t know how important reproducibility is when you just milk them for proteins instead of studying them, but at least for the general titular question, we considered this important enough to write a paper about it.
For vitamins, I expect the benefit for reproducibility to be less, since they are not as omnipresent and less resilient to cleaning procedures as trace elements.

Adding trace elements (Fe, Co) and vitamins will increase the growth rate of E coli quite significantly.
However in the context of protein expression, more is sometimes not better. The proteins produced under high yield conditions may be miss-folded and non functional. The only way to know is to test it out.

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text:
Identification of an unusual tree
Location : Lyon, France

I think it's one of the laziest trees I've ever seen XD

It looks like a cypress topiary. The form is most definitely not natural and trained to grow that way.

As Sudachi has commented it has been pruned, probably over many years, to take on this form. It is not natural shape.
I would say that it is not possible to identify the exact species of tree without a close up of the leaves. From zooming in it looks like it could be a Lawson Cypress (Chamaecyparis lawsoniana) although it could be a Leyland Cypress (x Cupressocyparis leylandii), or a number of other possibilities.
One way to investigate this further if you want to know for certain, apart from posting a close up of the foliage which may help, would be to find some specimens of cypresses that you can find the name of. Perhaps in a garden centre or an arboretum, then compare the smell of the foliage when you pinch and crush it between your fingers. Different species have a characteristic smell that is a useful method for identification.


text:
Martian Abiogenesis?
In the Miller-Urey experiment the probability of the chemical origin of life under (hypothetical) early Earth atmospheric conditions were assessed. For that water, methane, ammonia, and hydrogen were sealed in a bowl, heated and struck by artificial lightning (see this for the experimental setup). After cooling the mixture down several complex organic molecules (e.g. amino acids) were found by paper chromatography.
So my question is what would happen if instead of using early Earth gases, one puts a concoction similar to current or early atmospheric gases found on/expected to once be found on Mars.
Is it possible to foresee how well that experiment might do and what results it could bring?

Welcome to Biology.SE. I think your question is valid but please do not use references as parts of your questions. Rather (briefly) describe the experiment (the Miller-Urey experiment will probably known by almost everyone around here) and provide a reference for deeper reeding. I edited your question accordingly. Feel free to add anything to or change my edits.


text:
Is there a theoretical maximum on the number of sexes a given species can have?
Background: To the best of my knowledge, most sexually-reproducing species of organism have two sexes, although there are also sexually-reproducing species of organism (flatworms come to mind) which have only one sex. (Depending on one's definition of sex.)
Many species of fungi are both sexually reproducing and apparently have more than two sexes. (Depending on one's definition of sex.)
There are also species of lizards with more than two biologically determined "gender morphs". It is even more debatable than in the case of fungi whether these morphs should be considered separate "sexes" or not, since their mating compatibility network is bipartite.
Question:
Is there a theoretical maximum on the number of sexes a given species of organism can have?
Elaboration:
There would also be a lot of different possibilities -- already with three sexes, one can imagine at least two different means by which sexual reproduction could occur -- any one of three combinations of two individuals from two distinct sexes (most likely in "rock-paper-scissors" fashion), or the combination of three individuals from all three distinct sexes.
How, for example, might either of these two scenarios be maladaptive compared to sexual reproduction of two individuals in species with two or fewer sexes?
I am asking about species with more than two sexes/mating types in general, not necessarily about situations where more than two sexes are involved in a single reproductive event. (Contrast with this related question.) I am also not restricting to animals, or even multi-cellular organisms, or even eukaryotes, since these restrictions might affect the answer. (Contrast with this related question.)
Note that this answer to the second related question implies that we should expect the mating compatibility network of anisogamous sexually reproducing organisms to be bipartite. But note that, as in the example of the side-blotched lizards, this doesn't necessarily preclude having more than two sexes, nor does it give a theoretical maximum to the number of possible sexes. And since I don't want to necessarily restrict to anisogamous sexually reproducing organisms (i.e. isogamous ones would also be fine), then that answer also does not provide a theoretical maximum for isogamous sexually reproducing organisms either.

Why was the question down voted?

@Remi.b Can you explain why this is a duplicate? I already explained in the question why it isn't a duplicate. Admittedly I didn't explain it very well, but I did do so.

@GerardoFurtado Maybe you could give a summary comment? I would obviously love to hear your thoughts; this question has been bugging me a lot.

@Remi.b All of my examples are animals, that is true, since I am most knowledgeable about animals, but my question is not restricted at all to animals or mammals (as the "duplicate" question supposedly is). The answer to that question explaining the topic of anisogamy is only a partial answer, since it explains why, for special organisms the mating compatibility network would have to be bipartite, but not necessarily restricted to two nodes (as the example with the lizards suggests). But the example of fungi mentioned also makes clear that these assumptions don't hold generally for

arbitrary organisms http://blog.mycology.cornell.edu/2010/06/02/a-fungus-walks-into-a-singles-bar/ But even if they did, that answer itself would, again, not necessarily preclude having more than two sexes, it just would force the compatibility network to be bipartite (as is the case for the side-blotched lizards). So then the question, even in that special case, would still be unresolved by the answer to the other question.

