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Why do we need deep sequencing?
Why do we need deep sequencing? Why cannot the sequencing technologies read all the nucleotides correctly at the first read? Sorry since this question is too trivial, I don't have a biological background at all, and I have just started doing research in CompBio. Thanks.

Short Answer
In a nutshell, DNA sequencing technology has a limit to how long a stretch of DNA it can read in one go.
Long Answer
So what most commonly occurs is the length of DNA you wish to sequence needs to be (almost randomly) chopped up into given lengths (depending on the technology) and each length or read is sequenced in parallel. But now you don't know which lengths to stick together! i.e. the ordering of these chopped up lengths. So you sequence it many times over (deeper) and this way you can align contiguous ends of these lengths together like a jigsaw puzzle. The more times you sequence the more accurately the 'contigs' will be aligned.
DNA Assembly Diagram

Comment if you want more details, but the technical term you want to google is "sequencing assembly".
Here's the wiki
:)

Thanks, this helps a lot! One more trivial question, and I will get it completely :) The sources I checked on "sequencing assembly" usually assume some background which I don't have, so they don't answer my following question: Why the lengths that would be read are chopped almost randomly which would require this alignment stuff, and not chopped in sequential order of the DNA stretch and just augmented to each other after being read in parallel? I am sure you are smiling at this question right now :) But thanks in advance!

Actually it is a good question because I must have been quite ignorant in my past lectures since I do not "know" the answer but I can make a good guess: It is because you cannot handle the DNA like that, remember it is a chemical! You put it in a solution and you cant just "grab it" with a tweezer, snip it here and there with scissors. You chop it with enzymes that make cuts at highly repeating regions along the sequence - the pieces that result just diffuse around and boom you have a broken jigsaw to solve

If comments or answers have helped don't forget to "up vote" to help the community :)

Thanks! This helps a lot, too. I accepted the answer, but cannot vote up yet because I am new here so I need 3 more reputations for that :)

^^ restrictions... what field is it you are from? and why the Bioinformatics question?

I have Computer Science major and started PhD in CompBio.

@user5054. I just re-read this now, if you find Bioinformatics terminology tricky, then you would benefit from reading the "Glossary" sections of well-established Bioinformatics resources. Example: https://www.vectorbase.org/glossary

Deep sequencing is naturally error prone.  Sequencing will never be perfect, because no enzyme will ever perform 100.00000% perfectly.
In Illumina sequencing, you put your starting molecule down on the flowcell, then the polymerase makes a cluster of copies around it.  But at each step of building each copy, there's a chance the polymerase will make a mistake.  Then at sequencing, a single complementary labeled dideoxynucleotide is added to the complementary chain.  But there is always a chance the enzyme will make a mistake.  Then after the base is read, the label needs to be cleaved.  Another step where the enzyme might make a mistake.  Then the base is converted to deoxy, another possible error.  Even if each step is very unlikely to fail, after a lot of steps, there will be enough problems that the cluster won't show the correct color uniformly.  The software tries to compensate, but the result is that you will have reads with inaccuracies.  That's why you have to have depth.

Another important point is that we almost always sequence a population of cells, not just a single cell. Cancer cell populations, for example, can have multiple sub-populations of cells with different genetics (subclones). Deep read sequencing allows us to see this heterogeneity, and also measure the abundance of each sub-clone. Even with a single cell, we can see the abundance of different alleles... Usually 50-50 in normal cells, but can get pretty crazy in cancer.


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Why can cats interpret things on a monitor/tv, but dogs cannot?
E.g. you can see a lot of videos where cats are smashing some mouse or spider on an ipad, but I have never seen it with a dog. I have a dog myself and I know that he sometimes responds to the sounds from the TV, but not to the images.
Why is that?

Cats and dogs can both view tv screens & monitors ... though their viewing experience is a little different to ours thanks to differences in cone structure leaving them color blind and giving low acuity.
Both species have lower levels of color vision than humans. Cats see slightly more color (in the blue green and yellow end of the spectrum) than dogs do so they may get more of an immersive experience from watching TV.
Further, cats and dogs need a higher frame rate than humans to make it appear as a smooth film, a phenomenon known as flicker fusion, in humans we require 15-20 frames per second, dogs require 70fps and cats about 100. Before the frame rate of televisions increased in recent years it would appeared to them to be flashing images, similar to when you point a digital camera at a screen which may explain why the dog is not interested in the TV, it'd be like staring at a strobe for hours on end. Here is a paper which discusses flicker rates and color vision in dogs.
To summarize there are several factors which influence the "enjoyment" an animal can take from watching a TV - their response to TV imagery will depend on the frames per second, colors, contrast, clarity, movement, subject matter, and (perhaps most importantly in my opinion) the temperament of the animal, for all of which there are difference between the species.
From sciencenordic.com:

"We humans need about 16 to 20 images a second to perceive what we see
  as continuous film, whereas dogs need about 70 images per second.
So a few years ago, Fido was probably confounded by his master's
  behaviour of sitting for hours staring at a flashing succession of
  images. With modern resolution and quicker imaging, dogs have become
  potential television viewers.
This has not gone unrecognised in the USA, for example, where hopeful
  TV producers have started special TV channels for dogs.
If you have other pets, however, you need to think twice before
  placing them in front of the TV.
Birds need at least 100 frames per second to see TV images as a moving
  picture. Having a bird in the same room as a TV with a lower frame
  rate than that will be very stressful for the creature."

@derfder I've added some more content for you to make more comparisons between dogs and cats.

Some dogs definitely react to TV, otherwise I don't see how people came up with channels specifically for dogs like this one: https://www.dogtv.com

source: Stack Exchange

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sort: votes


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Mass production of bacteria
Is there a way to mass produce a certain species of bacteria?
Answers I am looking for should not involve a Petri dish: I am only interested in protocols involving, perhaps, more efficient mediums to grow the bacterium-in-question.
Is it done with any yet? In a factory or where etc?
How is it done?

The fed batch culture is a means of bacterial production that is used in industrial setups. Nutrients are fed into the chamber with controlled ideal conditions for growth of a particular species of microorganisms.
Upon reaching the desired yield temperatures can be increased (depending on the species of bacteria) to facilitate spore formation for eventual harvesting.

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By what mechanism can hypoglycemia induce fainting?
Hypoglycemia (Low blood sugar) is said to be among the potential causes of human-faintings. I was wondering by which mechanism this happens. Google search results are abundant; there are lists of various causes and solutions, but I couldn't find a direct answer to my question.
Is it a controlled reduction of heart function to save energy? Is it an uncontrolled shock reaction (malfunction)? I'm looking for an answer along those lines.
Thanks.

The following article may be of relevance: http://www.ncbi.nlm.nih.gov/pubmed/1437055

There are regulatory mechanisms that may prevent moderate hypoglycemia to progress to a more severe state, however these mechanisms act before lack of conciousness sets in. The progression of hypoglycemia may depend on overall health and medical status and vary between healthy and diabetic persons, for example.
Rosenthal et al. (1) write that

The brain is normally dependent on glucose for oxidative metabolism
  and function. Acute iatrogenic hypoglycemia, occurring as a result of
  insulin excess during the treatment of type 1 diabetes, can cause
  clinically significant cognitive impairment. In health, such
  hypoglycemic cognitive dysfunction does not occur. Endogenous
  counterregulatory mechanisms are activated in response to a small
  reduction in circulating glucose, preventing more profound
  hypoglycemia. In diabetes, the inability to reduce circulating insulin
  levels (1), the failure of glucagon responses (2), sometimes
  accompanied by defective autonomic and adrenergic responses (3), can
  allow plasma glucose levels to fall low enough to result in detectable
  disturbance of cognitive function, ranging from a subtle slowing of
  reaction times (3) to coma (4).

In short, the brain malfunctions due to lack of glucose (the sole energy source for the brain). Note that cognitive impairment and unconciousness can also occur in otherwise healthy persons, for example in the case of prolonged exercise combined with lack of nutrition. The exact cause of cortical dysfunction is not known:

Impairment of brain function is a recognized consequence of acute
  hypoglycemia. It is known that different brain functions have
  different susceptibilities to acute hypoglycemia; for example, the
  triggering of autonomic activation, a hypothalamic function, occurs in
  response to quite modest decrements in circulating glucose
  concentrations (5,6,7), whereas significant cortical dysfunction
  requires more profound glucose deprivation (3). Even within different
  cortical functions, there is variation in hypoglycemia susceptibility
  (26). The mechanisms of cortical dysfunction during hypoglycemia are
  not known.


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How credible is the Remenko's two-component color vision theory?
I've come across an article (in Russian), which describes a nonlinear two-component color vision theory made in 1975 by S. Remenko. The article heavily criticizes trichromatic theory as very imperfect. There's a whole page related to the criticism. Some of the citations there refer to Feynman's lectures vol. I ch. 35, where also some doubts are expressed. See e.g. the part by Feynman:

Using the three different kinds of color blindness, the three pigment response curves have finally been determined, and are shown in Fig. 35–8. Finally? Perhaps. There is a question as to whether the three-pigment idea is right, whether color blindness results from lack of one pigment, and even whether the color-mix data on color blindness are right. Different workers get different results. This field is still very much under development.

