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what are average, median, and minimal dna closeness of stranger peoples, compared to closeness of relatives?
i thought: a parent closeness to a person can be marked as 50%. seems that is 50% of all parts of dna of humans that have variability across all human population. i heard that chimpanzees are 98% close to humans by their dna, so, 100% here may match like absolute 1 or 2 % of dna.
then, if to say only about siblings with both parents same, for simplicity, a sibling also must have 50% closeness in average. then, an uncle has 50% * 50% = 25% . (because he is sibling of a parent). a cousin has 12,5%. (child of uncle). a grandfather is 25%, his sibling is 12,5%, son of his sibling is 6,25%, and grandson is 3,125%, that is, second cousin. third cousin should be 0,78125% .
and here a question appears: so, this number goes very low very quickly, when going to farther relatives. but it should not go to 0, because stranger people also must have some similar genes by chance.
so, i want to ask, what is that average level of the similar genes by chance? what is median level of it? and what is the distance between 2 of the most far persons?
i think, maybe this question is not possible to answer nowadays. because i searched, browsed in wikipedia, and saw that, seems, it is not known, to how many parts chromatids are split in meiosis. so, must be, it is not known, how much is that variability of human dna. i think, maybe this question may stay waiting for future answers.

this seems to give info for that: https://www.google.com/url?sa=i&url=https%3A%2F%2Fwww.biorxiv.org%2Fcontent%2F10.1101%2F716662v1.full&psig=AOvVaw0_Jvz-G-KdHgzCPIiTukBP&ust=1689930420026000&source=images&cd=vfe&opi=89978449&ved=0CBEQjRxqFwoTCKjTwsX3nIADFQAAAAAdAAAAABAw  would the fourth image on this page give the information that you wish for? https://www.quora.com/What-two-human-ethnicities-are-the-most-genetically-different

Everyone is related, it just gets harder to know exactly how related you are when you go beyond a handful of generations. When you talk about "shared" DNA with close family members, you're talking about shared variation. When you talk about "shared" DNA between chimps and humans, it's more like you're talking about similarity of the average. These are two very different, not-comparable measures.

The 1-2% difference refers to SNPs in coding regions. There are drastic higher-order differences like chromosome fusion (chromosome 2a/b) and deletion or reversion of long stretches in MB level. What you are calculating is theoretical inheritance of alleles by identity of person from which it comes, which is abstract and has nothing to do with the actual sequences.

I am speaking of chimpanzee vs human.

0.1% and 0.
the average person varies by around 0.1% from another random person, or two random people are 99.9% the same. Humans actually have very low genetic diversity as a species. Total variation is around 0.4% by copy number. Of course the catch is it all depends on how you calculate difference. Different ways of calculating it will give you slightly, but not insignificantly, different answers. For instance you have issues with duplication and deletion, humans can have multiple copies of the X chromosome with little effect, is a translocation one difference or do you count each difference in a 1:1  base pair map, do you count genes if we don't know if they code for anything, ect. There is a whole rabbit hole of competing ways to calculate genetic difference.
the 50% you are referring to for relatives is really 50% of the parts that vary, or 50% of 0.1% thus 0.05%, or you are roughly 99.95% identical to each parent and 99.6% identical to the most unrelated person on the planet, again depending on how you calculate it.
The minimal difference is 0, identical twins who don't know each other exist. Also the cutoff for relative is completely arbitrary, there are humans who don't share 100% of genes within themselves.
Mean in this case does not make a lot of sense, the closest you might get is something like a genetic distance map, because it is not a single variable axis. there is a whole wiki devoted to human genetic variation if you want to dive deeper. https://en.wikipedia.org/wiki/Human_genetic_variation
More sources
More on how relatedness works.


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What's the difference between tumor cells and host cells?
When you talk about cancer, is there a difference between tumor cells and host cells ? What is the role of immune cells ? in a nutshell ?

I think this is way too broad to be able to answer. There are many different type of tumor and "host" (normal body) cells, and they differ in a variety of ways. It sounds like you're pretty much asking to sum up all of cancer biology ...

In the comments of FrankyG's answer I posted a review of the hallmarks of cancer. For that reviews purpose, cancerous hallmarks can be subdivided 6 major ways. Consequently, you can subdivide either of those six hallmarks into multiple specific pathways, each of which could merit their own graduate-level course exploring. For SE's purpose, the scope of your question is very broad! Here's my recommendation: (1) Search the site, there are good answers buried somewhere, and (2) read up before you ask your question so it has some specificity!

This is far too broad. Asking "what is the role of immune cells?" in cancer is the subject of literally thousands of research papers every year.

This question is a bit broad but I'll try to narrow it to be specific in the terms of "tumor" vs "normal" cells.
 (Source)
Basically a tumor contains cells which have a part of the cell cycle regulation broken (very broad way of saying this). There are literally thousands of things that can cause this. Broad groups of things that cause this could be knockdown of a protein (of which many are involved in replication), mutation of a gene (most likely), etc etc. Basically any type of DNA damage can lead to cancer.
 (Source)
So what creates damaged DNA? Well here is a small list:

UV light (Can cause DSBs)
Carcinogenic chemicals (eg: Ethidium Bromide)
Replication proteins getting stuck or loosing function

 (Source)
Well how does that compare to a "normal" cell. Normal cells have a proper cell cycle with all the "checkpoints" working normally to essentially throw away any cells that detract from the cycle in any way. They also have mechanisms to fix DNA that has been damaged before it gets replicated. If none of that works they have mechanisms to basically commit suicide so they never replicated. When all of that fails you get cancer.
In summary, a cell becomes cancerous when the following things happen:

DNA is damaged by one of the above methods
The DNA damage repair mechanisms fail to fix the damage, or cause further problems by attempting to repair (NHEJ is a repair mechanism for DSBs that is implicated in causing cancer)
The DNA damage causes abnormalities in the cell cycle (replication)
The body fails to recognize the particular cell with abnormalities in order to kill it
The abnormal cell is allowed to replicate without hindrance from the body's checkpoint mechanism
You now have cancer

As for the role of immune cells that question is too broad as there are many different types of immune cells. Their "general" role is to clean the body of foreign agents but there are differences even in that role. There are many different types of them.
 (Source)
While I love teaching this stuff I do feel like you could find A LOT of this by doing google searches. Please try that next time.
EDIT: Updated with plenty of sources.

Nice answer. However it would have been way better if you could have added references to your points and images.

True but to be fair a lot of this is found with simple google searches which is what I told him to do next time at the bottom.

I agree. But you should try to give scientific references if possible. And definitely image source.

For these types of questions I feel Hallmarks of Cancer: The Next Generation is an informative survey of the differences between cancerous and healthy cells (It's also open access!). I suppose it also requires a little background in what constitutes "healthy," however.

@FrankyG just because something shows up on a Google Image Search doesn't mean it can be reproduced, especially without a citation. This is a science site, and scientists expect citations. Unsourced material may be challenged and removed.

@MattDMo I'm well aware of what scientists expect (am one myself). This was an oversight of mine, I apologize for that. Dexter already made me aware. As you can see I changed it.

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General transcription factors vs. DNA Binding transcription factors
I know that DNA binding transcription factors are trans-acting, but what about general transcription factors?
Are they cis or trans acting?

Hi there and welcome to biology.se. For this site users are expected to do a little background reading before asking a question. What sources have you looked at that lead to this question?

From Wikipedia: A defining feature of transcription factors is that they contain one or more DNA-binding domains (DBDs), which attach to specific sequences of DNA adjacent to the genes that they regulate. So, there's no differentiation between "DNA-binding transcription factors" and "general transcription factors". In order to be classified as a TF, a protein must be capable of directly binding DNA.

When we say trans we mean that a diffusible factor, or agent is involved. So a molecule synthesized at one location, that can have a regulatory role in another location in the cell is said to be a "trans-acting" factor.
When we say cis we mean physically linked to, in such a way that the biological regulation only affects other molecules that are attached (in other words, something that is "cis-acting" cannot be freely diffusible).
So prokaryotic operators or promoters, and eukaryotic enhancers and promoters would be examples of cis-acting sequences, or elements.  All protein transcription factors, or even DNA-binding proteins, are therefore trans-acting.

General transcriptional factor complexes bind to DNA at promoters of genes via DNA binding proteins such as TATA-binding protein.
It is quite clear that it is trans-acting.