@GerardoFurtado I like your suggestion for the title, my only reservation/qualm being that I don't  necessarily want to preclude organisms for which the concept of species is more-or-less ill-defined.

@GerardoFurtado Definitely the former, if a given species (each individual organism expresses only one sex or combination of sexes at a time) can have more than 2 sexes. Although to be fair, if a given organism of a species can express more than 2 (combinations of) sexes throughout its lifetime, then that must mean that the species as a whole has more than 2 (combinations of) sexes, so the latter option would be a special case of the former. But anyway my point being that I am most interested in the full generality of the former (a given species).

I reopened the post! @GerardoFurtado Feel free to post your answer. I note as a comment only that the post is a possible duplicate of Why do only two sexes exist for animals?


text:
What happens to the red blood cell in CaCl₂ solution?
Here's the problem:
One red blood cell is placed in a hypertonic solution of NaCl, another is
placed in a solution of CaCl2 equimolar with the NaCl solution. What
would you expect to happen and why?
My reasoning is that the red blood cell will shrink due to water loss by osmosis when placed in hypertonic NaCl. It will shrink even further due to the larger osmosis gradient due to there being such low concentration of Ca2+ normally in the cell. However, I'm not sure if this is right so could someone please explain the correct answer?

The reason why the cell would shrink more in CaCl2 solution is because it has a higher van't Hoff factor i.e. total number of dissociated ionic species per solute molecule (it is 2 for NaCl whereas it is 3 for CaCl2).
(Nonionic solutes do not dissociate and will therefore have a van't Hoff factor of 1)
Osmotic pressure (and other colligative properties) are proportional to van't Hoff factor. Therefore osmotic pressure in CaCl2 solution will be 3/2 times of that in an equimolar NaCl solution.
Note that the ionic chemical potential is not what drives osmosis; it is the differential concentration of water (or any other solvent) that drives it.

The osmolarity of the CaCl2 solution is higher than of the NaCl solution.


text:
Does the body have a gate control for pain
I understand it is not the most accurate source but I recall a House episode where he claimed the body had a control mechanism for pain in which only the most painful thing was felt. Is that true? and if so how does the body control which injury we feel and could we use this to our advantage?

Speaking from personal experience, no, the body does not just focus on one area of pain, allowing only it to be felt and other injuries not to be. It just means you hurt in more places.

Afaik there is something like that by cold and pain (aka. cryotherapy). http://www.spine-health.com/conditions/chronic-pain/modern-ideas-gate-control-theory-chronic-pain

Pain receptors, more precisely pain signal propagation, can be inhibited in several ways. One is, for example, fine touch receptors (mechanoreceptor in illustration) inhibit propagation of pain signal in spinal cord (a lot of pain processing happens in spinal cord):

That is why humans often rub skin around or nearby injury, whether it is in joints or something more superficial. You should find more information about such control in any textbook on pain. See this page for short primer.
Next, pain propagation is modulated -- still in spinal cord -- by descending pathway from brain and brain stem. See this page for more, or address Kandel's textbook.
Now, I don't know whether or not it is identified how/where brain "selects" to what pain pay attention. My hypothesis is that it happens by competition, e.g. several signals compete by inhibiting each other via some mechanism, probably, related to stress-induced analgesia.

Firstly you have to take into consideration that nociceptors do not adapt to stimulus. This means that a nociceptor will not only fire at the beginning of the stimulus, as seen in mechanoreceptors that have phasic responses, but will fire as long as the stimulus lasts. This type of response is called tonic response (see figure). Figure A shows the tonic response whereas figure B shows the phasic response.

So by this, we can conclude that, peripherally, every noxious stimuli, will induce action potentials as long as that noxious stimulus lasts. During the ascending propagation of the action potentials induced by the noxious stimuli, other neurons will have the "opportunity" to inhibit the response. Some ways that the pain transmission can be inhibited is by the release of endogenous opioids by descending neurons from brain parts in mid-brain and medulla.
The other mechanism is the one explained above by aandreev. And as you mention in your title, this mechanism is called the gate control theory.
Ref: Purves et al (2012).,Neuroscience 5th ed.,Sinauer associates.
http://www.ucl.ac.uk/anaesthesia/StudentsandTrainees/PainPathwaysIntroduction [2015-04-30]


text:
(Updated question) Problem with Fold-change mean compared to absolute data (in qPCR)
For the problem below I am aware of the statistics involved but just can't get my finger around the following:
In biology we use qPCR to measure gene expression or basically number of mRNA copies. It does this by counting how many cycles of amplification (2^) it needs to reach a threshold. So to simplify everything lets assume that 1024 copies would require 10 cycles (2^10). If there are more copies it would take less cycles to reach the threshold, therefore 2024 copies would take 9 cycles, 512 copies 11 cycles etc.. Now imagine the following scenario:
We have the following samples:
Sample 1. 1024 copies of gene A and 4096 copies of gene B
Sample 2. 1024 copies of gene A and 16384 copies of gene B

Now we want to compare sample 2 to 1, with gene B in relation to gene A:
In absolute numbers this would be:
Sample 1. 4096 / 1024 = 4x more B
Sample 2. 16384 / 1024 = 16x more B
The average amount more B = (16 + 4) / 2 = 10x more B

Now with qPCR the same samples from above would look like the following:
Sample 1. Gene A 10 cycles, Gene B 8 cycles.
Sample 2. Gene A 10 cycles, Gene B 6 cycles.