But the only English-language place I've found mentioning Remenko's two-component theory was the book "Computer Systems for Healthcare and Medicine" by Piotr Bilski and Francesca Guerriero, where the first name also looks suspiciously Russian.
So I'm somewhat skeptic about credibility of all this Remenko's theory and the criticism of the trichromatic theory. But having not much expertise in color vision theories, I thus prefer to ask the experts: is the theory by Remenko actually credible? Is it even known outside of Russian-speaking world? Has it been falsified? Is trichromatic theory really flawed in any significant way so that a replacement theory would be required (are Feynman's remarks out of date?)?

We have the physiology of colour vision nailed down pretty precisely, across a broad suite of species. There are some subtleties (there aren't, strictly, only three receptors involved in vision, and the number and properties of the receptors differ between species). But the general theory is still basically trichromatic theory. If the mechanisms in 'two-component theory' are very different, then that theory is very wrong. See https://biology.stackexchange.com/questions/39882/are-some-animals-like-dogs-and-cats-color-blind-and-how-do-we-know-that/39890

answering your sub-Q: Remenko's theory of color vision is not really shows up on Google search. So it is likely very esoteric

This is a confirmation of the theory of Remenko.
https://www.pnas.org/content/113/29/8206

It's not: Remenko's theory doesn't use any chromatic aberration to explain anything; moreover, it's two-component while the paper you link is about one-component+chromatic aberration.

That era produced a lot of very questionable science from Russia; there is no good reason to doubt the three-component color vision theory, and it's also the basis of all RGB TVs and computer monitors. However, I can't read Russian so I don't have any idea what this two-component theory is.
Typical humans have three cone cells, which is the biological origin of having three components for color vision. Colorblind individuals who lack one of the three cones have color discrimination issues consistent with the three component model. I am not aware of any credible research that questions this.
The lack of further study into the theory you refer to probably puts it into the category of "not even wrong" - based on such flawed reasoning or premises that it isn't worth disputing.

Nathans, J., Merbs, S. L., Sung, C. H., Weitz, C. J., & Wang, Y. (1992). Molecular genetics of human visual pigments. Annual review of genetics, 26(1), 403-424.

Please see the edit to the question. I've added some relevant part of the Feynman's remarks about validity of trichromatic theory.

@Ruslan Color-blindness is slightly more complicated because not everyone's color-blindness is because they are missing a particular cone. The others are because of shifts in the wavelengths the pigments are sensitive to.

It is worth mentioning hte other component of color vision which is how our brain processes color and how opponent colors work. https://en.wikipedia.org/wiki/Opponent_process

Remenko’s theory may only be dismissed (in favor of the L/M/S-cones theory) after obtaining a conclusive evidence of blue-sensitive (S) cones in humans; or at least, some primates.
How did Nathans, Merbs, Sung, Weitz & Wang (or anybody else) prove that OPN1SW is the “short wave sensitive opsin”? Has OPN1SW been extracted from a cone? IMHO various Internet “authorities” merely replicate opinion pieces. Hopefully science doesn’t work like this, where linking to Wikipedia, having the ♦ thing, 25k rep, and bashing USSR for Lysenkoism is sufficient for a heap of upvotes.

@IncnisMrsi You are free to write your own answer.

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Is it possible to simulate tetrachromatic vision in a trichromat?
Suppose we are able to stimulate the whole matrix of cones of a human retina, targeting each cone individually¹. Normally we would project an image in the LMS color space onto the cones, in such a way that each sub-image of particular color channel would get to cones of corresponding type. As the eye moves, this image would be adjusted so as to create an illusion of real surrounding (similarly to a VR headset).
Suppose now we think up a new spectral sensitivity function $P(\lambda)$. We choose a subset of e.g. M cones to represent this type of sensitivity, making sure that this set is scattered enough around the M cones so as to avoid clumping the same color channel cones. And then we try to simulate tetrachromatic vision by replacing the M-channel sub-image in the projection by a special sub-image that an actual sensor with $P(\lambda)$ would capture.
Would this result in a sensation of a new color having appeared in the image, or would this be simply a lot of noise in the visual field?

¹The technology is not quite there, but on the way: see e.g. this answer.

I think your question would be better if you provided more background information — at a minimum adding links for things like "LMS color space" will make your question somewhat more accessible. In addition, the material about eye-tracking seems superfluous and to me distracts from the question. Finally, my (non-specialist) understanding is that people with tetrachromatic vision have been identified, which perhaps obviates your question?

@tyersome OK, I've added the link to LMS color space@Wikipedia. Regarding the existing human tetrachromats, no, this doesn't obviate the question: I still wonder whether the people who don't have corresponding phenotype are able to have tetrachromatic-like sensations, and whether the choice of the type-four cones makes it any different. Moreover, there might be some limitation in the brain, restricting, if not potential for tetrachromacy,then maybe for pentachromacy—or there might not be—which is what I'm also interested in.The eye-tracking material was a description of the thought experiment.

I think the thought experiment contributes to this questions seeming too speculative (i.e. any answer would be primarily opinion and thus would not meet the criteria for this site). ——— Are really really interested in whether adults can adjust to new color inputs? If so, there are reports about people acquiring UV vision after cataract surgery.

@tyersome well, UV vision is not a new color: basically, just an extension of S cone sensitivity. Namely, those people see UV simply as violet, which isn't a new color (the same cones are stimulated by 370 nm light as by 400 nm). I'm not looking for opinions, but rather an answer from the position of modern neuroscience theories about how brain functions regarding the processing of the input signals from cone/rod cells.

And finally, I'm interested in how color vision works from the POV of my thought experiment: e.g. whether the neurons connected to different cone types are predefined to particular color channels, or it's possible to repurpose them for a different sensitivity curve by some kind of modification, so as to get completely new colors and higher-dimensional color gamuts.

The experiment on squirrel monkeys is much closer to my idea than aphakic human UV vision, but it still leaves some doubts because the species already has large percentage of trichromats (77%of females), so the male brain may be genetically prepared to handle third cone type thus enabling the success of this experiment. In humans, OTOH, only 12%of females have 4 cone types, and only a small fraction of these are actually tetrachromats.That does leave some doubts on whether every trichromatic human can be made tetrachromatic,more so penta-.

I think it's an interesting question, but there are 4 sub-questions that share little overlap in some cases. It's best to ask focused questions. Feel free to split them up in multiple posts

@AliceD OK, I've removed the sub-questions that depend on the first one. However, I think there's no use in asking them in multiple posts until this one is answered, exactly because they depend on the first question.

Surely a great thing to wait with asking a fellow up question. Good luck!

How is this different than what is done now with false-color photography?  If I understand correctly, all you're doing is mapping the (R,G,B,UV) color space into (R,G,B), which doesn't result in any "new" color sensation.

@jamesqf the difference here is that e.g. you repurpose part of the set of e.g. M cones to another sensitivity curve. This could result in two possible outcomes: 1) The human sees a noisy image, as if looking at raw undeveloped Bayer-pattern image, but with the pattern following the direction of looking akin to an afterimage. 2) Due to fine dispersion of one set in the other, the signal from the retina is somehow demosaiced by the brain, resulting in a smooth new color. I wonder which of these outcomes would actually happen.

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How close genetically is the most human-like chimpanzee to the most chimp-like human?
I understand that:

Chimpanzees are the closest species to humans genetically. Only 1%-6% of their genes are different.
Within any species there is genetic diversity, i.e. no two individuals have the same exact DNA sequence.
This variability applies to humans and chimps.
Thus, there exists a pair consisting of a human and a chimp that will have the smallest number of different (edit: genes) DNA base-pairs within the two populations. One can say that the pair forms an "inter-species genetic gap".

Question: What is the smallest estimated inter-species genetic gap between humans and chimpanzees?
Edit: I changed the last point to base-pairs instead of genes. Most of the comments seem to suggest the population genetic variabilities are much, much smaller than the genetic distance between the populations. Visually, that looks something like this:

Is this a fairly accurate picture of the human-chimp genetic distance?

This closest pair of human-chimp is probably very negligibly more related than a random pair of human-chimpanzee. (But I haven't go through any evidence it is just a gut feeling).

As far as I know, all humans have the same genes. Ditto for chimps. Variations within humans aren't due to possessing different genes, they are do to having different variations (alleles) of the same portfolio of genes. Again, ditto for chimps. Your fourth point is suspect as applied to genes. Although, it is possible for a particular chimp and particular human to share a more similar package, compared to other individuals, of alleles for the genes that are in common.