I agree, all transcription factors are trans-acting. I just am not sure that I agree with you first sentence completely. Some of the proteins bind to other proteins and don't themselves have a DNA binding domain. I might be wrong in the sense that these proteins may not be canonically considered TFs, but they do exist.

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How to estimate heritability from breeding data
I have a lot of plant-breeding data (tens of thousands of results) that are composed of phenotypes of parents and offspring. The plants however went trough years of selection and it is not balanced. Moreover, I have a lot of inbreeding data. What is the best way to estimate heritability from this type of data, having the exact pedigree relations and the phenotypes (But no accurate environmental data).
Moreover, how would you estimate heritability from nominal traits (like color or resistance)?

The (biometric) heritability of a trait is the slope of the regression line of the mean phenotype of offspring on their mid-parent. When you have multiple traits, you need to use a general linear model rather than a simple linear regression. The GLM accounts for underlying genetic correlations among traits. Nominal data poses no problem, you simply assign numeric values to each category. For example, red = 1, blue = 0. For the relevant theory, I would consult Falconer & Mackay (1996) "Introduction to quantitative genetics". Also look up the 'multivariate breeder's equation'.

http://www.d.umn.edu/~jetterso/Ecological%20Genetics/documents/Anecologistsguidetotheanimalmodel.pdf

Thank you very much, it was very helpful. I went on trying with the REML/MCMC methods, and will check how it goes.


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Area under the curve in a drug concentration curve
I am not from a background on pharamacokinetics and trying to learn some concepts.
I noticed that the definition for AUC involve the first 24 hours. For example in here AUC is defined as "the area under the concentration–time curve over 24 h
divided by the MIC."

Is there any reason why this 24 hours is selected?
Say I test 2 treatment strategies. Strategy 1: 500 mg tablets given 3 times a day (500m g×3, 8 hours apart) and Strategy 2: 500 mg tablets given 3 times a day for 2 days (500 mg×6, 8 hours apart).
In this case if I simulate the change in the drug concentration over time assuming exponential decay, then the two concentration curves would have the same values for the first 24 hours. Therefore the AUC obtained in the first 24 hours for these two strategies are the same. But strategy 2 performs better than strategy 1. So, in this case isn't the total area under the curve above MIC a better index than consdiering AUC in the first 24 hours?
Is it wrong to inform why a particular dosing strategy is effective than the other one using 'Total area under the curve (rather than of the first 24 hours)'?

The link in the question body isn't working, could you please correct it? Thanks.

This definition of AUC is non-standard.
The usual definition does not involve the MIC or 24h: it is the area (~ integral) of the plasma concentration curve as a function of time, from first administration time $t_0$ time to infinity. (You will sometimes see it subscripted as $\mathrm{AUC}_{0 \to \infty}$)
In the case of so-called time dependant antimicrobials (beta-lactams, macrolides, vancomycin), the bacteria are inhibited from replicating as long as the concentration stays above the MIC (minimal inhibitory concentration). Often a second threshold, the MBC (minimal bactericidal concentration) is defined corresponding to the required concentration to kill rather than just inhibit replication.
As you stated, the second strategy has indeed a longer duration above MIC. It is more effective from a purely kinetic standpoint. Whether than translate to clinically relevant effects depends on the antibiotics, the bacteria and the tissue under consideration.
A second point is whether a higher AUC is beneficial if the time spent above MIC or MBC is the same (nb: not the case here). However this also depends on factors beyond just pharmacokinetics.
As an aside, some antimicrobials like the aminoglycosides display a "concentration dependant" effect where the peak drug concentration determines the effect, dictating different dosing schedules.

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How do steroids travel in the bloodstream?
Cholesterol, which is hydrophobic, cannot simply travel in the bloodstream, and instead is enclosed in lipoprotein (LDL, HDL). Steroids, which are derived from cholesterol, are also hydrophobic (right?). So how do they travel in the bloodstream? If they are enclosed by anything, what is the molecular mechanism of their entering the target cell?

Steroid hormones are transported in an inactive form bound to proteins in the bloodstream. Androgens and estrogen are bound to Sex hormone-binding globulin (SHBG), while glucocorticoids and progestins are bound to transcortin.
References:

Transport of steroid hormones: binding of 21 endogenous steroids to
both testosterone-binding globulin and corticosteroid-binding
globulin in human plasma.
Plasma protein-mediated transport of steroid and thyroid hormones.
The Functions of Corticosteroid-Binding Globulin and Sex
Hormone-Binding Globulin: Recent Advances

They also bind to albumin.


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How and why can cold inflict pain?
I was carrying a can of very cold liquid, had something heavy in my other hand so couldn't switch hands. After a few minutes, I started to feel very intense pain. I was very surprised. cold is just atoms moving slower. This makes more sense if you think about how heat, or burns can cause pain. But heat can cook tissue and disable it, it makes sense it would hurt.

What about frostbite? Did you read anything about injuries from the cold? What can you add to your question so that it isn't so broad?

also read about nociception. Extreme cold can activate pain pathways

One mechanism through which low temperatures cause pain is through vasoconstriction.
Cold environment causes constriction of blood vessels in the periphery. This will cause decreased blood flow and the muscles will cramp due to lack of oxygen. The cramping is due to the accumulation of lactic acid (due to activation of anaerobic pathways of metabolism) and carbon dioxide. Both these chemicals will lower the pH which cause pain.


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An unknown band appearing in my gel electrophoresis
I am having trouble understanding what is the source of band "2" in the following gel-electrophoresis:

In this experiment, we took an E.coli transformant colony and ran its nucleic acids in the gel, after adding a restriction enzyme which cuts the recombinant plasmid molecule into two corresponding bands ("3" and "5" ["5" is very weak in the scanned version, but is well seen in the "hard copy" )  . I know the first line ("1") corresponds to possible genomic DNA we took from untransformed bacteria, and that the fourth line ("4") corresponds to a plasmid molecule without an insert. 6 is also well understood.
My question is-
What is the source of band "2" which contains more base pairs than any of the parts of the plasmid and its insert , and in particular more base pairs than the insert?
WIll someone please help me understand this ?
Thanks in advance

I think you need some controls. If you can purify the plasmid away from the genomic DNA, run that plasmid alongside this lane. Would also be good to have genomic DNA without plasmid, such as from your untransformed control, in another lane. This should tell you if the mystery band is from the plasmid or the genome. If it's plasmid DNA, are you sure you're getting complete digestion? Uncut plasmids usually produce more than 1 band because supercoiled DNA migrates at a different rate than open circle, which is different from linear. Incomplete digestion could have left supercoiled and circular.

Hi user137, thanks for your answer, as for your suggestions:

I ran four transformed colonies in four different lanes, and this is the only lane when this mysterious line appears, so I guess the problem is not incomplete digestion.
I currently have no possibility of redoing this experiment with other controls. I am sure about the bands I told about, but still have no idea about this one.

As mentioned here:
http://biology.stackexchange.com/questions/19114/why-isolated-recombinant-plasmid-dna-without-any-restriction-is-often-detected
the circular form should run a little bit

less fast than the linear one, so I don't think it is reasonable that this line corresponds to a circular plasmid, since "4" is the line corresponding to a linear plasmid without an insert.
WIll you please help me figure it out ?
Thanks a lot !

So you combined different plasmid digests with genomic DNA from different samples of bacteria and ran it all in 1 lane? Please describe the digestion in more detail. Band 4 is empty vector, but what are bands 3 and 5?

I would also suspect single cut DNA here. Can you give us some details on the digest?

OK. I took a plasmid (containing one restriction target for BamHI) and an insert (containing one more restriction target for BamHI) , and inserted it into E.coli bacteria. I then put the bacteria on a selective bed, and took a colony, homogenize it and then ran the nucleic acid part in electrophoresis. Just notice, that on the bed , around the main colony, I had very small colonies corresponding to non-transformant bacteria that are able to grow only because they feed from the food the main colony is providing them.
As I said before, bands 3 and 5 are the two restrictions products I get

after digesting the plasmid+insert with BamHI.
Got any idea?

The most likely explanation I can think of for band 2 is an incomplete digestion, that the BamHI is missing one of the cut sites and creating a linear plasmid that is longer than band 3 because it also contains band 5. Without further controls I can't really know. And was the selective media using an antibiotic such as ampicillin or kanamycin? Because if so the satellite colonies aren't eating food from the transformed colony, they are surviving in the antibiotic depleted region around the main colony.