Now using the methods standard used for qPCR data we first take the difference between Gene B and A. Followed by the mean of the difference and this is taken 2^.
Sample 1. 10 - 8 = 2 cycles
Sample 2. 10 - 6 = 4 cycles
The average amount more B = 2^((2 + 4)/2) = 8x more B

All publications / software tools etc will compute an average of 8x more B. And I am aware this originated from a log2 scale, however why does this statistically correct method differ in outcome from absolute numbers?
Update
I oversimplified my question therefore below some more details of my "problem".
Condition 1 biorep 1. 1024 copies of ref and 1024 copies of gene X
Condition 1 biorep 2. 1024 copies of ref and 1024 copies of gene X
Condition 2 biorep 1. 1024 copies of ref and 4096 copies of gene X
Condition 2 biorep 2. 1024 copies of ref and 16384 copies of gene X

So to compute in absolute numbers the average amount more of gene X in condition 2 versus 1:
We can forget the reference gene here as cDNA amounts are the same, therefore:
Condition 1 biorep 1 & 2: average (1024 + 1024) / 2 = 1024 copies
Condition 2 biorep 1 & 2: average (4096 + 16384) / 2 = 10240 copies
Condition 2 vs 1: average 10240 / 1024 = 10x more gene X in condition 2 vs 1

Now with qPCR CT values based on the numbers above:
Condition 1 biorep 1. Ref_CT 10 and GeneX_CT 10
Condition 1 biorep 2. Ref_CT 10 and GeneX_CT 10
Condition 2 biorep 1. Ref_CT 10 and GeneX_CT 8
Condition 2 biorep 1. Ref_CT 10 and GeneX_CT 6

Now using the official qPCR calculations:
Condition 1, Ref_CT mean (10 + 10) / 2 = 10
Condition 2, Ref_CT mean (10 + 10) / 2 = 10
Condition 1, GeneX_CT mean (10 + 10) / 2 = 10
Condition 2, GeneX_CT mean (8 + 6) / 2 = 7

Ref_deltaCT (10 - 10) = 0
GeneX_deltaCT (10 - 7) = 3

delta_deltaCT (3 - 0) = 3
Difference Condition 2 vs 1 = (2^3) = 8x

This equates to 8x more of Gene X on average in condition 2 compare to condition 1. Here now is the difference of 8x vs 10x. Also any program you will use to fill in these CT values it will result in a ratio of 8 compared to 10.
Is this perhaps as this method equating to 8 should only be used for technical replicates, and bioreps should use a different equation resulting into 10?

Sample 1. 4096 / 1024 = 4x more B
Sample 2. 16384 / 1024 = 16x more B
The average amount more B = (16 + 4) / 2 = 10x more B

That is not the right way to go about. You are calculating average expression of B in both samples. It does not mean there is 10x more B. There is just 4x more B in Sample-2 relative to Sample-1.
Gene-A does not change its expression between samples and can be used as a reference gene.
If you calculate by threshold cycle the fold change $ = 2^{8-6} = 4x$
See this post too.
The average is calculated between replicates, not between different experimental conditions.
Sometimes the average of two experimental samples is calculated — this is typically done in a MA-plot analysis which is done to filter out genes which show very high fold changes just because of their overall low expression (1:4 vs 100:300).
Answer to your Edit
You should not take the average (arithmetic mean) of Ct. They don't scale linearly with expression (and so is the converse).
For any non-linear function $f(x)$:
$$f(x+y) \ne f(x)+f(y)$$
$$f\left(\frac{x+y}{2}\right) \ne \frac{f(x)+f(y)}{2}$$
Furthermore, for a convex function:
$$f(E[x]) \le  E[f(x)] $$
$$ Jensen's\ inequality $$
where $E[x]$ is expected value of $x$
$a^x$ is a convex function with respect to $x$ ($a$ is any real number > 1). So you can apply Jensen's inequality to Ct values and expression.

I totally agree with your answer, I think I over simplified my question, above I edited my original post to clarify a bit more my question.

The answer you give in your edit is also the answer I expected. However all (commercial) tools assume that the Ct values are on a linear scale and therefore you take the arithmetic mean of the Ct, resulting into 8x. And as you take 2^ of Ct the absolute values are not. This means you would have to take the geometric mean of 4096 and 16384, which is 8192 (which is 8x 1024). Apparently all published methods consider the absolute values not to be on a linear scale, and actually the Ct values are. Which biologically speaking is difficult to grasp.