@bpedit In reaction to: Variations within humans aren't due to possessing different genes, they are do to having different variations (alleles). There is lots of copy number variation in humans (Redon et al. 2006).

I updated the last point, changing genes to base-pairs. That seems to be a more clear way to phrase the question.

Do you expect a theoretical expectation or an empirical observation? Empirically, I am afraid we have sequenced way too few chimps and sampled humans for sequencing in a way that is way too biased (96% of sequenced people are from european descent) to answer this question. One could probably draw some conclusion from theoretical work though.

I see. Right, it would basically require sequencing every human and every chimp to get the exact answer. I think even something that approximates the gap between the 95% CIs of the two populations would be acceptable.

But would you be happy with a theoretical prediction (which I could do but it would take me some time; would be a good exercise for me though) or are you looking exclusively for an empirical observation.

Yes, theoretical prediction should work as well.

You may be interested in this 2005 Nature paper from the Chimpanzee Sequencing and Analysis Consortium: Initial sequence of the chimpanzee genome and comparison with the human genome. It breaks down the most common categories of genetic variation:

Single-nucleotide substitutions occur at a mean rate of 1.23% between copies of the human and chimpanzee genome, with 1.06% or less corresponding to fixed divergence between the species.

So if we accept their analysis, ~1% (it says "or less", but elsewhere in the paper they estimate a lower bound of ~0.96%) of the genome difference consists of fixed single-nucleotide differences between species.

Small insertions and deletions: On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ~90 Mb. This difference corresponds to ~3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies.

So another ~3% comes from small insertions and deletions, which gives around a ~4% fixed divergence between populations. This rough estimate of the fixed genetic distance between humans and chimpanzees is probably a reasonable estimate of the distance between the nearest human-chimpanzee pair.
If you also want to know how far apart the two furthest humans are, as @Remi.b mentioned, the populations we've sequenced don't span the whole diversity of our species, but it is likely much smaller. You could look at some of the HapMap or Human Genome Diversity Project papers. For reference, when Watson's genome was sequenced, they reported around 0.1% of the sequence to be different from the reference genome, but that isn't a particularly diverse comparison.
You may also be interested in this paper comparing the human, chimpanzee, and bonobo genomes: http://www.nature.com/nature/journal/v486/n7404/full/nature11128.html.

The answer given by leekaiinthesky and partially in the comments on the question give a good general picture. I also think that the variation within the respective species is way less than between the species. Keep in mind that also archaic humans like Neandertals fall outside of the variation of present-day humans when you do a genome-wide (nuclear genome and mt-chromosome) comparison (see Briggs et al. (2009) for the mt-genome, and Green et al. (2010) for the first draft nuclear genome and Prufer et al. (2014) for the high-quality genome. Looking at Meyer et al. (2012) you see that even Denisova genomes falls outside of Neandertal variation for whole genomes); this means that looking at phylogenetic trees of either nuclear or mt-genomes, the Neandertal always forms an outgroup, independent from what present-day human populations you are looking at. This is roughly quantified to 1% difference between humans and chimpanzees, 0.2% difference between present-day-humans and Neandertals and 0.1% difference within present-day humans. The latter two seem to be fairly close, but: there are no fixed differences between present-day human populations, and this will blur the differences in intra-present-day human populations compared to the differences of present-day humans and Neandertals or chimpanzees.
However, there is one aspect that has not been discussed here which I think is very important for your considerations: trans-species polymorphisms (TSP). In the first part of my answer I was careful to always pronounce that major differences can be observed genome-wide, but genomes have a mosaic structure. When you look at specific parts of the genome, i.e. genes or haplotypes, these major differences do not hold and TSP are a very interesting special case of that. TSP are basically just gene variants, i.e. alleles, that are shared between species. This means that individuals between species might have the same variant, but individuals from the respective same species might have other variants. In simple terms this can be seen as individuals between species are more closely related at a given gene locus than individuals within species. Shared polymorphisms between species can in principal be caused by three mechanisms: (i) Genetic admixture and introgression, (ii) molecular convergence and (iii) TSP by either incomplete lineage sorting or splits in the lineage of alleles that predates the split of the species and both alleles are maintained in both species [Těšický and Vinkler (2015)]. This figure from Těšický and Vinkler (2015) shows the three mechanisms (see the green genealogy for an incompletely sorted lineage and the red genealogy for a lineage with an early allele lineage split).

The first two are fairly unlikely in our case, even though there is some evidence that admixture between humans and chimpanzees happened after the initial lineages split [Patterson et al. (2006)]. Incomplete lineage sorting or early splits in the allele lineage, i.e. the TSP variants are identical by descent, can be seen as TSP in a narrow sense. And this type of TSP has been described between humans and chimpanzees especially for immune-related regions (see Azevedo et al. (2015) for a review) that are under long-term balancing selection. You can think of this as a selective pressure that is fairly constant in time, acting on different species over a wide geographical range, and triggering a similar selective response in the species involved. Given that, it makes sense that the candidate genes are immune-related as most likely that selective pressure is mediated by pathogens. Azevedo et al. (2015) also note that maintenance of TSP variants by balancing selection is most likely mediated by heterozygote advantage or frequency-dependent selection - both make sense in a pathogen co-evolution scenario. So far, the number of reported TSP loci is really low (really just below a dozen or so), and there might be two reasons for this that are not mutually exclusive: First and obvious, there might be very few TSP. Second, these loci are very, very difficult to detect (as you want to exclude loci that are identical-by-state due to e.g. recurrent mutation) and we might simply not yet have the tools and power to find most of them.
To draw a bottom-line and come back to your question, I would suggest that your inter-species genetic gap model needs a minor modification. Even though the general picture seems to fit, i.e. there is a significantly larger difference in variation between species than within species, there also is overlap in the far tails between chimpanzees and present-day humans. These overlapping variants are not identical-by-state, i.e. due to random effects or recurrent mutations, but are signatures of polymorphisms in the ancestral population of chimpanzees and humans that are still maintained independently in both the split lineages.

I found at least one example of genes where the same genes and the same alleles exist in both humans and other primates but the frequencies of the different alleles are different in different primate species and those are the genes/alleles associated with the AB0-blood system that humans and other primates share. Citations from this site:

Of the Old World monkeys, the chimpanzee has been the most studied
  (Socha et al., 1984).  Interestingly, they have predominantly blood
  type A and in rare cases blood type O, but NEVER blood type B (Socha
  et al., 1984).  Most blood systems found in chimpanzees also exist in
  man, but there are some species specific characteristics.

.

In contrast to chimpanzees, gorillas have been found to possess ONLY
  blood type B.

Now you can use some kind of statistic tool often used to determine genetic distance within species, such as the Fixation index on the genes regulating the AB0 blood system.
Using that tool you can say that your genetic distance to gorillas are less if you have blood type B than if you have any other blood type. If you have blood type A your genetic distance to Chimpanzees are less than if you have blood type 0 and your genetic distance to chimpanzees is the largest if you have blood type B. You can do a google image search on "Cavalli Sforza" and find a lot of interesting diagrams where this method is applied to humans.
You could in principle do the same procedure on all genes that Chimpanzees and humans shares but the allele frequencies differ and try to find who has the least genetic distance to the present day chimpanzee population.
According to a study referenced here such areas in the genome are found in genes relating to fighting off diseases, where you might have an evolutionary advantage if you have a different allele than people around you that catches a disease because your allele makes you immune.

A genome-wide analysis searching for evidence of long-lived balancing
  selection -- where the evolutionary process acts not to select the
  single best adaptation but to maintain genetic variation in a
  population -- has uncovered at least six regions of the genome where
  humans and chimpanzees share the same combination of genetic variants.


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Do prey animals fail to see incoming pythons/snakes?
I understand that pythons are considered ambush predators, and I was under the impression that they tend to employ the sit-and-wait strategy: quietly staying in a coiled position near a trail frequented by prey animals, and striking when a prey passes by. However, this is in contrast to the stalk-and-strike strategy I encountered in every video I could find of snakes hunting prey in the wild.
In this video compilation of pythons hunting prey (warning: it's graphic), in every instance shown, the snake can be seen closely approaching the prey, the prey appearing to not notice the snake, and striking when the snake's head is within a few cm/inches of the prey animal.
This seeming appearing-to-not-notice-a-large-snake-nearby behavior can be seen in different animal species:

Pigs: Here
Mice/rats: Here, here, here, here, here, and here
Rabbit: Here
Bird: Here
Possum: Here

Similarly, the-fail-to-notice can be seen another video and here too.
Question: Is the stalk-and-strike strategy the more common hunting strategy that snakes tend to employ? Do the prey really fail to notice a looming large snake? Or do they "play pretend to not see it" as a some sort of adaptive strategy?
My sample of videos could also be biased, but it seems that the sit-and-strike strategy would be more easier to film and thus should be more easy to find in popular video sharing sites. No?