Can you put up the plasmid map?


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How and why did mammals go back to the oceans?
If I understand evolutionary biology correctly, mammals first evolved on land as small, rodent-like creatures, in a time when reptiles were dominant on land. Eventually, they diversified into the species we know today. Some of these species, however, are aquatic - whales and dolphins readily spring to mind. Why did the ancestors of whales and dolphins leave the land to go to the oceans? How did they evolve from their original form to their superficially ichthyoid appearance today?

I'll focus on whales and dolphins (cetaceans) as you mention them by name and they are representative for other marine mammals such as seals or manatees. The evolution of cetaceans was one of the fascinating evolutionary mysteries. Clearly, they were mammals, but which mammals were their closest relatives? Clues to solve this mystery began to appear in the 1980s and 1990s.
During the 1980s and into the 1990s, paleontologists discovered several fossils that were clearly land-based mammals but shared many skeletal features with cetaceans. These fossils, including Pakicetus [(Gingerich et al. 1983)] and Rodhocetus (Gingerich et al. 1994), shared skeletal features that are unique to whales and to the Artiodactyla, commonly known as the even-toed mammals. Artiodactyls includes deer, sheep, pigs, bison, and hippopotamuses. Artiodactyls and the fossil whales share a unique skeletal feature of the ankle called an astrogalus, shown in the picture below. The astragalus is a "double pulley" structure that contributes to the ankle joint. This picture is taken from an excellent summary of whale evolution, provided by the Understanding Evolution site hosted by University of California at Berkeley. The astragalus is not present in other mammals.

The fossil whales and modern cetaceans also share unique features of the skull around the area of the ear, called a tympanic bulla. Although all mammals have bullae (plural of bulla), the bullae of cetaceans and the whale fossils is unique compared to other mammals. For more on the bulla, see this Talk Origins page. More on fossil whales can be found at the Berkeley Comparative Museum of Paleontology. The many fossils that have been found are transitional forms that link artiodactyls and modern cetaceans.

Source
Around the same time as the fossil discoveries, genetic analysis added additional evidence supporting a relationship between the artiodactyls and cetaceans (Milinkovitch et al. 1993). Although early genetic analytical techniques were not as robust as they are today, many genetic studies have since supported and refined the conclusions of Milinkovitch et al. Current evidence shows that the closest living relative of cetaceans are the hippos (see, for example Price et al. 2005 and Agnarsson and May-Collado 2008). The relationships are shown below in this figure from the Agnarsson and May-Collado paper. The dark lines are the artiodactyls and cetaceans, formally called the Cetartiodactyla.

The question remains: why? The most likely explanation is that cetaceans evolved to exploit an unfilled ecological niche or adapted to new niches that formed as a result of plate tectonics or other types of environmental changes that occurred 50-55 million years ago. The niche describes all of the living and non-living resources needed by an organism to survive. Although land-based mammals were increasing in diversity, few or none were present in the oceans. The basic hypothesis is that the early whale-like artiodactyls, like Indohyus and Pakicetus were land-based (terrestrial) mammals that spent most of their time near the water's edge. Over time, they adapted to the niches in the ocean. Fossils like Ambulcetus and Rodhocetus showed clear evidence of swimming ability, with flattened tails and the enlarged rear feet. In addition, the nostrils shifted from the front of the face to the top of the head, which we recognize as the blowhole.
The shift to the aquatic habitat allowed these species to exploit resources that were not available to land-based mammals, thereby reducing competition for the resources. Reduced competition allows more individuals to survive and reproduce.
Similar scenarios are very likely for other marine mammals, such as seals or manatees. They evolved to take advantage of ecological niches that were not filled by other organisms. This basic concept, evolving to fill available niches, is a common outcome of the evolutionary process.
The of adaptation of cetaceans and other mammals to the oceans may be similar to that of the hippopotamus. Hippos spend most of their time in the water, and they show many adaptations that allow them to live in the aquatic environment.  The eyes and nostrils of the hippo are high on the head, which allows them to remain almost entirely submerged but still see and smell, as shown below.

(Hippo photo by Johannes Lunberg, Flickr Creative Commons.)
Hippos feed underwaters, they are heavy enough to walk on the bottom of the river, and the mate and give birth underwater. The young can suckle underwater. Clearly, hippos seem to be another mammal that is "returning to water." Similar types of processes must have occurred in cetaceans for them to adapt to the marine habitat.

Citations
Agnarsson, I. and L.J. May-Collado. 2008. The phylogeny of Cetartiodactyla: The importance of dense taxon sampling, missing data, and the remarkable promise of cytochrome b to provide reliable species-level phylogenies. Molecular Phylogenetics and Evolution 48: 964-985.
Gingerich, P.D. et al. 1983. Origin of whales in epicontinental remnant seas: New evidence from the early Eocene of Pakistan. Science 220: 403-406.
Gingerich, P.D. et al. 1994. New whale from the Eocene of Pakistan and the origin of cetacean swimming. Nature 368: 844-847.
Milinkovitch, M.C. et al. 1993. Revised phylogeny of whales suggested by mitochondrial ribosomal DNA sequences. Nature 361: 346-348.
Price, S.A. 2005. A complete phylogeny of the whales, dolphins and even-toed hoofed mammals (Cetartiodactyla). Biological Reviews 80: 445-473.

+1 - Exactly. Because the seas were there, full of food. It's a great example of how evolution works.

Nice write up!  I can see how a deep wader like a hippo might have started getting fins and going further out into the water, much the way manatees and sea lions seem to be doing.  The phylogenetic tree really helps.

@shigeta Thanks for reminding me about the hippos. I meant to include them in my answer. It was late though and I got sleepy, so went to bed instead. :)

While "filling niches" always sounds nice, it must mean that the niche is there, i.e. that no other already existing species is living there. Given that water based animals are probably more likely to adapt to niches in water I think there must be another advantage that mammals had over those that tried to filled the niece from water. Maybe something with changing water levels(tide)?

@PlasmaHH You're correct that the cetaceans could have adapted to a newly forming niche. It is also possible that the niche was there and empty. For example, the plesiosaurs and ichthyosaurs may have filled the niches. Their extinction would have left the niches empty. It is not safe to say that existing aquatic organisms were more likely to fill those niches, given the nature of the evolutionary process. Besides, the niches were filled first by reptiles.

@PlasmaHH Also remember that this did not happen all in one great leap.  Something land dwelling evolved to be slightly more aquatic, and that animal more aquatic still, and so on until we had fully aquatic whales.  Though this is very very much not what happened, it's easy enough to imagine something raccoon-like evolving into something otter-like, and seal-like, and whale-like in turn.  Each step in the chain provides a benefit to the species, but the niche that the last species filled never had to exist for the first.

@MikeTaylor Thanks for the answer; this is pretty in-depth and definitely answers my question.

Sorry for arriving so late to this discussion - a very illuminating write-up, @Mike Taylor, nevertheless. On the subject of why mammals were better suited to exploit the niche than piscine and reptilian competitors, I’d guess that warm-bloodedness gave them an advantage.

How did they evolve from their original form to their superficially ichthyoid appearance today?

This is an example of convergent evolution. Fish appear as they do (streamlined body shape, wide tail, fins, etc.) since these are adaptations to the underwater environment they're living and evolving in. These features are only "ichthyoid" or "fishy" because the fish 'got there first'. Instead, we can think of such features as "ocean-favourable".
Reptiles evolved on land, and hence have a generally different appearance from fish, but those which went back into the oceans to become the ichthyosaurs adapted again to live in that environment. Since they faced similar problems as fish (drag from the water, the need to maneuver in 3D, etc.), natural selection would favour the same "ocean-favourable" features as the fish (but not exclusively; for example, turtles have a rather different appearance, which is "ocean-favourable" but not as "fishy").
When mammals ventured into the oceans, they also faced these same problems and the same selection pressures, so they also gained a more "ocean-favourable" appearance.

Great answer. The idea of convergent evolution makes a lot of sense, and it's a pretty cool mechanism.