If someone is interested in average Ct then they may very well do it. But we are not interested in that are we. Independently the values are not in any scale. They scale with other value as per some function. So expression scales exponentially with Ct. So $ Expression = f(Ct)$. I should clarify about it. Edited


text:
Is this formula describing the loss of unfixed genes from a population accurate?
In the 1954 science fiction novel Search the Sky by Frederick Pohl and Cyril M. Kornbluth, a formula is featured that "quantitatively describes the loss of unfixed genes from a population".
$$L_T=L_0 e^{-T/2N}$$

"A final word. There has been much loose talk among the troops about the slogan of the Joneses, which goes $L_T=L_0 e^{-T/2N}$. Some uninformed people actually believe it is an invocation which gives the Joneses supernatural power and invulnerability. It is not. It is merely an ancient and well-known formula in genetics which quantitatively describes the loss of unfixed genes from a population. By mouthing this formula, the Joneses are simply expressing in a compact way their ruthless determination that all genes except theirs shall disappear from the planet and the Joneses alone survive. In the formula $L_T$ means the number of genes after the lapse of $T$ years, $L_0$ means the original number of genes, $e$ means the base of the natural system of logarithms and $N$ means number of generations."

Is this formula indeed an accurate description?
Or was it made up by the authors? I find it suspicious that it contains two different measures of time, years and number of generations, while they seem related to me.

An earlier version of this question omitted the minus sign in the equation. I noticed it when finding it again on Google Books.

Honestly, you should really look at some scientific literature in this area. Do not judge it by speculation. If you can not find anything, then assume no.

@RadekMartinez - I assume that the point is to ask the experts, who might already know the right equation.

I also find this formula odd. Isn't the length of a generation generally fixed? And if so, shouldn't the number of generations in a given time be proportional to time, rendering T/N independent of time?

Number of generations would be proportional to number of years, but every species would have a different ratio. Since P & K were talking about only humans, that would be a constant. But it appears to be a more general formula with generation length independent of number of years. But you're right, It seems odd.

I have edited your title so readers have an idea what the formula relates to without having to read the question. Helps them and you. (Gentle hint for any future questions you ask.)

The expression is based on a real one, but missing a minus sign (EDIT: not anymore! See updated question), and the explanation is garbled. For the actual equation, see "eigenvalue effective population size" in, e.g., WJ Ewens, Mathematical Population Genetics. There should be a negative sign in the exponent: $L_T = L_0 e^{-T/2N}$. Note that you need this minus sign so that "genes" (actually heterozygosity) are lost with time rather than growing exponentially in number!
As for the errors in the explanation: $T$ should be measured in generations rather than years, and $N$ should be the number of individuals (or rather the "eigenvalue effective number") instead of the number of generations.

Oh yes, you are probably right! +1. So, the definition of the symbols were wrong (generation vs years), the meaning of the equation was wrong (loss of genes vs loss of heterozygosity) and the equation was wrong (minus sign missing). Wow, that's quite a distance from the original formulation!

I keep my answer for information purpose but the right answer is @DanielWeissman answer. It is made very clear once the OP noticed the missing minus sign.

I think this formula comes from nowhere. The supposed meaning of this formula is very unclear. As you said, it makes little sense to have two measures of time (in years and in generations) in the same equation.
Fixation of new alleles
I am not sure what is meant by gene loss. I would suppose, it refers to fixation of new alleles. Under the assumption that all mutations are neutral, then the probability of fixation of new alleles is $\frac{1}{2N}$, where $N$ is here the population size. If the neutral mutation rate is $\mu$, then the number of new mutations per generation is $2N\mu$ and therefore the rate of fixation of new alleles is $2N\mu\frac{1}{2N} = \mu$. Per consequence, after $t$ generations the number of new alleles $L_t$ is $L_t = L_0 + t \mu$ (assuming it makes sense to talk about the number of newly fixed allele at time $t=0$).
Loss of genes
Muller's ratchet (typically on the Y chromosome in mammals) does lead to systematic loss of genes. There are here a number of models and a final expression for the rate of loss of genes is not that easy.


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Why are there no tree-like plants that grow in lakes?
Looking at aerial photos of boreal forests, with dense woods clear-cut by quiet lakes, I wondered why exactly are the woods so clear-cut at the edge of water? Why won't trees develop adaptations that will let them grow from a shallow lake bottom, with the lower part of the trunk in the water and the crown above the water?
It seems to me that this would give them some significant advantages. Lake bottoms are rich in organic nutrition, and insolation will also be plentiful above water, at least at first when there's little competition. So why are lakes' surfaces so clear and open, instead of overgrown? Of course there are aquatic and semi-aquatic plants like water lilies, Scirpus or Typha, but they are a far cry from the nearby terrestrial forests, in terms of biomass. Why don't they develop into large amphibian trees, or why don't terrestrial trees try to re-colonize lakes?

Just a guess really, but maybe for whatever reason they can't outcompete aquatic plants.

Mangroves grow in the water...

@MattDMo Think he is talking about boreal forests while  Mangroves belong to the tropics

http://www.mangrove.at/images/mangrove/forests/overwashed/overwashed%20mangrove%20community.jpg

I remember seeing a documentary (David Attenborough perhaps?) that showed a particular plant where part of the plant grows underwater and part grows above water (i.e. not just floating on the surface). The stem is strong enough to support the weight of the plant above water and the airborne leaves are radically different from the aqueous leaves. Still, it is not big enough to be called a tree.