It looks like being close to the ground and having certain patterns send little information to prey about their motion or they blend into the environment.  They tend to be silent also. https://academic.oup.com/beheco/article/24/5/1237/256081


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Effect of single nucleotide deletion or insertion on primer annealing
How is primer annealing, and, consequently, PCR amplification affected by single nucleotide deletion or insertion inside the primer ?
Imagine a primer like this:  GCGTCATAAAGGGGACGTG (primer)   and the corresponding part of template DNA has one G missing, so it looks like this:  GCGTCATAAAGGGACGTG (template).
The possible pairing could be
GCGTCATAAAGGGGACGTG primer
GCGTCATAAA_GGGACGTG template
or
GCGTCATAAAGGGGACGTG primer
GCGTCATAAAGGG_ACGTG template
 or anything in between.
Is it possible that amplification with such primer would be completely disrupted in normal real time PCR at 60°C annealing? Could this completely disrupt the amplification?
If the mismatch was substitution-like, I would be pretty confident, the primer would be still functional and amplification would occur. In the extreme case, it would be at least residual amplification at late Ct. There are a lot of data, how substitution mismatches affect primers and I also have a lot of personal experience with that.
Unfortunately, the deletion mismatches are less studied plus googleproof. The only indication I have found is this work:
Lipsky RH, Mazzanti CM, Rudolph JG, Xu K, Vyas G, Bozak D, et al. DNA melting analysis for detection of single nucleotide polymorphisms. Clin Chem. 2001;47:635-44.
In that work, single nucleotide deletion had similar or lower affect on melting temperature than substitution mismatch. But it was about longer oligos.  Examples:
Effect of deletion:
133 bp fragment, 67 % GC, deletion SNP at position 43, delta Tm (homo-hetero duplex) = 1.2°C
Effects of substitutions:
152 bp fragment, 43 % GC, substitution T to C at position 68, delta Tm (homo-hetero duplex) = 0.9°C
100 bp fragment, 41 % GC, substitution T to C at position 42, delta Tm (homo-hetero duplex) = 1.4°C
163 bp fragment, 60 % GC, substitution C to T at position 86, delta Tm (homo-hetero duplex) = 2.2°C
110 bp fragment, 59 % GC, substitution G to A at position 66, delta Tm (homo-hetero duplex) = 3.8°C
Questions:
1. Can you recommend me literature about how deletion mismatches inside (not at the very end of !!!) primers affect annealing and PCR ?
2. Would You guess the primer in my example would be still functional , at least partly, or would You expect no amplification at all ?

EDIT after your inputs:
This online application " mfold.rna.albany.edu/?q=DINAMelt/Two-state-melting " thinks, deletion mismatches are more destabilising than substitutions, at least for short primers. For my own example, it calculated delta Tm (homo-hetero duplex) = 12.9°C .
If I try substitution mismatches instead, delta Tm (homo-hetero duplex) is in interval 3,8°C to 5,7°C.
New question  If you have experience as similar as possible to my case, which is 19 nt long primer with single nucleotide deletion in the comlementary template at position cca 6 - 9 from 3' primer end, annealing temperature used at 60°C, please let me know if You achieved amplification or not.  Please, give me a respective reference, if you have it, so I will quote it in my review :-) .
Also, I am still interested in general info, as long as the topic is narrow enough to be about single nucleotide deletions or insertions in primers. (Not substitution mismatches).

primers would be functional as long as the 3'ends match properly and the mismatch is not huge. You can calculate the changed melting temperature using UNAfold DNA-DNA hybridization server.

Very neat application, thanks ! For the benefit of others - I have found where exactly one enters the sequences at the server: http://mfold.rna.albany.edu/?q=DINAMelt/Two-state-melting

Similar to @Chris, I've used longer, even ultra-mers to cause deletions.  I've been curious about how small I could make the primers, but I've always had the luxury of being able to make them pretty long without worrisome 2ndary structures.  Have you considered trying this on a test template to see how it goes?  Wouldn't be too costly to test (I've considered it).

We used this kind of primers to generate out of frame mutations or to add additional bases. In my experience your PCR will work (probably a a lower efficiency) and you will get a product with an additional base. We used primers with bigger differences in PCR based site directed mutagenesis of plasmids, there up to 10 bases didn't match but the primers where also longer. For single nucleotide mismatches (either + or - one base) we used primers around this size.
Regarding the literature, this publications might be useful:

A guide to the design and use of mismatched and degenerate
primers
Effects of primer-template mismatches on the polymerase chain
reaction: Human immunodeficiency virus type 1 model studies
The Effects of Internal Primer-Template Mismatches on RT-PCR: HIV-1
Model Studies
Effect of primer mismatch, annealing temperature and PCR cycle number
on 16S rRNA gene-targetting bacterial community analysis

Especially the first publication contains a lot of other interestings references.

If you do not wory about your identity, would you mind sending me a reference for your publication, where there was primer of this size (cca 19 nt), had a single nucleotide deletion or insertion, and still worked ? ( Iknow I am probably too demanding, because you have sent me 4 publications already. It would just be convenient to have reference for this specific example right away).

No big deal: Look at this paper, the sequences are in the supplemental data. The shortest primer pairs are 25mers. The length is dictated by the surrounding sequence.

@Barbara What I forgot: I recently used sligtly shorter primers (21 and 22mers) but this results are not published yet.

@ Chris: Thanks, at least I have assurance, it can work this way. But if by chance you'll remember you have a poster presentation where those short primers are mentioned, please, let me know.

@ Chris again: The articles you listed say nothing about single nucleotide deletions, with the exception of Kwok 2014, which says minimum. (Kwok says, the primers can be used to indtroduce indel SNP and that they should be placed in the middle of 24 - 36 base oligo.) Your own article mentions only long (46 nt) oligos spanning 3nt indel. Am I overlooking something ?

Yes, you do. In the supplemental document there are 25mers documented.

@ Chris  The only 25 nt long primers are N278D-F and N278D-R. Blasting them against nrnt database shows, that N278D-F has a central G, where most mice have A. N278D-R has a central C, where most mice have T. It looks like substitution mismatches, not indels. (Limiting blast to Homo sapiens does not give good primer matches). In which primer is an indel mismatch and which template should I blast it against to see the indel myself ?

I never talked about indels, for this purpose you will need longer oligos. This short primer was used to introduce a point mutation. Which worked quite well according to our sequencing results.

@ Chris  Where does the information come from, that (single nucleotide) indels are more destabilising to annealing than substitutions ? (Maybe we use different definition of indel and point mutation. What I was talking about are single nucleotide insertions or deletions. But not substitutions)

what do you mean by indels ? In your vocabulary, is single nucleotide deletion or insertion a subtype of indel ?

I name this small changes point mutations (when we only change one nucleotide to another to express a different amino acid). Otherwise I stick to the definition of indel, that you find in the Wikipedia: "In germline and somatic mutation studies, indel describes a special mutation class, defined as a mutation resulting in both an insertion of nucleotides and a deletion nucleotides which results in a net change in the total number of nucleotides, where both changes are nearby on the DNA."

Your answer confuses me further. For clarity, let us just speak about frame shift mutations caused by only one nucleotide insertion or deletion. Do you have citation about 25 nucleotide long (or shorter) primer, which harbors single nucleotide-based frameshift mutation in the middle ?

I haven't done frame shift mutations since this doesn't occur in the transcription factor would analyze (it would be embryonical lethal). What we have done is to introduce point mutations (exchanging single nucleotides against others) and here relatively short primers can work (the N278D mutation in the paper mentioned above is done with a 25mer).

Thanks. Now, which part of Your main answer (not comments) pertains to single nucleotide-based frameshift mutation ? Did you previously work with cca 19-22 nucleotide long primer with single nucleotide-based frameshift mutation in the middle ?

Adding another reference. This group looks at the effect of different mismatches (e.g. A>T vs A>G) and also looks at positional effects.

Our results show that single mismatches instigate a broad variety of
  effects, ranging from minor (<1.5 cycle threshold, eg, A–C, C–A, T–G,
  G–T) to severe impact (>7.0 cycle threshold, eg, A–A, G–A, A–G, C–C)
  on PCR amplification. A clear relationship between specific mismatch
  types, position, and impact was found.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2797725/

I was interested in deletions, not substitutions. No matter how much stress this out, people keep sending me info about substitutions in every forum ever.


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

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

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

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

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

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

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

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

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

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

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

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

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

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


text:
Are there sterilisation methods that do not denature proteins as heat does?
Context:
Most countries require milk to be sterilised through radiation or heat to remove possible harmful bacteria. Both of these processes denature the proteins in the milk (ref).
Are there methods of sterilisation that will not denature proteins?

does radiation denature protein?

Why would a denatured protein in milk cause problems in the human body? Could you provide source / example for this?

About what problems in the human body are you talking? Please provide a source for this claim.