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Are there any animals that maintain white fur year round?
Besides examples of rare albino animals, it seems animals only have white fur during the winter.  Additionally, and not coincidentally, the examples I've found live in the northern latitudes with predicable snow cover and have different colored coats in the summer months.  Are there any examples of animals that maintain a white coat of fur year round, or are there simply no environments that such a trait would be beneficial in?

https://en.wikipedia.org/wiki/Sheep :)

White Cats

Relatedly (but not fur), all-white colouration is not restricted to animals that experience snow. Consider the white tern, a tropical seabird. https://en.wikipedia.org/wiki/White_tern.

Are you asking about only wild animals?  Because there are numerous domestic animal varieties that have breeds that are white.  There's also the white tiger: https://en.wikipedia.org/wiki/White_tiger  And then there's the old argument about the zebra: is it white with black stripes, or vice versa?

@jamesqf: Yes, only wild animals.  Sorry, I should have been more explicit in my question.

Polar bears (Ursus maritimus) have white fur all year long.

There are probably several other examples. @L.Diago gave sheep as example. There are also all white troglodyte species.

This may be splitting hairs so to speak but the fur of a polar bear is actually transparent and gives off a white color due to reflection of snow. https://polarbearfacts.net/why-are-polar-bears-white/

@wanderweeer It is actually a good point. I have never been able to fully understand the polar bear fur but I would note that on the second picture, on a green background, the polar bear still look white.

@wanderweeer: That explanation seems a bit confused. As Remi.b says, a polar bear can have fur that will still look whitish even when there is no snow around. The fur is (more or less) colorless and scatters the ambient light, so it looks whitish. Many "white" objects/substances are built of smaller parts that are somewhat translucent or transparent; e.g. salt and snow

@Remi.b: I think it's closer to being blue and black tbh

@Remi.b & sumelic: I wish I knew more about how the lack of pigmentation in the polar bear hair works optically and I'd agree that it has more to due with scattering the ambient light than it's surroundings.  I don't ever remembering hearing a similar explanation for the white fur of other arctic animals.

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What advantages do birds gain when they mimic other bird species calls in the wild?
I've read that birds such as crows and blue jays often mimic other bird species calls.  There seems to be evidence that birds do learn and react to other bird species calls, specifically when they relate to danger.  What I'm curious about is what advantages do birds gain when they imitate other species calls?

There are a number of reasons birds will mimic other birds mostly for deception, but not always.

Impressing a mate: Songs are a large part of bird courtship behavior, and a more varied song that includes different mimicked tones can help attract a better mate. Because mimicked tones are learned, a bird with more vocal variety is demonstrating its intelligence, ability to survive, and other characteristics a mate would find desirable.
Safeguarding Food: Using a hawk or owl call, or the sound of a cat, dog, or other predator, is an effective way for a bird mimic to claim a food source. When it utters such a call, birds monopolizing feeders or nearby bushes, trees, or other feeding spots may scatter, letting the mimic take advantage of a less crowded food source.
Defending Territory: Songs are crucial for many birds to claim territory, and adding mimicked tones into the song can demonstrate the resident bird's strength. Extra sounds may also trick other interested birds into believing that there are far more birds in the region than there actually are. The newcomers may then simply move along rather than challenge the resident mimic bird.
Social Acceptance: Baby birds learn many songs from their families and other birds of their species, and if mimicked sounds are included, young birds will learn them as part of their initial repertoire. This helps birds fit in with their flocks, which will also help them eventually defend their own territories and attract mates. Many pet birds that mimic speech are doing so for social acceptance, as they consider humans to be their flock.Bird to bird mimicry
I have personal experience with one of these where a Blue Jay would come to our feeder imitating the screech of a hawk and all the other birds would scatter so he/her had the feeder to themselves.


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Is there any evidence of blue jays preying on other birds?
Are blue jays known to prey on other birds?  I've found that they are known to raid nests of eggs and young, but have not found any evidence of them actually preying on other birds.
Background:  A few years ago while raking leaves this time of year (late Oct/early Nov) the head of a house sparrow fell on me.  I looked around in the spruce tree I was under and saw a blue jay eating the rest of the house sparrow.  This was approximately 10 feet from my bird feeders.  I can't say that it wasn't dead beforehand, but it's proximity to the feeders made me wonder.

I know European Jays kill sparrows if they have an opportunity. So do crows. This is titled blue-jay but it's different than american blue jay. https://www.youtube.com/watch?v=VmeUcIxLTwk

@com.prehens.ible.  Thanks for the link.  It is pretty much exactly what I witnessed - including the decapitation.  Unfortunately it starts when it already has the other bird so we don't know if it was scavenged or actively caught.

Yes! This article gives an account of a Blue Jay killing and consuming a Cedar Waxwing, and further it clearly states that at times Blue Jays do predate on fledgling and adult birds, and gives a hefty amount of sources to back that up, if you're in the mood for further reading.

WOW.  Exactly what I was looking for.


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Are freshwater jellyfishes really jellyfishes?
Articles from the aquaticcommunity.com and the Nature Conservancy suggest that freshwater jellyfish, Craspedacusta sowerbyi, are more closely related to the Genus Hydra. From the Nature Conservancy article:

It should be known that though Craspedacusta sowerbii is touted as a
  jellyfish, some argue it is more   related to the family Hydra than a
  "true" jellyfish. Many researchers still call it as such, but others
  may simply refer Craspedacusta as a jelly. The main difference between
  Craspedacusta swerbii and "true" jellyfish is the presence of a velum.
  Its velum is a thin, circular membrane around the cap that helps
  propel, or move, the jelly forward.

An articles from the US Geological Survey (USGS) states that Craspedacusta sowerbyi is a hydrozoan that can take the form of a jellyfish. From the USGS:

Craspedacusta sowerbyi is a hydrozoan (Phylum Cnidaria, Class
  Hydrozoa), which is most easily identified when it takes the form of a
  small, bell-shaped jellyfish, known as a hydromedusa.

The Merriam-Webster dictionary defines a jellyfish as follows:

a free-swimming marine coelenterate that is the sexually reproducing
  form of a hydrozoan or scyphozoan and has a nearly transparent
  saucer-shaped body and extensible marginal tentacles studded with
  stinging cells

This definition, to me, seems to suggest that Craspedacusta sowerbyi is a jellyfish, however there must be some other reasoning that I'm missing that makes others believe that they aren't. Any clarification would be greatly appreciated.


text:
How do I go about traveling with DNA extract samples?
I am traveling from Fairbanks, Alaska to Vienna, Austria in six weeks and need to bring 10 very small (~50 ul) samples of extracted arctic ground squirrel DNA with me.
I need to travel with these on dry ice in a little carry-on cooler.
Has anyone flown with DNA samples? Any advice on how to go about it? Questions to ask customs?

I think it could also be asked at Travel.SE for a better answer.

Dry ice is classified as "dangerous goods" in most countries, probably because it can explode! It depends on the airline how much or if you can carry it with you. As an example, Swiss Air allows up to 2.5 kg per person with prior registration. See this question for carrying DNA. As these regulations vary by country and airline, you'd probably be better off if you contact your airline before going to the airport.


text:
Are amino acids of viruses L or D enantiomers?
I read a note saying that the amino acids of viruses are D enantiomers but I can't understand how that's possible since their human host can't even recognize that type.

I'm voting to close this question as off-topic because it's apparently based on a complete misunderstanding. Unless the person can post the "note" that ostensibly makes this claim, there's no utility for SE.bio site here.

Viral amino acids would almost exclusively be L-enantiomers considering they use host cell resources and machinery to build their proteins and the host cells are built on L-enantiomers.
With that said, you could always have nonstandard exceptions as xusr mentioned, if a virus somehow requires oxidase for example.


text:
What is reaction time of a single c. elegans neuron?
What is the reaction time of a single c. elegans neuron?
Is sensory neuron reaction to stimulus is similar to intermediate neuron passing a signal to motor neuron? What about chemical and electrical synapses?
I want to make a simple real-time artificial network model using existing c. elegans connectome projects, but I can't find anything defining time scale.


text:
relationship between cytokines
This is for a mathematical research. I am building a model to identify severe dengue patients through the interaction of cytokines S1P,IL1b,TNFa,PAF and IL10.
For this I would like to know if there are any relationships among these cytokines. That is for example: when PAF increase S1P should decrease. or when IL10 increase Il1b too should increase likewise.
There are seperate articles on the individual effect of these cytokines but I couldn't find any that exhibit any kind of relationship among these cytokines.