Trees need:

Deep roots to get more water and anchor their growth.
Strong trunks to support themselves against gravity.
A vascular system to move water and nutrients throughout the tree.
Small leaves that can be supported high by the trunk to compete for sunlight.

Water plants need:

Just enough root to anchor its location.
No vascular system. Water is everywhere.
Leaves that are more substantial than the stems to gather as much sunlight as possible through the cover of water.

So the kind of body that has to develop under water to thrive is in many ways the opposite of the kind of body needed to thrive on land.
Water plants would have to waste energy on

Vast roots.
A strong trunk.
A vascular system.

...Things it wouldn't need till later while receiving little sunlight on small leaves. It would have to shed its thirsty skin like a snake on the above water parts. Too complex and little or no demand for it.

If water plants had evolved a way to turn oxygen into helium and keep much of it trapped within its leaves, then we'd have tall ocean forests. The plants could grow just like they do now  but with slightly fluffy leaves. As soon as it broke water surface, the abundance of oxygen would ramp up helium production and really fluff them leaves. The slight stems would have to be scrappy instead of massive.
There would be Greek mythology that Gaia was married to Helios but left him for Poseidon the Gaia-Shaker. Poseidon and Gaia were cursed with children (the vast ocean forests) who rebel against them and adopt a lifestyle where they are always reaching out to Helios and later in life shedd their bodies to be closer to him in spirit. Some early humans tried to rob the Helium spirits of the ocean forests by inhailing them out of their plant bodies. They were cursed and turned into chipmunks with only their hands to remind them of their past humanity.

Edit to add reference: A piece by Mickey Walburg on eHow.com
Though I would call mangroves amphibian trees, I wouldn't call them large and I was trying to ascertain the spirit of what @kai teorn was asking rather than let the question sit unanswered when I believe I can answer it.
You learn something new often if you're looking and today @MattDMo introduced mangroves into my awareness. If he thought it was the answer to the spirit of the question post, he might have elaborated on it as an answer instead of a comment. I could be wrong about that.
Mangroves are mostly coastal. They are usually at the edges of the water. The ones that are a few meters in the water are usually more like shrubs than majestic boreal forest trees. They end up shooting roots everywhere and kinda lounge around compared to the typical tree standing straight reaching for the sun. Also the incidences of Mangroves in the ocean away from the shoreline are of maybe a handful bunched up, hardly a species wide return to the the oceans. Seen from aerial photos, Mangrove concentrations look like boreal forests surrounding lakes, not swamp lands.

Why are there no tree-like plants that grow in lakes?
Looking at aerial photos of boreal forests, with dense woods clear-cut
  by quiet lakes, I wondered why exactly are the woods so clear-cut at
  the edge of water?

I think the spirit of the next question is about trees in general in lakes. Not the few instances peppered around the world. Also some lakes grow and shrink throughout time, sometimes long enough for trees to gain a little ground and survive lake growth. But I don't think those trees as a species have developed adaptations to grow from shallow lake bottoms.

Why won't trees develop adaptations that will let them grow from a
  shallow lake bottom, with the lower part of the trunk in the water and
  the crown above the water?

... and from the end of the post ...

Of course there are aquatic and semi-aquatic plants like water lilies,
  Scirpus or Typha, but they are a far cry from the nearby terrestrial
  forests, in terms of biomass. Why don't they develop into large
  amphibian trees, or why don't terrestrial trees try to re-colonize
  lakes?

... I eliminated mangroves from qualification. Interesting but I still don't think it's what @kai teorn had in mind. I think @MattDMo introduced mangroves as a comment to enhance our knowledge.

Please consider adding references. I dont think u can generalize trees that way as one of the comments do mention that mangroves send roots in water

For boreal forests, lake freezing is probably also hindering mangrove-like growth: freezing may be resisted if you're wholly out or wholly in the water, if crossing the air/water interface then there's much more danger of mechanical damage to a plant.

The question of "why are there no/few aquatic trees?" can be approached in two ways.

Why are land trees tall?
Is it harder to be tall in a lake?

Land trees are tall to shade competitors and spread their seeds and fruits. To get tall, they need extensive root structures to anchor and provide enough water to the trunk. If there are no competitors to shade out and the water provides long-distance seed dispersal, why bother growing tall?
It's much harder to be tall in a lake. Nutrient uptake is a problem, as is proper anchoring. Large amounts of organic biomass may exist, but iron, phosphorus, and other micronutrients are more important. A large oak can be 15 tons, which is harder to support using only sediment on the lakebed. It's also understandably difficult to germinate and sprout if you're an aquatic tree. See mangrove propagules for an example of the problems and how to get around them(sort of). Most mangrove species need lenticels in the trunk to provide enough oxygen, and long roots require periodic pneumatophores to provide oxygen to the roots.
Looking at all the pressures on plant life in lakes, it's a lot of work to be a tree, and much easier to be a lilypad. More of the biomass can be concentrated on photosynthesis, and structural concerns are a lot less troublesome. Additionally, many lakes simply do not have the nitrogen or phosphorus content to support tree-sized growth. See trophic state index in lakes. If the lake can't support algae, there's no way it can support a tree.