Read about pasteurization. Plus denaturing the native proteins won't cause any problem unless of course it coagulates to form an insoluble mass; in any case it is going to be digested in the stomach

I'd recommend removing the claim about human health as it's very questionable. Sterilisation by heat can, depending on the actual temperature, indeed denature proteins. Similarly, strong radiation will ultimately break molecules. I can't tell you whether the levels used to sterilise milk are sufficient to denature anything contained in it though. In general of course, "Are there sterilisation methods that do not denature proteins as heat does?" should be a valid question.

Filtration through a 0.45 micron filter is how we used to routinely sterilize laboratory solutions that we could not sterilize in the autoclave (or if we were in a hurry). This works primarily based on molecular size, so, for example, the viruses, bacteria, and fungi that are larger than the pores  will be retained on the filter, and everything else in the solution will pass through. There are filters available with different sized pores. I have never tried this with a colloid like milk. It seems like this Question was placed "On Hold" so I don't think I could "Answer" it, hence a comment.

Most countries require pasteurization and not sterilization of milk (https://en.wikipedia.org/wiki/Pasteurization), but that also involves heat. It doesn't result in denaturation of the proteins however - who would drink curdled milk?


text:
What do you see if you look at your own retina with the same eye? (optical feedback)
When you record a video while pointing the viewfinder towards the screen showing a live preview you create optical feedback: video example. An anoalogous effect occurs when you turn your microphone towards the speaker.
Once you look at your own retina with the same eye, does our brain create a similar effect as recorded in the video? Or could it be something different all together?
Obviously the best way to find out is to 'just go ahead' and see for myself, but it seems as if I don't have the proper conditions to test this at home: The pupil gets too small in the mirror and thus the retina is plain dark. Such an experiment would require eye drops to force widen the pupil and allow for more light onto the retina.

Dear mods, I'm not confident if this question is fully appropriate for your site or if it's better to post at http://cogsci.stackexchange.com/. Please decide if you need to migrate this question.

There wouldn't be any feedback loop, because retina is not an "output device". You'll need to wire the eye to the visual cortex or something to have a feedback loop you want.

@Memming Indeed, thanks! This is what I have been trying to say in my answer as well.

@gentmatt - why do you link to a youtube video which is private/unaccessible ?

There was an answer posted here and deleted again - which I think has found the error my question. Please undelete it :)
What the eye observes once it glances at the retina is a physically constant image of the retina.
In order for the optical feedback loop to work however, the retina image 'in' the mirror would need to be affected by what is projected onto the retina of the observing eye. Since the retina image in the mirror is constant (there is no link of any kind between whe mirrored retina an the observing retina) the projected image onto the retina of the observing eye is constant as well.
The loop is broken and there is no optical feedback.

I deleted my question just after posting it because I had some doubts and wanted to improve my answer (which I didn't finally :)). But re-reading it, I bet you were right I shouldn't have deleted it.

You would see your retina and that's all. There would have no "mise-en-abyme".
In order to experience this feedback loop you describe, you need to see something which includes the total picture of what you see. For example: You might see a woman holding a frame of the totality of what you see.

When you look at your retina, you can't see something which includes the total picture of what you see, you just see your retina! It would probably work if the retina was a mirror (or any output device)
This question might not really a good fit for Biology.SE. You might have a chance to make a good fit by asking a question on the mechanistic nature of the process called mise-en-abyme on Phylosophy.SE. And ask wether one can live this same process with any of their sense (perception). You can ask whether the Larsen effect (audio feedback) is a similar process to the one we experience when looking at this picture and in what terms they are similar and in what terms they differ. If you ask such question, I welcome you to add the link on this post (except if the post get closed)!

Feedback means that the output from a device is fed back to it as new input. You can feed input to a retina, but cannot take its output.
You will get no feedback if the microphone is not linked to a speaker, or cannot hear the speaker.
You will get no feedback if the video camera is not pointing to the display.
Your eye consumes input, but this input is only used to change the state of your brain in mysterious ways. No output is produced. There is no "Kodak" organ in the human body which reproduces with fidelity the image seen by the retina*. Without output, there is nothing to feed back - same as how you can't get feedback when a camera is not linked to a display. A display, with human beings, would be analogous to a magic machine that reads your mind.
If you looked at your retina, you'd see your retina. Just like a camera pointed at a mirror would see a camera.
The closest thing you can do is imagine yourself, imagining yourself, imagining yourself... Although you would probably need to take mind-altering substances to experience this fully.

*: I say no organ exists, but it is possible for humans to reproduce an image they've seen. It's called "painting". Some famous painters apparently have included an image of themselves in their picture, depicted while painting the picture.
This isn't really a classical painting, but to give an example:

The trouble is that actually painting a picture takes a long time, so the feedback is very slow - each iteration may take days.


text:
How to identify the age of a "living" person?
An Indian old man claims he is [180 years old] now.
We are not able to tell he is 180 or 181 probably. But can we tell he is 90, 120, 100 or 150?
Different people may age differently.
A 60-year old person may appear to be 80, while somebody else could appear younger than their mathematical age. Some other people may have progeria.
What is the most accurate way to identify a living person's age nowadays?
Are there reliable parameters to measure?
C-14 needs a long time base line. Hence, it is suitable for the bone of dead people.
What kind of method can guarantee it can distinguish a 30y and a 80y old person?  What's the error bar of that method?

Cut off a limb and count the rings

possible duplicate of Can we determine a person's age by dating methods or other means?

Birth certificate, I presume :P

@WYSIWYG: Assuming that you a) Have one (and only one); and b) Haven't done some creative editing on it.

@WYSIWYG By the way, a person celebrates his/her birthday on the correct day only for (max) 4 years after his/her birth.

We can tell he isn't 150. People just don't live that long. He almost certainly isn't 120, and very likely isn't 100. The unusual thing about people who lie about their age is not their age. It is that they lie about their age.

@mmesser314  You mean biologically we are not able to tell he is 80 or 180?

@questionhang Scientifically no, we'd have no standard of comparison since people don't live that long.  If there is something that happens to the body post 120 years, we'd have no idea.

@questionhang - Or more realistically, yes. If he was 180, he would have been dead for 60 years at the very least.

@Mercury - A person is a year older when the Earth has gone around the Sun exactly once. This takes about 365 1/4 calendar days. Most calendar years have 365 days. So every 4 years we add a day. This keeps the calendar birthday happening at the right time. Every 100 and 400 years, there are additional leap year adjustments to account for the "about" in about 365 1/4 days.

You have the wrong impression about carbon-14 dating, the long time horizon doesn't have anything to do with not being able to use it to date the age of a living organism. Living things are constantly replenishing the very limited supply of carbon-14 while they are alive. It is only after the organism dies that the carbon-14 clock starts to tick. A dead organism no longer replenishes its supply of carbon-14 and the carbon-14 it did have begins to decay into nitrogen-14. We can then measure the percentage of carbon-14 left in the remains and date them to when they died.

The most accurate method known so far may be Horvath's methylation dating algorithm, which uses 353 CpG sites (Genome Biology research article, Nature news article).
From the Nature article, this method was validated with at least one population.

[After the publication in Genome Biology] Marco Boks at the University Medical Centre Utrecht in the Netherlands applied [the algorithm] to blood samples collected from 96 Dutch veterans of the war in Afghanistan aged between 18 and 53. The correlation between predicted and actual ages was 99.7%, with a median error measured in months.

However, I did not read the original research article and it seems that the dating method works poorly on cancer patients.

DNA methylation is susceptible to environmental factors.

Good article. This may replace teeth as the gold standard.

@anongoodnurse, I was actually hoping someone would argue that dating using teeth would be the best way to estimate the age, since I'm not familiar with this literature.

@Jonathan - See the possible duplicate. I think it's close. I almost posted an answer, but the Nature article surprised me. Plus, you don't need to pull a tooth.

My question is about the error bar in fact. Look at the boldface sentence please.

@anongoodnurse - Besides, a 180 year old man probably doesn't have any teeth left to pull.


text:
How can frogs tolerate freezing while humans cannot?
A wood frog can tolerate the freezing of their blood and other tissues. (wiki, news2), but human beings can not.
Some people plan to freeze their bodies/brains after death, and some of them have done that.
Can wood frogs help us learn how to freeze our brains safely?

@Dexter has the correct answer. Human cells are made mainly of water, it should be fairly obvious what the problem of freezing is. Water expands as it freezes, so the cells begin to rupture due to the expanding ice crystals. Cryoprotectants used to protect cells when they are frozen in Liquid Nitrogen in a lab setting are very toxic. You have a very short window of opportunity when thawing cells to exchange the cryoprotectant with growth medium before the cells start to die. Now multiply this a billion fold and you get an idea of what it would be like when unfreezing a whole body.