Probably you used bad keywords. It is called cytokine (or interleukin) network what you are looking for. There are several articles in the topic.
For example:

Cytokine patterns during dengue shock syndrome
Multiplex cytokine profile from dengue patients: MIP-1beta and IFN-gamma as predictive factors for severity

You can find here more:
https://scholar.google.com/scholar?q=cytokine+networking+in+dengue

Thanks for the links. But all they  say it that for example IL1b was depressed and returned to normal or IL1r was significantly elevated in DHF patients. They have findings like that. But what I want is to know if there is any relationship or association between the cytokines. Like when  cytokine A increases since it has some kind of ineraction with cytokine B, then the cytokine B too should increase. These kind of relationships do they exist?

@sam_rox I don't know. I'll check it in the afternoon.

@sam_rox Sorry, I forgot this question. I think I have found what you need, check this article: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527385/


text:
metabolic heat generation and exercise intensity
Is there a relationship between bio heat equation (found here) and exercise intensity as described here
That is I am trying to include the effect from exercises to the tempertaure variation in skin. I am trying include the term $Q_e$ which measures the heat generated from exercises,
 to the known bio heat equation

So that it would be modified as
.
So I would like to know if there is a relationship between metabolic heat generation and exercise intensity.


text:
Natural Killer Cell and Cancer
NK cells are very effective in destroying circulating cancer cells before their extravasation into the organ, However they have only a minimal inhibiting effect on already established micrometastases.
Anyone knows why ?
Regards.

So we know that NK cells work by receiving activating signals through receptors, and then degranulate such that cytotoxic molecules enter the target cell, and induce apoptosis. NKG2D is such a receptor, and cells that are becoming transformatively stressed by mutations and the like upregulate expression of NKG2D ligands on their surface for elimination. This is one example, and NK cells have different subsets of activating receptors, such as NCRs. NKp30 and NKp44 are examples of NCRs and activate NK cells through detection of heparan sulfate compounds on the surface of tumor cells. The question, then, is what happens to cancer cells that can: (1) downregulate NK cell receptor ligands on their surface, or (2) abrogate NK cell receptor function in their vicinity?
In an earlier study, it was shown that mesenchymal stem cells broadly inhibit NK cell activity through activity of prostaglandin E2 and indoleamine-2,3-dioxygenase, which downregulates each of the three aforementioned NK cell surface receptors. A later study using melanoma cocultured with NK cells again came to the conclusion that the same cancer cell secretions would inhibit NK cell activation in their vicinity.
By the same token, if we consider a cancerous cell that upregulates MIC expression, NKG2D receptors will recognize this and activate the NK cells. A cancerous cell with a truncated MIC that lacks an extracellular domain will fail to activate surrounding NK cells through that pathway. Keep in mind: many mutations go into making a cell cancerous, and many more go into giving it enough fitness to avoid getting killed from the start. These are just examples of critical pathways that result in immunoevasion.
As for why are small masses more immunoevasive than single cells? This goes into a sort of power in numbers logic. A single tumor cell doesn't produce as much inhibitor compounds as a mass of tumor cells. This is an interesting concept because in the hunt for pro-angiogenic compounds, a problem for a while was you would remove a large mass, and a smaller unknown mass would quickly begin to grow. They found that although large masses secreted more pro-angiogenic compound, the tumor cells also secreted so much inhibiting compounds that smaller tumors in the vicinity were effectively inhibited. Once the large mass was removed, this inhibition got lifted.


text:
Can Allergy and Auto-immune diseases be the signs of hyper-vigilant immune system?
Allergy sufferers are much less likely to get some types of cancers. Theories regarding  allergy - cancer link are mixed.
Many say it is due to hyper-sensitive immune response.  But the correlation between allergy and lowered glioma risk is also difficult to explain, due to blood -brain barrier.
However there was one interesting theory, saying that, allergy is an evolutionary anti-cancer protection. Allergy sufferers simply do not let some of the carcinogens to come into their body.
I am computer engineer. When we setup a protection at a system (antispam, antivirus, firewall) there is  sensitivity level that we have to select.  Higher sensitivity offers better protection but also results in more false positives.  However not all false positives are due to higher sensitivity. Some can simply be due to faulty protection system.
So my question is,  can  allergy or auto-immune diseases be sign of high-sensitive immune system which will have advantages and  disadvantages  or just a sign of simply faulty immune system which will have only disadvantages?

Could you add some citations of where you came across these theories?

@MattDMo  http://jnci.oxfordjournals.org/content/early/2012/02/20/jnci.djs153.full


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Engineered CD8 T-cell therapy for HIV infection
CD8 T-cells are effective in controlling HIV during the early phase of the infection. However by the time, the virus mutates and develops an evasion mechanism against CD8 T-cells.
Since cancer cells also develop immune evasion mechanisms, and scientists are using several technics to block those mechanism, i think it would also be possible to control "viral escape".
I made some research regarding HIV immunotherapy, however the only thing i found was antibody based immunotherapy.
My question is, would it be technically possible to engnieer custom CD8 T-cells which will targed HIV infected cells ?

And drive the patient into AIDS even sooner?! The problem is that CD8 cells do their job and wipe out all of the infected CD4 positive cells. Once someone is infected, our current course of action is keep viremia low and don't allow for escape mutants, you do this by attacking multiple pathways using HAART.

If you have access to Janeway's Immunobiology 8th edition, read the Acquired Immune Deficiency Syndrome section in Chapter 13. It will give you a good feel for why you don't need better killers (CD8+), you need ways of blocking the virus from propagating, keeping as large a population of uninfected CD4+ cells as possible. There will always be a reservoir of the virus that has been integrated into the genome of cells that lays dormant, that's how lentiviruses behave; well except for the Berlin Patient.

@AMR , Since you are expert in immunology, my questions may sound too elementary. Sorry for this, but i have one more question if possible. Once patient is at a early stage of infection, Are all of the CD4+ T Cells infected ?  As far as i know, we can't complately eradicate HIV from body because HIV drugs don't affect HIV hiding in resting CD4+ T cells. My Question is,   assuming,  the patient still have uninfected CD4+ T cells at the early stage of infection, May killing all infected CD4+ T by CD8+ T cells, and killing the virus itself with drugs may be an effective treatment method ?

There are protocols that allow people like healthcare workers that have been accidentally infected,  to go on HAART very soon after exposure. This will usually prevent the infection from taking hold. The way HAART does this is through 1)Entry inhibitors 2)Nucleoside Reverse Transcriptase inhibitors 3) Non Nucleoside Reverse Transcriptase inhibitors 4)Integrase inhibitors, and 5)Protease inhibitors. If you can keep the viral genome from integrating into the host genome, the virus will clear. Once the infection has integrated, you will never get rid of it; only happened once with Berlin Patient.

T-Cells aren't the only cells that have CD4. Macrophages, Dendritic Cells, Monocytes, Precursor T-cells, Natural Killer Cells. Let's say you have any of these infected cells encounter a cytotoxic T-Cell with specificity for the HIV amino acids, but the provirus is dormant and is not expressing its genes, then the CD8 cell will not identify any problems and will not kill the cell. Months, years, even decades after, the provirus can activate and start producing virons. The strategy currently is don't get it, block it ASAP if you are exposed, or suppress it with a multi drug regimen.

but the provirus is dormant and is not expressing its genes  -  I think even this sentence alone is  enough to explain why CD8+ T cell therapy would not be  useful.  Thanks

HIV is a difficult problem, but this might be a step in the right direction and hold promise for the future of HIV treatment. http://www.nature.com/articles/srep02510

People in the comments suggest that this would "Drive the patient into AIDS sooner", or that this will be ineffective because of dormant virus.  Neither is correct.
The question is asking about engineering CD8 with engineered T cell receptors specific for HIV.  This is a logical approach, and multiple groups have tried it:

In Vivo Suppression of HIV by Antigen Specific T Cells Derived from Engineered Hematopoietic Stem Cells
Reconstitution of anti-HIV effector functions of primary human CD8 T lymphocytes by transfer of HIV-specific alphabeta TCR genes
Development of CD8+ T cells expressing two distinct receptors specific for MTB and HIV-1 peptides
T-cell engineering by a chimeric T-cell receptor with antibody-type specificity for the HIV-1 gp120

A brief search on Pubmed will turn up many other articles. Some of these approaches have entered clinical trials; for example:

Redirected High Affinity Gag‐Specific Autologous T Cells for HIV Gene Therapy

The problem with this approach is not that it will "drive the patient into AIDS sooner".  A strong CD8 T cell response controls HIV well, and although it might be one contributor to CD4 T cell loss it's no longer believed that it's a major cause, especially in the early stages of HIV infection.
The general problem with CD8 control of HIV is that the virus is capable of mutation to avoid control by CD8s. Essentially, every case of HIV is effectively controlled by the CD8 T cell response in the early stage of infection, but the virus then mutates and escapes control, then the CD8 response adapts and controls the virus once again, and the virus mutates and escapes ... This can and has been tracked in many patients, showing repeated rebounds of the virus in the blood correlated with CD8 changes.
Better CD8 control of HIV is linked to a broader CD8 response -- that is, attacking many viral proteins, so that viral escape requires multiple simultaneous mutations (exponentially more difficult for the virus).  (Alternatively, the CD8 response can attack a small number of proteins that are very constrained, so that the virus can't successfully mutate them.  However, for reasons related to MHC restriction, that seems to only work in a small minority of people.)
An engineered CD8 T cell response will inevitably be to one or a small number of viral proteins.  That's conceptually similar to the natural situation following HIV infection, meaning that the outcome could be the same -- viral mutation and immune escape.
Because engineering the TcR means you can pick your targets rationally, you might be able to do better than the natural situation, but it's not obvious.  Overall, the fact that groups have been working on this approach for decades, without a breakthrough cure yet, suggests that it might be useful but isn't going to be a slam-dunk.

You have three ways that HIV leads to AIDS: 1) Apoptosis: The cells recognizes it is infected or integrase messes up the cDNA insertion and the cell undergoes programmed cell death. 2) Lysis: Budding of HIV destroys the cell 3) CD8 targets and kills infected CD4 cells. Escape mutants are much more of a problem for Immunoglobulin neutralization than CD8 cells because CD8 is only "looking" at the primary amino acid sequence of the viral proteins that the infected cells are presenting. and if viral reservoirs weren't a problem then we could cure people with HAART and time or BMT. We can't.

Escape mutants are much more of a problem for Immunoglobulin neutralization than CD8 cells because CD8 is only "looking" at the primary amino acid sequence - this makes no sense, and is immediately proven wrong by the frequency of HIV CD8 escape mutants (rapid and repeated) vs immunoglobulin escape mutants.  Very basic HIV biology here.

Love the downvotes.  Want to explain?


text:
Alpha-gamma co-activation
I am having trouble visualizing/grasping the necessity of alpha-gamma co-activation. My understanding is the following:
When an external load causes stretching of the sensory muscle spindles, the 1a afferent fibers travel via the DRG and synapse on both alpha and gamma motor neurons in the anterior horn of the spinal cord. The alpha motor neuron then relays an efferent signal to the extrafusal muscle fibers and induces a contraction. Almost simultaneously, the gamma motor neuron relays an efferent signal to muscle spindles, causing the contraction of the intrafusal muscle fibers at their polar regions, and stretching at their equatorial regions. The stretching of the equatorial regions is what causes the 1a sensory fiber afferents to relay signals to the spinal cord.
Herein lies my problem. If muscle spindles can only relay their afferent signals to the spinal cord AFTER gamma activation, but gamma activation requires muscle spindle afferent signals, wouldn't this be a catch 22? Also, I read from a few sources that gamma activation, while almost simultaneous, occurs after alpha activation. Wouldn't the converse make more sense as gamma activation would trigger higher alpha firing frequency?
I hope my question makes sense. This is my first time making a post on this forum so I do apologize if the syntax of my question is not in accordance with proper question formatting.


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And another insect from SE Brazil Oct 2017

Photographed in the low areas of the Brazilian Atlantic Rainforest - Oct 2017 and about 2cm in length.

Great answer from @Charles: I was still humming and hawing between a zelurus species and another of the zelus species such as the longpipe that has the distinct red colour. (I had to leave for a couple hours...)  Like him, I was having trouble finding one that looked really similar.  But I found one, labeled as the Zelurus Circumcintus:

However, further research revealed that this is a fairly undocumented species.  The only source I could find with pictures of a distinctly red one was Flickr, such as this one:

I'm guessing it actually is the zelurus circumcintus, but I have yet to find any official sources that back me up.

Zelurus species will be fine guys - brillient


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Why can't neurons undergo cell division?
Many cells in the human body can divide and reproduce, making healing possible. Neurons, however, cannot reproduce, which makes diseases affecting the brain particularly crippling. Why can't neurons divide - that is, what makes them different from "normal" cells? Are there any ways to artificially stimulate neuron cell division?

Neurons do not divide due to the reasons mentioned in Cornelius's answer. However, some new neurons can be generated in adults (Ref: Neuroscience, 2nd edition).
Generation of new neurons in adults was first demonstrated in birds, where labeled DNA precursors could be found in differentiated neurons. Experiments in mammals and humans demonstrated later that new neurons are created in the central nervous system (CNS) in adults, although it seems to be restricted to some particular regions: granule cell layer of the olfactory bulb and dentate gyrus of the hippocampus. These new neurons seem to be local circuit neurons and interneurons (i.e. no long distance neurons).
How are the new neurons produced if neurons cannot divide? They come from neural stem cells (NSCs) that were preserved in the sub-ventricular zone during development. NSCs are presumed to play a part in brain plasticity in the adult brain. However, they have therapeutic potential. Check the brief information in wikipedia), or this perspective in Nature neuroscience that may contain further details.
References:

Neuroscience, 2nd edition. Purves D, Augustine GJ, Fitzpatrick D, et al., editors.
Sunderland (MA): Sinauer Associates; 2001.
Gene therapy: can neural stem cells deliver?  Müller FJ, Snyder EY,
Loring JF. Nat Rev Neurosci. 2006 Jan;7(1):75-84. Review. Erratum in:
Nat Rev Neurosci. 2006 Feb;7(2):167. PMID:
16371952 [PubMed -
indexed for MEDLINE]

There are also NSCs in the hippocampus which is the part of the brain responsible for memory. This and neuroplasticity of existing neurons makes new memories.

Morphological point of view
Neurons cannot divide because they lack centrioles.

Because centrioles function in cell division, the fact that neurons lack these organelles is consistent with the amitotic nature of the cell [1].

Functional point of view
New cells in the nervous system wouldn't do any good. The whole nervous system is based on interneuronal connections, so adding an extra neuron would mess up these connections and alter both the functionality and the "stored" information.

Each nerve cell has a specific place in our nervous system. Its job is all about taking a signal from one specific place to another one. Adding new nerve cells would mess up these very specific connections in a very complex system [2].

References:

SEER Training. NERVE TISSUE. Available from http://training.seer.cancer.gov/anatomy/nervous/tissue.html
UCSB Science Line. Available from http://scienceline.ucsb.edu/getkey.php?key=1710

Although I agree with your comment the notion that "New cells in the nervous system wouldn't do any good" is untrue. New neurons are generated on multiple sites in the adult brain. For example learning as well as recovery from injury may be accompanied by formation of new neurons from stem cells.

I'm not sure if I should write it here but I have a related question. How does the body recovery from stoke which is actually death of nervous tissue? @Cornelius

I agree with AliceD in saying the second point there is a bit confusing. The primary goal of cellular replication (and coincidentally what people mean when they ask about neurons not being able to do so) is to replace and heal the original cell. This is a bit like asking "why can't we regrow limbs like lizards can?" and answering with "there's no point in having a third arm, two is the most efficient system we evolved to have for the least amount of energy."

I would like to propose an "answer" from a personal belief (no sources) based on an evolutionary approach to this question.
If neurons were readily capable of division, that is, healing, they would require a different form, thus mandating a different function; ultimately, they would be less efficient at what it is they are supposed to do (transfer electricity)--thus, not advantageous for the organism (during the evolutionary period); thus, did not occur.
Think of this for a moment: in physical space, what would happen to the other neurons if one were to divide? It would push into them, possibly 'disconnecting' a pathway, or impairing it's ability to fire (possibly below the activation threshold)--a whole new host of diseases could emerge.
Perhaps plausible, there was at one point something similar to what I've described above (a mitosing nervous system). The question is, though, would it be more efficient than a non-dividing nervous system? Would it have fewer diseases?