Cypress swamps are an example of tree like plants in lakes. There is even a lake in Louisiana called  Cypress Lake


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Questions regarding Scapulohumeral Rhythm
I'm actually an artist, but I wanted to ask this because it will help a lot in my figure drawings.
My artistic anatomy teacher taught me about the Scapulohumeral Rhythm. He said that in during the first 30 degree of rotation of the humerus, neither the scapula nor the clavicle moves. But after that, for the next 60 degree of rotation of the humerus, its rotation is distributed in a 2:1 ratio to the Scapulathoracic joint.
He said that beyond that, the Humerus is locked into the socket with Acromium and Coracoid Process. So the Glenohumeral Joint is frozen. Additional elevation comes from the Clavicle.
My first question is how true is that?
My second question is what happens to the Scapula after the 90 degrees rotation of the Humerus? I noticed that the Scapula keeps rotating even after the Humerus is rotated beyond 90 degrees, but is there any consistent ratio?
My third question is what is the maximum elevation of the Humerus in degrees?
Forgive me if I looked liked an annoying dumbass, I'm just an artist. So, please explain in a simple and understandable way.


text:
Simultaneously using both hands - How does that work?
Is some part in one hemisphere the decision maker and "calling the shots" - controlling the opposite side's hand "directly" and controlling its own side's hand through the corpus callosum. Or: is there some "Gestalt" of parts in both hemispheres working as one making the decision?
If the latter - it would seem counter intuitive to have a deciding part which is not "unified" in one region, having to go back and forth through the corpus callosum for deciding.

Why can't the hemispheres coordinate? Even though control of muscles on one side of the body may primarily originate in the opposite hemisphere, inter-hemisphere communication and coordination is vital to proper functioning of the body.

@MattDMo Yes. I can't seem to formulate the question clearly. Perhaps better phrasing would be to ask: Is one side dominant in the decision and "calling the shots" or is it some "Gestalt" of the two hemispheres working together on the same "level"?

@user133943 This article should interest you http://faculty.washington.edu/chudler/split.html

@MattDMo I edited my question. Thank you for your response.

@TheLastWord I edited my question. Thank you for your response.

I am not sure I fully understand your question, it's a little unclear. But if I understand the question correctly it is how to we coordinate movement on both sides of the body?
Well this can occur because we have connections between both hemispheres of the brain. The major connection is called the corpus collosum, this is a white matter tract that allows signals from one side of the body to pass to the other side of the body.
In some rare cases there have been individuals who have had this connection severed, for these individuals each side of the body may perform tasks of which there other side of the body is unaware.

I tried upvoting your answer because it answers my question as originally posted. But I don't have enough reputation for upvoting. I have also edited my question.


text:
What triggers programmed cell death in humans (from outside the cell)?
What triggers programmed cell death in humans? Is it decided by the brain (for the entire body)? Or is it a local decision of a cell by its environment? Something else?
I realize that there might be different cases. But I'd like to get a general idea of where (and why, actually) does this happen.
EDIT
As linked to by a comment below - one type of cell-death (Necrosis) just "happens" to a cell. And perhaps there are other types that are decided by the cell.
What I'm asking about (and trying to understand more) is about the idea that cell-death might be initiated externally to the cell because it would be beneficial to the whole organism. Such as "the separation of fingers and toes" mentioned in Wikipedia  .   "Who" would initiate it? Are there examples of the CNS initiating it? Notifying the cell by nerves? By hormones? Are they initiated by neighboring cells? (And if so - what cells have the "clout" to send such signals?)
What I'm trying to understand is who decides when a cell dies in those cases where it's not the cell itself.

Have you read the wikipedia article on apoptosis? If not, please read it, then [edit] your question to narrow it down to a specific question about the process. As it stands now, this question is far too broad, as there are many different ways of triggering apoptosis, and many different pathways within the cell for effecting it.

@user133943 you should edit your question to specify that you mean regulated cell death (as it applies to development). As it is written, your question is too broad

The answer is, in part, it depends. Let's think of the PI3K/AKT pathway. Akt actively phosphorylates BAD which abrogates the Bax/Bak apoptosis pathway. RTK's at the plasma membrane activate this pathway when bound with survival factors. In the absence of survival factors, Akt would become dephosphorylated and you'd have a net movement toward apoptosis. In a particular form of cell death called anoikis, this could be as simple as detaching from the extracellular matrix. So anything that halts the binding of survival factors could play a role.
In the case of immune response, activated Tc cells can induce apoptosis by secreting pore-forming enzymes as well as enzymes that directly activate caspases. The Tc cells also express Fas on their membrance which is involved in the extrinsic apoptosis pathway. TNF (tumor necrosis factor) may also bind cell surface receptors as sort of a death factor, and push towards apoptosis.
These are just examples, some generic searches about apoptosis, necroptosis, entosis, and a myriad of other programmed death mechanisms will yield a very comprehensive overview.

Thank you. If I understand you correctly - the first type you mentioned is (very generally) - an example of cells having a built in mechanism to detect a condition (such as being detached from their natural surroundings) that warrants cell death. The second - more pertaining to my question - would be: the immune system. (Please feel free to correct me if I'm wrong.)