Generally frogs are cold blooded animals (more specifically ectothermic or poikilothermic) . Wood frogs can maintain their body temperature by production of cryoprotectants which a human body cannot produce from normal metabolic processes. Such molecules depress the freezing point of tissue and avoid ice formation. Here is a scientific report on the physiology of wood frogs and what helps them survive at freezing temperatures. There are also other mechanisms which cold blooded animals use to survive such conditions.
Now for the human part. Humans are warm blooded (more specifically endothermic). We always try to maintain their body temperature (our normal body temperature is $37^{o}$). That is why we cannot tolerate freezing temperatures, because our physiology does not have a means to avoid cell damage at that temperature. The company which you mentioned uses vitrification methods which uses various artificial cryoprotectants (which wood frog makes naturally).
There is research going on in this direction already. Researchers are using extremophiles and their metabolic products in cosmetics and medicine (like this, this and this).

how long can a wood frog keep frozen if they live in human-controlled cold environment?

No idea. I know for bacteria though. We can keep bacteria for many years in $-80^0$. I have recently used bacteria stored in $-80^0$ after 6 years!

It is  interesting to test how long can wood frogs keep frozen. For bacteria, Russian people are doing the similar things. [http://www.dailymail.co.uk/sciencetech/article-3243056/Is-key-elixir-life-3-5-million-year-old-eternal-bacteria-boosts-longevity-immune-scientists-claim.html]

You should specify that the body temperature provided is in Celsius to avoid a bit of confusion :P.

@JohnOdom $37^0$ F will be frog's body temperature during hibernation :P


text:
what is the difference between homozygous and heterozygous duplication?
In a genetic test result it's written
homozygous duplication

or
heterozygous duplication

Does it mean four copies of the same gene for homozygous duplication and three copies for heterozygous duplication?


text:
Does common X-like picture represent one doubled chromosome or two homologous chromosomes?
What is on common X-like picture of chromosome?
Here is the image from Wikipedia:

Are (for example) lower petals homologous to each other?
If yes, then why (1) is entitled as chromatid: one-half of two identical threadlike strands of a replicated chromosome? Homologous parts are similar but not identical.
If no, then why does human chromosomes are often denoted by Xs:

Do we have 23 Xs (females) or 46 Xs?

You should the wikipedia legends on the post

I have cited important one.

Sure, but if you give more info and thoughts, it might be easier for us to understand what is unclear to you. This seems particularly important as I don't understand your comments below my answer.

@Remi.b note that I am absolutely agree with your answer and this is my "zero hypothesis". But I am confused, that sometimes X-like patterns are apparently used to depict homologous chromosomes.

Ok. If the legend under the figure (wherever you found it) says that it displays homologous chromosomes, then the legend is wrong! A single X-like shape always represents a single chromosome.

Please indicate the source of your second image.

The "X" you see is a chromosome. The two strands that forms the X-shaped chromosome are called chromatids. As they are bound together (by the centromer), they are called sister chromatids. Note that chromosomes look like that only during the metaphase. Note also, that not all chromosomes have a centromer that is in the middle of the chromosome as it is obvious from the picture in your question.
Many species (including humans) have two sets of each chromosome. If you add the other chromosome in the picture, you would see a pair of chromosome. One chromosome of the pair is said to be homologous to the other one. Below is a cladogram during the metaphase of a human (I let you figure out the sex) showing each pair of chromosome.

Sister chromatids are identical (except for mutation during the last chromosomal replication). Homologous chromosomes are similar but not identical. Crossover occurs in between chromatids of homologous chromosomes.
Further comment on your figure
There are 23 pairs of chromosomes, that is 46 chromosomes. Your picture shows only one chromosome per pair, that is your picture shows only 23 chromosomes. In other words, your picture shows the haploid genome and not the diploid genome.

See the picture of human genome. It is depicted as 23 Xs (some not fully formed).

I don't understand your comment. Can you develop? Do you think I answered your question?

So, pictures, depicting 23-24 X-like feutures are just incorrect?

See my update. I have added a picture. These pictures are common. Search human genome in google images.

Sure, I see the picture. I don't understand what you think would be incorrect on this picture based on my answer. Can you please develop further what is unclear? Note that your picture only show a single chromosome (two chromatids) of each of the 23 pairs.

Regard object #1 on my picture. There are ~ 23 of such objects in my picture. Hence, this object is representing 1/23 of genome. Hence, it represents 2 chromosomes. Probably, homologous ones. This object is depicted as X. Hence, strands are homologous, not identical. But you said strands are identical (not regarding mutations).

Please see edit "further comment on your figure"  and let me know if it helps.

To whoever is concerned: Please leave a comment when downvoting. Such downvotes are really not helpful at improving the answer.

I didn't downvote

I never thought you did. No worries!


text:
Is organ transplantation race dependent?
I watched (IMHO canibalistic) movie "Seven Pounds" where protagonist donated many of his organs to other people and I noticed, that most recipients were black also as protagonist was.
Is race really taken into account when organ transplanting?
UPDATE
The question is not just about if interracial transplantation really good or bad. I can imagine, that transplantation is done same-race just in case, in favor of "do not harm" principle.

Interesting that pillay et al. (1990) contradict organedono.gov. Organdonor.gov don't have any reference but the article is quite old (1990) while oraganedonor.gov is probably frequently updated. We'll need some more recent research in order to answer this question.

No, race is not a factor taken into account. However, due to higher genetic similarities between people of the same race, it is usually easier to find a match within a race.
Source 1
Source 2

The two statements seem somewhat contradictory. Can you add some explanation?

Race is not taken into account in the sense that they do not use it as a factor in finding a match. E.g., if you are black and need an organ, they do not look only to black donors. However, it is more likely that someone from your own race is a match simply because of genetic similarity. Therefore, it is going to be more common to see people have a donor of the same race only because the probability of a match being the same race of a recipient is higher than the probability of a match being a different race.

It makes sense. You might want to rephrase the question just to avoid the confusion. I also first thought that you were contradicting yourself.

Also keep in mind the most likely match is  direct family which of course will tend to be the same race.

Here is a really interesting article discussing this topic and finding no statistically significant difference in survival rates between donations across race and those within a race.

Everyone is correct, it depends on which organs are being offered.With kidneys and pancreas the HLA (the tissue matching) is used and important for graft survival. Since our HLA will more likely match another of a similar race then you could say race may matter with those organs. There are some interesting studies that are emphasizing that race does play a factor in the success of the kidney transplant, as well as the HLA. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2826243/#__ffn_sectitle   In liver transplant, race still does not matter for the success of the organ transplant.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2954674/

Welcome. Can you add sources or references to your answer? Without those, people can't background read on your post.


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From 46 human chromosomes, is each one from a single parent?
Humans have 23 pairs of chromosomes. Each chromosome in pair is homologous to another one in pair.
Does this imply, that the entire chromosome in any cell is obtained from only one parent? I mean entire single chromosome from one parent, and entire homologous one -- from another parent?
This is obviously true for sex chromosomes, especially in boys. They get Y from father and X from mother.
Is similar true for any other pair of chromosomes?
Or they are exchanging genes during mitosis too?
I.e. parents data is distributed grouped by chromosome or by gene?

See Mitotic Cross-over. I don't know what is the cross-over rate during mitosis though.

To be clear, are you asking specifically about events after fertilization of the egg? Your question about chromosomes obtained "from only one parent" suggests a more basic question of how meiosis works.

Yes, each single chromosome came from one parent.  However, it is not true that each chromosome came from one grandparent.  Due to crossing over in meiosis, the copy of Chr 1 that you got from your father is partially from his father, and partially from his mother.  And the same for all the rest of your chromosomes.  You will not pass on a whole chromosome as you inherited it onto your children, crossing over will happen in your gametes, so that your kid will get whole chromosomes that are part from your mother, and part from your father.  The sex chromosomes are exceptions, because in men, they can't do crossing over, since men have a mismatched pair.  (At least in biologically "normal" men.)

No homologous chromosomes do not imply that each cell has genetic information from only one parent.
Let's just talk about one chromosome - and call it Chr1. This chromosome has genes A, B, C, D, and E.
When an egg is fertilized by a sperm, the resulting egg will have a pair of Chr1. One of the Chr1 would have come from the mother (egg) and the other from the father (sperm). These two are a homologous chromosome pair and they both have genes A, B, C, D, and E.
The mother and father contribute different alleles of the genes. So the mother could contribute A.1, B.1, C.1, D.1, and E.1 where as the father could contribute A.2, B.2, C.2, D.2, and E.2.
Then the child has two homologous chromosomes A.1/A.2, B.1/B.2, C.1/C.2, D.1/D.2, and E.1/E.2.
Hope that is a bit more clear.


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How can botox cure wrinkels?
How can botox cure wrinkels?
Do wrinkles caused by tension of some muscles in the skin?
Can these muscles be relaxed by hypnosis or training?

To avoid down-voting of your question, perhaps first read about Botulinum toxin and if there's something that you still don't understand come back and amend your question.

@vkehayas you can downvote if you wish; I have read articles about botulinum toxin, but I need positive statement like wrinkles caused by tension of muscles.