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Why do some cuts leave scars, while others do not?
Last year I got a moderately-deep cut on my finger, and it left a scar. Six months later, the scar is still there. On the other hand, I've had lots of other cuts on my fingers, though none have left scars. Why is this? Is scarring related to the severity of the cut, or something else?

Similar question: http://biology.stackexchange.com/q/20129/6422

This depends on a number of factors. Here are the first two that come to mind:
1) Is the cut deep enough to reach the dermis (this is the layer below the epidermis) where scar tissue will form?
2) What is your general state of health, and was there an infection at the site of the cut, which would have altered the normal healing process.
Basically, not all cuts are created equal, especially if some are deeper than others and become infected.
This article studied scratch depth
http://www.ncbi.nlm.nih.gov/pubmed/17440346


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How reactive are reduced antioxidant molecules?
When antioxidant molecules stabilize free radicals, they themselves become unstable and reactive but to a lesser degree. How reactive are these reduced antioxidant molecules? And what substance stabilizes reduced antioxidants?

How do you measure "reactiveness"?

Shouldn't this be better suited for http://chemistry.stackexchange.com/?


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C.elegans and antioxidants
How would you test the effect of antioxidants on C.elegans lifespan?
Is this done through feeding E.coli with antioxidants and then C.elegans with E.coli, or is there another method?

base on a article they do the test of nano-Pt, kind of SOD, and they do the experiment in several steps, first choose C. elegans strains and growth conditions, meanwhile prepare the nano-pt. then, do the lifespan assay. thired is Oxidative stress resistance. the last step is Fluorescence microscopy. in the mictoscopy they do several steps, include Measurement of lipofuscin accumulation, Detection of ROS, Measurement of SOD/catalase activit, Thermotolerance and Effects of dietary restriction

You can simply add the molecule of interest in the NGM or Liquid medium.
From this paper.

The worms were bleach-synchronized as follows: 2 mL of 6% NaOCl were
  mixed with 1 mL of 5 M NaOH per 7.5 mL of concentrated worm
  suspension, and shaken for 4–7 minutes until the carcasses dissolved
  as monitored by direct observation. The remaining eggs were then
  washed 3 times by pelleting at ~1150 g for 2 minutes at room
  temperature, followed by aspiration of the supernatant and
  resuspension in 50 mL of 0.1 M NaCl. A final pellet of eggs was
  obtained by centrifugation at ~1150 g for 2 minutes at room
  temperature, followed by aspiration of the supernatant. Eggs were then
  added to a 250 mL liquid culture, as described above. For experiments
  without RNAi treatment, bacteria were heat killed at 80°C for 60
  minutes. The worms were cultured at 20°C and monitored until they
  reached adulthood (~72 h), at which time FUdR was added to a final
  concentration of 400 µM. Worm viability was scored every two days by
  taking ten 10 µL drops (initially ~20 worms per drop) of the culture
  and counting the living worms under a microscope. The average number
  of living worms was then calculated. S medium or deionized water
containing 10 mM malate, succinate, or fumarate was added back every
  three days to compensate for metabolism of the compounds and
  evaporation, and S medium containing FUdR and bacteria was replaced
  every 6 days. At least two replicates of each experiment were
  performed.


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Hormones and body mass
I was wondering how some animals (bulls, elephants etc.) become so large by only eating grass or plant based material and why some humans can build large amounts of muscle and mass without a proper diet.
1. How do both get their essential amino acids in order to build muscle and mass?
2. Can hormones independently build muscle and mass regardless of the food or amount of calories ingested?

All life has amino acids. That bulls and elephants are alive suggests that they can obtain any amino acids that they can't synthesise from their diet.

hormones are only signals - how the organism responds to hormones is tuned by evolution in each organism.

The amino acids to build muscle and lean mass come from essential amino acids that must be consumed via diet that contains these, which most plants do not.

Could more hormones then possibly send a signal to extract more nutritious material from food in order to build more mass?


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How likely is it that through dog breeding, tail-wagging has been disassociated with happiness?
I am not a biologist, so sorry to anybody for misinformation in this post.
If I understand correctly, dogs evolved the ability to show emotions through various sounds and tail-wagging in order to better communicate with their symbiotic partners, humans. Is it possible that recently, dog breeding has disassociated this with the communication of emotions due to the fact that humans like dogs which are more naturally happy? Considering that they have been tamed, and therefore their actions wouldn't be a good indicator, it seems plausible to me.
Please correct me on misinformation.

Welcome to Biology.Beta. Just to make sure I understand your question: You ask whether it is plausible (or whether it really happened) that dogs do not feel anymore happiness but still waggle their tail because they are selected to make humans think they are happy but not to be happy per se?

I am asking about plausibility, unless there is some accessible source of knowledge to answer definitively. Other than that, yes- that is what I am asking.

Well...yes that sounds plausible to me! I guess one answer should incorporate some elements of the additive genetic covariance between traits and how such covariance evolve in order to address whether it is likely or not to have first evolved both traits together because they were correlated and then correlation fell down (eventually because being always happy is not a good thing) so that traits could evove independently.

Evolution of the G-matrix is still poorly understood today. Hopefully we won't have to discuss too much about the M-matrix. If I feel courageous I may try to give an answer along these lines later.

Dogs are very cunning. Wouldn't surprise me one bit if they evolved tail-wagging without being happy, just to get another biscuit.

P = zero, or so close to zero as to not be worth contemplating or discussing


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Do antioxidants interfere with chemotherapy?
Since most of the chemotherapy drugs kill cancer cells by damaging their DNAs by means of free radicals. So antioxidants, which will detoxify free radicals, should theoretically decrease the efficacy of the chemotherapy.
However clinical trials are proving the opposite. Saying, antioxidants does not decrease chemotherapy efficacy but also make chemotherapy more effective, thus increase the survival rate.
http://www.ncbi.nlm.nih.gov/pubmed/17283738
The question is, why antioxidants do not interfere with chemo, while they are supposed to do ?

That reference doesn't look very authentic. Four authors all named Simone (a family enterprise?), from the "Simone Protective Cancer Institute", which appears to be just a website (www.drsimone.com). This Dr Simone (self-appointed as "cancer's worst enemy") says he is endorsed by Ronald Reagan and claims broad expertise ranging from "the truth" about cancer to "how to save yourself from a terrorist attack", and peddles various anti-cancer diets (?) as well as health insurance plans. Stay away ...

Since it's a very broad argument I'll try to summarize in a few sentences.
First of all the sentence:

Since most of the chemotherapy drugs kill cancer cells by damaging their DNAs by means of free radicals. So antioxidants, which will detoxify free radicals, should theoretically decrease the efficacy of the chemotherapy.

is a bit inaccurate as of today. The chemotherapy today uses the "classical" chemotherapy drugs which IN PART use the mechanism of free radical but there are a lot of mechanism such as microtubule damage and so on which do not depend on free radical toxicity. Today there are also a lot of biological drugs and inhibitors of tyrosine kinase inhibitor which use a completely different pathway.
You cite a paper from 2007, a bit dated, I cannot access full text because it's an abstract. It seems it's not performed in a systematic manner (it's a not a systematic review or meta-analysis) and is published in a journal of alternative medicine. Maybe there are more recent paper but unfortunately at the moment I cannot have the time to check.
Finally you are comparing the effects of a chemotherapy drug administered usually in high dosage to the use of antioxidant which I cannot recall are sold as drugs used regularly, so it's a potential interesting biological question but practically it's a bit difficult to compare the oxidative effect of a cancer drug with the effect of an antioxidant one in real patients since I don't think there are randomized controlled clinical trials comparing chemotherapy to antioxidant alone.