@user It's a very textbook answer, here's a review of some apoptotic regulation mediated by extracellular signaling. It's a complex response that may be regulated by paracrine, autocrine, neuronal signals in addition to cell-cell interaction. There's a bunch of different pathways that all differ in their mechanism of action.

One event that comes to mind is the use of radiation on cancer patients. Radiation is an external event that can trigger apoptosis in humans 1. When cancer patients receive radiation, the treatment is localized. The brain isn't telling the cells to die it is the radiation effects on the cell.

Ionizing radiation can also induce apoptosis via the generation of free radical oxygen species 2.

Free radical oxygen species does this by searching for an electrons in the molecular make up of the cell 3.


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On evolution statistics
This basic evolution theory question has been haunting me since childhood and I'm kind of embarrassed that I can't explain it yet:
Consider a butterfly. It's wings have evolved to look like the eyes of an owl, so to prevent it's predators who are themselves preys of the owl to attack it.
From what I've learned (and feel free to indulge me in the very basics if I get this wrong), natural selection suggests that the butterflies that didn't have the owl's eyes in their wings would be eaten, leaving the ones with the eyes to survive, right?
But that implies that this useful trait appeared in the butterfly's wings by chance. Now, I know trillions of butterflies have been born before this, but trying to figure out the possibility of this to happen by chance doesn't look like it's plausible. Let's go through the things that have to work right before this trait is passed over:

For a butterfly to be born in a different wing colour, it should be a genetic mutation which doesn't happen this often, for what I know.
The wings are composed of micro-scales. For every scale to compose an image so similar that confuses even us, the margin of error is very slim. It could be anything. It could be a picture of Tom Selleck for all we know. The scales must be in the correct spectrum of colour by a small margin of error. So that is already a very unlikely thing to happen.
Then, this butterfly cannot be eaten out of bad luck (mind you, the wings don't guarantee it will not be eaten, just enlarge her chances).
It has to mate, which also is not a guarantee to happen, since nature deals with competition. If this butterfly we are considering is a male, the female must find the wings hot, instead of being afraid of those creepy eyes.
The genes of this mutations must also be dominant, so when it mates and generates offspring, at least part of the new butterflies inherit this trait.

And this is a simple example. There are animals that evolved so smartly I can't even start to think of the possibilities.
My question is, more precisely, how likely is it for a species to evolve into complex solutions?

And still: Mutations happen by chance. Having a relationship where one of the participants is eaten when his mimicry isn't good enough puts a strong selection pressure on the related genes. So you will gradually collect mutations which are responsible for this pattern.

As link only answer are discouraged here is a link only comment; See On the Origin of Species (1859)

This is the OP's only post and basically is asking an ID sort of question that has been answered elsewhere at great length.

have you stopped to imagine that it is us that associate random patterns on butterly wings with different identifiable features like eyes .. It could be anything that scares off predators.. It supposedly looks like eyes doesn't mean that this is the only pattern that came with mutation.. There would have been many others among which this particular pattern was probably more effective at its job..

Thanks @Chris! You started to enlighten what Remi.b and prooffreader tackled in larger detail.

@daniel I am sorry, I tried to build a lightheaded question, otherwise people well above this knowledge level would feel like they wasted their time reading (since it ended up longer than I expected). But now I see that I exaggerated the beginning. I am not that guilty of not looking for an answer though. I searched around, but my vocabulary on the matter is not as vast, as you can notice. I thought on making an effort to change the question, but since you already pointed it out and both answers were more than satisfactory, the change would be frivolous. Promise to be careful next time.

@TheLastWord Yeah, as the others pointed out, it makes more sense that more detailed images come up in time.

what exactly is your question? Is it "How many years would it theoretically take to achieve this?" ?

@daniel.. Actually I am sympathetic towards the OP. The wikipedia article on evolution or any other online discourses and even most books on evolution do not emphasize on the timescales associated with the process of evolution. The OP is not hinting at ID. I think they are just flabbergasted about the fact that such a complex process is generally explained in one line without a substantial explanation. A good book on phylogenetics is what I can suggest to OP (such as Molecular Evolution & Phylogenetics by Masatoshi Nei).

I am closing this question as too broad.. I still think this is not off topic.

Ok, @WYSIWYG I think I found a way to ask what I was curious about simply. Let me know if it's satisfactory.

@WSIWYG: Yes--OP responded reasonably and I deleted my longer comment. 'Too broad' works fine. I left the original comment because that reason for closure also applies. There is a history of such questions here, which is not the OP's fault.

@Digger. this is still very broad. There are two aspects to this. A general mutation rate giving rise to a phenotype and fixation of some mutations due to predation. In a question which encompasses all aspects, it is difficult to answer (one can write a review article rather:P). You can check this article out; it is about evolution of predator-prey interactions. Remi might know better about the best mathematical models for this.