I hope you didn't take my comment as a 'threat' but merely as a suggestion to improve the question. Based on your comment I would suggest that you could consider asking that question, i.e. "how do wrinkles form?"

@vkehayas then I would read about collagen, hyaluronic acid and etc loss which I don't want to

@vkehayas i.e. I need to clash the fact that botox works and common theories of skin aging

Botox works by inhibiting signal transmission at the neuromuscular junction preventing the signal sent by the nerve from reaching the muscle through the destruction of the receptors on the surface of the muscle. As the intensity of contractions decreases the overlying skin is able to recover from constant contractions and replenish the lines and wrinkles with collagen. To keep the wrinkles at bay you will have to repeat this every 3-4 months.


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Normal cell diffusion in normal organism?
We know, that cancer cell can travel across an organism.
Is this ABSOLUTELY impossible for NORMAL cells?
For example, is it EXACTLY ZERO probability to find some bone cells inside liver or some skin cells inside brain?
In non-living things and with molecules this is called "diffusion". Any two contacting things will penetrate inside each other after hundreds and thousands years.
Is something similar happening in living thing?
May be very slow?
Was this phenomenon searched for?
Are there some protection mechanisms against appearing wrong tissue cells inside another tissues?
I understand that cells appear in their places during grow, but in mature state I think it is not impossible for cells to travel.
UPDATE
I know that there are many cells that travel by nature, like blood cells.
The question is namely about "static" cells, those ones we normally regard as non-travelling.
Also, I understand that there are some mechanisms, making cells to prefer their normal places when they divide and grow.
But the question is what about all these mechanisms failed? And how often it happens?
For example, I am 40 y.o. So, how many bone cells from my legs are currently in my brains? Zero? One? Million?

hemotocyte (blood cell) travels quite a bit around the body. Lymphocyte cells go pretty. Lymphocyte (involved in immune system) can go in many different tissues. Does it answer your question?

Depends on your definition of "normal," probably. There are non-cancerous diseases, like endometriosis, which involve cells ending up in the wrong place.

Also, this is a potentially very difficult question because cell "type" is not as well-defined as you would like it to be. It is difficult to tell if a cell is in the wrong place ("ectopic") or just a strange variant of a normal cell type.

In a healthy body, cells travel.
But this is very dependent of the cell type. Some cell type will travel in all the body (lymphocytes, plasmocytes, etc) while other do not have any migration capability.
The concept of diffusion is wrong to apply here, indeed the scales at which you are looking are not molecular.
Moreover, there are very active mechanism to keep cell type in place, for example, a concept called preferential attachment will maintain the cells grouped by cell type. If you take two balls A and B and A attached more to A and B to B, and you shake, you will see appearance of clusters of A and clusters of B. But that is only one such mechanism and a lot of other take play here.
see this: http://www.ncbi.nlm.nih.gov/books/NBK26937/
Thus, the probability of finding a cell type NOT at its normal position (that is one that does not travel) is maybe not zero, but so close to it that you will not find a cell outside of their normal position.
I hope this answers your question ?
Reference
Cooper GM. The Cell: A Molecular Approach. 2nd ed. Sunderland (MA): Sinauer Associates; 2000

Looking at it on my desk, I can't really find a chapter on this, it is too broad a question, it encompasses things from caderine adhesion, to Blood brain barrier.
The most relevant thing I found to this question is probably this:
http://www.ncbi.nlm.nih.gov/books/NBK26937/

Agreed on that. It's very broad. Good attempt though. +1d already :)

The preferential attachment mechanism can't be 100% accurate as anything in nature. Even the very term "preferential" implies uncertainty, because it would called "exclusive attachment" otherwise.

So, the question is namely about cell types we normally regard as non-travelling. For example, can we find bone cell in brain or skin cell in eye? I agree that probability is not zero, but the question is how large is this probability?

The concept of diffusion is actually very relevant - it's one aspect of how you would model the motion of a single cell!


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Textbook Recommendations Covering The Adaptive Immune System
I will soon begin work on a project about immunology. I would like to read more about the main mechanisms of the immune system.
What books or articles could you recommend to me? In particular I am interested in the adaptive immune system.
I would appreciate if some of the recommendations are at an undergraduate level as I do not have a background in biology.
Thanks a lot.

@MattDMo 's answer is a great starting point. You probably also want to look through Nature Reviews: Immunology to get an overview of what is  currently occurring in the field today. From there, you can look at the referenced articles in more specialized journals for topics related to your project.

echoing @AMR 's sentiment, Annual Reviews of Immunology is also a great resource if you're looking to go deeper than textbook-level, although Nature Reviews in general has better pictures :)

There are two books that I see as "standards" in the field:

Cellular and Molecular Immunology, 8th Ed. by Abbas et al.
Immunobiology previously by Charlie Janeway, who unfortunately has passed, so it is now authored by Kenneth Murphy. Many people just refer to it as "Janeway".

These texts can be used both at an undergraduate and graduate level (I used them in both), and are updated every few years. The latest edition of Immunobiology is from 2011, while CMI is from 2014, so you may want to start with that one first.
An earlier version of Immunobiology is also available for free on NCBI's Bookshelf, but unfortunately you can't read directly through it, you'll need to search for what you're interested in.

+1 for Cellular and Molecular Immunology. My undergrad immuno course used Parham's The Immune System and I really didn't like it. There are very good figures in Abbas' text, and I think it's also more in-depth for those of us who want to know more without multiple textbooks.

The Immunobiology book (previously by Janeway) - is awesome! Used it for my graduate school course on immunology. Great pictures and explanations - even for someone who didn't have a strong background in immunology. I would recommend that to anyone interested in learning more about immunology.


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Why does HIV belong to a group of retroviruses called lentiviruses?
HIV is an enveloped retrovirus. Each virus particle contains two copies of an RNA genome. The virus also has a number of enzymes: reverse transcriptase, integrase and viral protease. But, once I also find that HIV also belongs to lentiviruses.
I am not very familiar with the relationship between retrovirus and lentiviruses. And does here have somebody know why HIV is a kind of lentivirus?

In Latin, lente means slow, so lentiviruses are retroviruses that are characterized by long periods of latency.

lentivirus A group of retroviruses that include human immunodeficiency virus, HIV-1. They cause disease after a long incubation period.
latency A state in which a virus infects a cell but does not replicate.

-Janeway's Immunobiolgy, 8th Edition, Kenneth M. Murphy
HIV-1 is characterized by long incubation periods. It can often take months before the virus is detectable on HIV tests.
It is also known that HIV reservoirs will exist in a patient, such that even if they have undetectable viral loads when on Antiretroviral Therapy, once they come off of the treatment, they will begin to produce virons again. The likely reason for that is that the immune cells that they infect can be very long lived, and as the viral genome has been incorporated into the host cells genomic DNA, it is incredibly stable. It will stay dormant for years until it is able to replicate again.

There're 6 genuses under the family"orthoretrovirinae": alpharetrovirus, betaretrovirus, gammaretrovirus, deltaretrovirus, epsilonretrovirus and lentivirus. So the question came down to the differences between lentiviruses and other retroviruses. Here are some major differences:
Lentiviruses have a cone shape capsid while other retroviruses have a icosahedral capsid.
Retroviruses share 3 common genes: gag, pol and env. While lentiviruses share 2 additional genes: tat and rev.
Lentiviruses have an overlap between gag and pol, and a gap between pol and env. While retroviruses have no overlap between gag and pol and an overlap between pol and env.
Retroviruses can only infect mitosis cells while lentiviruses are capable of infecting non dividing cells.
Pathogenesis of retroviruses and lentiviruses are also very different.


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Why do feces vary so little in color?
Why do feces vary in color so much less than the food they are results of? E.g. you may eat food of all kinds of different colors but the resulting feces will almost always be some shade of brown.

Answer the questions what is the cause of variations of colors in living organisms, such as plants and what happens to molecules during digestion, and you will have an answer. Maybe look at an Organic Chemistry and Biochem text book.

The reverse can also be true - products of newborns in their first weeks range from tar black, to green, yellow and brown, all on amniotic fluid and mother's milk :)

The colors in feces can vary tremendously - the bilirubin answer posted below explains the brown tinge that's always present, but other colors can also be present, depending on the type of food and the presence of dyes or other chromagenic molecules.

feces color can vary with the food you eat. ever tried beets or eaten too much broccoli?

The main reason for the color of our stool (or feces) is the presence of bilirubin, a breakdown product of the hemoglobin. The amount of it causes different variations from yellow to dark brown. When the passage time of the food in the intestine and the amount of bilirubin is constant, the color changes very little. Illnesses like diarrhea, which cause a lower passage time have therefore a ligher color because a lower amount of bilirubin can accumulate.
The color of the stool can also indicate illnesses of the internal organs, white stool (or pale clay like colored) can for example indicate problems with the biliary system (drainage system of the gallbladder, liver and pancreas).
You can find some more information here and here.