@WYSIWYG Oh, both answers below were exactly what I was looking for and beyond. I'm also reading new articles about the subject (together with The Selfish Gene, although it doesn't seem to go over this broad question). So what I'm trying to do is find a question that the answers below correspond, otherwise it would seem as if they didn't answer me correctly. Since I'm already satisfied, the idea is to make this post searchable, right?

This question is only off topic if evolution has nothing to do with biology.

Remi.b's answer is great, but here's something less technical if that's what you're looking for:

Genetic mutations happen ALL THE TIME. Every time a cell divides, there is an error rate of about one per billion. That's a very low error rate per division, but when you multiply it by the number of divisions, times the number of cells, times the number of individuals, times the number of years the species has existed... well, that's a lot of mutations. Mind you, way fewer mutations will get passed along to offspring, because the vast majority of mutations are non-advantageous (because there a lot more ways to make a bad butterfly than a good one). But that's the job of selection, not mutation.
Evolution is a step-by-step process. There doesn't just have to be mutation and advantage, there has to be an advantage every step of the way. If big circles were selected for, that means intermediate forms (smaller circles, perhaps?) were selected for too. A blob that sort of looks like Tom Selleck will not confer as many fitness advantages as a blob that looks a lot like Tom Selleck (assuming the butterflies' predators hate Magnum P.I., which as far as I'm concerned is a perfectly reasonable assumption ;-)
Lots of butterflies get eaten by bad luck. But it's unlikely any trait was the result of one mutation in one individual (although it does happen sometimes). There are lots of mutations happening, and if one individual doesn't pass it along, another will. Think of this: maybe 100,000,000 years ago some butterfly developed a mutation that would be ten times more effective at discouraging predators than the owl-eye circles ... but then it got stepped on by a dinosaur. You'd never know it happened, and you're left eons later wondering how a way less impressive mutation happened.
There's natural selection, and there's sexual selection. Maybe the females don't like the owl-eye wings so those butterflies mate half as often as their more attractive brethren. But if the resulting offspring is four times more likely to survive, that ugly butterfly just won the gene pool lottery.
That's a common misconception, traits don't have to be dominant in order to be selected for. Think of this: lactose intolerance is dominant, but in many populations lactose intolerant people are in the minority, because after the domestication of the cow being lactose intolerant was enough of a disadvantage to make those people less likely to have offspring.

One of the concepts people most often lack when dealing with evolution is of scale. You're looking at a tiny, tiny, tiny fraction of all the mutations that could have possibly happened and thinking, "What are the odds that that happened, it seems so improbable!" But that's because you're not seeing the trillions and trillions and trillions of mutations that could have happened if random chance had taken things in an ever so slightly different direction. SOMETHING had to happen, it's the laws of physics. You're only able to see and be amazed by what did happen... well, because it's the thing that ended up happening. The more you think about it, the easier it is to wrap your mind around.

Incredible! Thank you! Putting it that way made me realize what I've been missing easily. It's wondrous to think that so many incredible mutations could happen that didn't move forward out of bad luck...

In your 5 points you basically cover several concepts of evolutionary biology.
1) The number of mutations depend on mutation rate. The mutation rate varies along genome sequences, species and individuals. According to the recent DECODE study (Kong et al., 2012) a human mother transmit on average 15 mutations to her offspring and a human father transmit on average $25 + 2(g-20)$ mutations to his offsprings, where $g$ is the age of the father and where the formula stands only for father older than 20 years old.
2) Mutations happen by chance and are not directed toward creating some specific feature. But it is much more likely to create a round of color on the wings of a butterfly than creating the picture of Tom Sellek. The reason has to do with the developmental and biochemical pathways linking the given mutation to its phenotypic effect. Looking at a given mutation, you can understand how it yield to the modification of some phenotypic trait by looking at the biochemical and devlopmental pathways.
3,4) The third point that you raise is called "genetic drift". Shortly speaking the concept of genetic drift may be called the good luck/bad luck effects. Stating differently genetic drift is the random sampling of alleles (gene variant) from a population. If some alleles are favored over some others at a given locus, then sampling is not 100% random but is not either 100% deterministic. The only case where genetic drift is absent is in infinite population (which is obviously an unrealistic case). Genetic drift is inversely propotional to population size and you'll understand it better by reading this post.
5) When the mutation is at very low frequency, the mutation needs to be dominant in order to be expressed, this is true. But an allele may increase in frequency due to genetic drift up to the point that some individuals are homozygous for this allele and therefore express the trait. Dominance and recessivity are just extreme case of a continuum and most often alleles have intermediate level of dominance. Pleiotropy is also something to consider. Note also thaat the frequency of the three possible genotypes $AA$, $AB$ and $BB$ are given by Hardy-Weinberg law (under some assumptions) $x^2$, $2x(1-x)$ and $(1-x)^2$ respectively, where $x$ is the frequency of the allele $A$.
Hope that helps!

@Digger There is no such think as a question in your post so please let me know if I missed your point or if I answered your question.

Thank you so much! Your answer not only enlightened my question but also gave me new vocabulary for me to know more about it. I will be reading more about the matter, specially your answer on my 2nd topic. @prooffreader's answer only got my vote because a few thing on your answer went over my head (not your fault, obviously). I wish I could vote on both your answers.