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Primer Design with Primer-BLAST over specific site
I am trying to design primers using Primer-BLAST such that the forward primer spans a specific base pair site.
I am looking at KRAS for which I believe the RefSeq ID is NG_007524.1 and the forward primer should span chr12:25398285.
However, I'm not sure how to restrict the design to accomplish this. Thanks.

Do you want to amplify the genomic DNA or mRNA?

I want to amplify DNA.

In any case, I always verify the primers on the UCSC In-Silico PCR tool (https://genome.ucsc.edu/cgi-bin/hgPcr). You can never make sure enough with genomic DNA...

I think various ways can be apply, but the easiest way could be to indicate the range to set a forward primer.
Decide the length of primer you are going to get.
Let's say you would like 25 mer.
You can set the range from chr12:25398261 to chr12:25398309.
When you identify where chr12:25398285 is in NG_007524.1, you are ready to design your primers.

If he had to sequence KRAS gene, he had to amplify fragments of a determined maximum lenght, depending of the platform used. Also, do not forget that many sequencers need some bases (20-40) to warm up, and some other to land. E.G. I want to sequence a fragment from bp 100 to 150 of a given gene: I will design primers starting from bp 50-70 and stop at about 170. Personally I design primers pairs for any coding exon of a gene.


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What are the metabolic concerns associated with hard water?
If humans can maintain a consistent blood pH, then what problems does alkalized water cause us?
Why is it recommended that we filter and boil hard water? Is the issue that hard water can affect the pH of our blood?

Could you add where you have gotten this advice? I have lived in many regions with pretty hard water, and never came across it. The only reason I could envisage is to improve the water's taste...

@Gerhard I don't remember, it is the conventional wisdom.

It might help mentioning where you are from, if you say that it's "conventional wisdom" :)

@Gerhard it isn't matter, filters are sold all over the world.

I don't know this area, but found a recent review http://www.ncbi.nlm.nih.gov/pubmed/24049611 on epidemiological studies on hard water. It seems there are no conclusive data showing a health risk. Water hardness will definitely not affect your blood pH, which is carefully regulated by buffering systems. I think the reason most people install water softeners is because higher salt content can in the long run damage pipes, valves, dishwashers etc.

@RS: no problem if you would like to keep your location a secret. It's just that I had never heard of such a claim neither in the south of Germany nor in England and was curious - and thought that there might be something more behind the recommendation than just the hardness of the water, which might depend on your location. And yes, water filters are on sale here, too, but exclusively to improve the taste of tea and coffee :)

Right now, there is no evidence shows hard water can cause any healthy problem.
Previously people were concerned about the high mineral content, such as calcium and magnesium, may cause disease such like cardiovascular disease.
But from the report World Health Organization published in 2003 Hardness in Drinking-water, it says "Although a number of epidemiological studies have shown a statistically significant inverse relationship between the hardness of drinking-water and cardiovascular disease, the available data are inadequate to permit the conclusion that the association is causal. No health-based guideline value for water hardness is proposed."
And the United States National Research Council thinks hard water can supply the calcium and magnesium ions that dietary need. Hard Water Hardness Calcium Magnesium Water Corrosion Mineral Scale
And at the same time, I have to say the filters cannot directly work for hard water because ions cannot be isolate by filter. We can filter the precipitation after boil the water. Boiled water is better because tap water may contain microbes in some country, that will be harm for our health. And also you don't want to feel some "precipitation" while you drinking water. That's it.
For my personal view, I prefer soft water because it tastes a little bit sweet.

Ions can be isolated and removed by filters.  That's the exact premise of reverse osmosis for water purification. They don't work as well for hard water over time because scale can build up on the filter and drop it's efficiency faster than expected.


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Can brain cells move?
I was discussing this with my brother. I'm pretty sure I read somewhere that they can move.
Thanks
EDIT: By movement I mean long distance migration (preferably within the brain only).

If I recall correctly, there is neuronal migration during embryonic development? If you have a better wording for this, tell me so I can edit my Q. Thanks.

Do you consider the cells of a malignant brain tumor "brain cells"? Because they do move when invading the tissue.

The question is relatively broad and one should take into account that the brain not only consists of neurons, but also glial cells (supportive cells) and pre-mitotic neuronal stem cells. Furthermore, as critical fellow-scientists have indicated, developmental stage is very important, as the developing embryonic brain is very different from the adult brain.
However, after sifting through various publications, the answer to the question is actually remarkably simple: Yes, brain cells migrate.
In  the adult brain glial cells migrate in the brain (Klämbt, 2009). Glial cells are involved in a myriad of functions, but a notable example of migrating glial cells are the oligodendrocytes that migrate relative long distances to find their target axons onto which they wrap themselves to form the insulating myelin sheath (Tsai and Miller, 2002).
Neuronal stem cells migrate over long distances in response to injury (Imitola et al., 2004) and they migrate from specific stem-cell locations (e.g., hippocampus and subventricular zone) to other regions (Clarke, 2003).
Post-mitotic, but non-differentiated neurons have been shown to migrate in the adult brain in fish (Scott et al., 2012), and in mammals and non-human primates as well (Sawada et al., 2011).
Not surprisingly, glial cells, stem cells and neurons also migrate during embryonic development. Most notably, post-mitotic neurons destined to fulfill peripheral functions have to migrate over relatively long distances from the neural crest to their target locations (Neuroscience, 2nd ed, Neuronal Migration).

Great answer. Glial cells (resident, supporting cells) also include resident immune cells, such as microglia, which are related to the monocyte lineage

"oligodendrocytes ... wrap themselves to form the insulting myelin sheath" - wait, what? TIL.

Not only that, I didn't know the myelin sheath is formed by having some extra cells migrate into place. I thought they were acellular and grew from the axon?

Yep, they are definitely cellular - follow the citing link, grab any neuroscience textbook, or everyone's best pal wikipedia: http://en.wikipedia.org/wiki/Myelin. Thanks for the typo though :)

To add to Christiaan's answer, I'll mention one striking example of long-distance neuronal migration in the adult mammalian brain: the so-called Rostral Migratory Stream found in rodents, in rabbits and both the squirrel and rhesus monkey.
Neuronal precursors originating in the subventricular zone (SVZ) of the brain migrate to reach the main olfactory bulb (OB), and it's quite a distance for the small cells.


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What would the resulting karyotype be if someone with Klinefelter syndrome fertilized an "empty" egg?

Endoreduplication: is a form of nuclear polyploidization that results in multiple, uniform copies of chromosomes. This process is common in plants and animals, especially in tissues with high metabolic activity, and it generally occurs in cells that are terminally differentiated.
Investigating the hows and whys of DNA endoreduplication. - Larkins, et. al.

What would be the karyotype of the sex chromosomes of a complete hydatidiform mole that was the result of a sperm (monospermy) of someone with Klinefelter syndrome (47,XXY) fertilizing an "empty" female egg?
I know that in a situation without Klinefelter syndrome the sperm inside the egg would double all it's chromosomes by endoreduplication (since the mother's chromosomes are all missing), but in this situation there would not be a need to double the sex chromosomes if the sperm already contains "XX" or "XY" (Since Klinefelter syndrome has 4 possibilities for a sperm : Y, X, XY, XX).
Or would it be that the cell doubles every chromosome if there are too many missing?

I added some links to your question for those that might be unfamiliar with molar pregnancy, etc - it's always a good idea to add links for clarity to help others understand your question


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Can skin be removed and replaced so that it maintains its original cellular structure?
The cells in our body that form tissue, such as our skin, are interconnected. I would think that cutting out tissue or trying to repair/replace it, as is done in surgery, or after an injury, could not be accomplished without damaging this network and creating irreparable damage.
Am I mistaken and is it possible to remove and replace skin, close a wound without damaging the underlying cellular structure and having scar tissue form?
When it is healing, is the tissue that is healing in some way weaker than the tissue that remained intact, say just beyond the margin of the wound?
If someone has surgery, can their skin be repaired completely with the proper amount of healing time?

As pertains to skin, no. As pertains to your other fears, that's a different question.
Every cut that extends into the dermis significantly (and to remove skin, it must include the dermis) will leave a scar behind.

Cuts that extend only very superficially into the dermis may hit some capillaries and bleed, but these will usually not bleed much, and can heal "seamlessly". But anything that extends deeper will bleed more. Those are the cuts that often get stitches if they are long enough, won't stop bleeding, etc.
Lifting and replacing a piece of skin would necessitate the damage of many cells and the destruction of a lot of fine blood vessels, but even with the best microsurgical techniques, a scar will form. The best techniques combined with the best pre- and post-surgical care will only minimize scar formation; it can't be eliminated.

In skin, the process of wound repair can be generalized into three cascading phases each with characteristic cellular events: 1) inflammation; 2) fibroplasia or proliferative phase; and 3) scar formation.

Wound Healing in Development

I have the honor :-) congrats on 10k :-D