There are many ways to damage the DNA of a rapidly proliferating population of cells; oxidative damage is one example—albeit a very broad example not especially specific to cancer cells, the cells we would like to eliminate.
Many non-targeted chemotherapeutic drugs exploit other mechanisms of depriving cancers cells of a high-fidelity genome, therefore reducing their competitive fitness or outright killing them due to a lack of functioning copies of essential genes. For an overview of such classes of drugs, see the Wikipedia page on Chemotherapy.
Alkylating agents covalently modify the DNA (along with protein and RNA) of affected cells, causing misreading errors to accumulate as DNA is replicated. Alkylated DNA bases cause misincorporation of nucleotides on the newly synthesized strand that sometimes escape proofreading, causing mutations to be passed on to all daughter cells. Also, if such survailance systems are working in cancer cells, alkylated DNA can cause cell cycle arrest or even programmed cell death.
Antimetabolites disrupt necessary cellular metabolic functions. One common mechanism is to interfere with any chemical reactions catalyzed by the folate family of vitamins/enzymatic cofactors. Folate is necessary for synthesis of some new nucleotides, which are necessary for replicating the genome. A lack of these nucleotides can cause low-fidelity DNA replication (introducing deleterious mutations into the genomes the cells) and cell cycle arrest, blocking division and proliferation.
Anti-microtubule agents interfere with the dynamic behavior of microtubules, a subcellular structure responsible for properly sorting the chromosomes during cell division; microtubules also contribute to cell shape and tissue-invasive locomotion. Preventing microtubules from functioning normally can lead to chromosomal missegregation during cell division, depriving some daughter cells of whole chromosomes (gene loss) and leading to genome instability, which can cause cells to loose fitness or loose genes necessary for life.
These are some examples of chemotherapeutics that do not rely on broadly oxidative mechanisms for their cell-killing action. The point of chemotherapy is to be more toxic to malignant cells than to the rest of the body's cells. Since malignant cells often divide more often than normal body cells in adults, many chemotherapeutic agents are employed with the idea in mind of being more toxic to rapidly-diving cells and less toxic to slowly diving cells.


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Safety of cobalt-chromium and nickel-chromium dental implants
How safe are cobalt-chromium and nickel-chromium alloys used in dental implants (porcelain fused metal)? IARC groups nickel and cobalt metals in group 2B and chromium in group 3 (hexavalent chromium is group 1!). But what is the likelihood of these metals leaching from implants and affecting the body? Aren't some of these metals already used for kitchenware (stainless steel vessels for instance contain chromium) and in industrial containers used for food processing? Is the risk much higher when these metals (not their more toxic compounds/salts though) are present in mouth when compared to their being used for food storage or cooking?

I would guess these are steel-alloys, right?

@MattDMo you can convert this comment to an answer.

Alloys have completely different chemical properties than their component elements. Elemental mercury is liquid, and is toxic, but when alloyed into amalgam with silver, tin, and some other elements it is perfectly safe, and has been used in dental fillings for a very long time with no negative effects. The same is true of cobalt and chromium alloys - they are chemically bonded to the other elements in the alloy, making a new molecule, and cannot "leach out" without the chemical bonds being broken, which cannot happen in the mouth or at standard cooking temperatures. Hence, they are safe for food prep and for fillings/implants.

But I have read reports in health columns warning that amalgams with some heavy metals can be dangerous in the long term since some tiny amounts of these elements will inevitably enter bloodstream occasionally, accumulate in some vital organs and hereby have the potential to cause chronic illnesses. I even saw a somewhat similar thing mentioned in a health awareness book written by a neurologist - that certain tooth fillings are suspected to be the cause of some degenerative neurological conditions. Are these studies flawed?

@so2 Please give some references to these "health columns" and the "health awareness book". Anyone can write anything they want, that doesn't mean it's true, or supported by peer-reviewed research.

Here is one of the many websites that mention amalgams can be dangerous: http://www.curezone.org/diseases/cancer/cancer_dental_risk.asp. Many of these websites mention names of doctors and medical institutions. I agree that the internet has a lot of misleading information and I also find an increase in the amount of health news that we cannot use, but was concerned about dental implants thing because I have also read articles in reputed newspapers that mention health hazards of heavy metal contamination in general, though they were not in the context of dental implants.

@so2 that page is full of random quotes from dentists, unsourced claims, and links to other unverified websites, without a single citation to reputable peer-reviewed literature or actual evidence - it's scare-mongering. Just because a doctor associated with a medical institution says something, doesn't mean it's true - you need evidence. Yes, heavy metals on their own can be highly toxic. However, as I described in my answer, amalgam is an alloy of different elements, and its chemical properties are entirely separate from the properties of the individual components that make it up.

Here is another one that cautions against using aluminum foils to store food while clearly stating that there is no strong scientific evidence showing these practices to be harmful to health: http://www.whfoods.com/genpage.php?tname=newtip&dbid=8. It also cites some studies. Atleast it provides a more balanced view & is not bent of creating a scare.
Would you mind updating your answer to state that no scientific study has given a conclusive evidence of long-term harmful effects of metallic dental implants, or if a study has proven they are perfectly safe, provide a link? Thanks!

Made the request to update your answer since I feel that at least when it comes to health, we have a much bigger moral obligation towards the society and hence must exercise more caution when we state something is perfectly safe. I want to accept your answer but would like to ensure that we either substantiate the claim of safety with some references or caution that the claim is based on studies done so far and leave room for future studies that may find some health effects.

@so2 I understand. I'll update the answer as soon as I can (I'm at work now, and a bit busy).

Thanks and no problem. Will wait for you to update whenever you get time


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How do geneticists compute the percentage of DNA shared between species?
It's not exactly clear to me what is meant when people say that humans and bananas share 50% of their DNA.

There is a good question in here I think. Currently it's hard to tell exactly what you're asking. Could you provide a citation for the 50%?

My source is MythBusters: https://www.facebook.com/MythBusters/posts/10150466971768224

That is atrociously irresponsible science journalism. The link they provide just takes you to some flashcards. I have no idea how they came up with that number. To get an idea of how people attempt to quantify homologous genomic material, checkout this article.


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What is the acceleration profile of a cheetah?
I'm interested in the time it takes for a cheetah to reach maximum velocity as well as the acceleration over time that's typical of a cheetah prior to attaining this peak velocity.


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Database of known human proteins
Is there an up-to-date database of known human proteins that is easily accessible using Python libraries?

GenBank includes human proteins and provides APIs for constructing HTTP requests to make searches. Examples are given in Perl, but if you prefer another programming or scripting language you are expected to write your own:

Equivalent HTTP requests can be constructed in many modern programming languages; all that is required is the ability to create and post an HTTP request.

This approach has always served me well.
Uniprot seems similar in this respect.
SwissProt provides a package for BioPython which may be of interest. I don’t know if this is the library you are referring to — you don’t say, and I don’t use Python.

The human proteome can be retrieved from the UniProt Knowledgebase (http://www.uniprot.org/help/human_proteome).
All data on the UniProt website is accessible programmatically via a REST API. The documentation http://www.uniprot.org/help/programmatic_access also includes a few python code examples (among other programmaing languages).
Please don't hesitate to contact the UniProt helpdesk if you have any additional questions.


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Is there a maximum size for an insect?
I have read in biology text-books that one of the most important constraints on the size of an insect happens to be the importance of the surface-volume ratio. It simply states that
if we assume constant oxygen levels and increase the size of an insect there would be a point where the insect's exoskeleton would no longer be able to support its weight.
Some textbooks go on to say that this is why we don't have insects the size of elephants. But, if this is true...is there a least upper-bound on the maximal body mass of an insect?

Also relevant are http://biology.stackexchange.com/q/13444/107 and  http://biology.stackexchange.com/a/20677/107

Also see http://biology.stackexchange.com/questions/17488/will-the-increase-in-atmospheric-carbon-dioxide-lead-to-larger-insects

I assume there must be a maximum size for insects, and I atmospheric oxygen probably has something to do with it. Insects do not breath like vertebrates, they have a series of tubes call trachea that run through their bodies and open to the surface at spiracles. Air passes through these tubes and oxygen and CO2 passively diffuse through the tissues. Insects can force air through the trachea to increase the diffusion rate, but they just aren't as efficient as vertebrates with lungs and hemoglobin to carry oxygen around the body.
In the past, oxygen levels were much higher. Higher amounts of oxygen could allow for larger invertebrates, and there were 6 foot long millipedes and giant dragonflies. Their size probably was not entirely caused by the extra oxygen, this was before they faced competition from vertebrates, so increased competition probably had more to do with their size reduction than loss of oxygen.
I don't know what the maximum size for an insect is at modern oxygen levels, but you'd have to eliminate the other selective pressures such as competition and limits on food before an insect could reach that size.

Good point. But, in that case I wonder why text books sometimes deduce with confidence that insects can't be as large as elephants? Unless a biologist has approximated the maximal size of a terrestrial insect...

Another limit on size is strength. An insect can't be directly scaled up to large sizes because an object's weight scales with the volume, but strength tends to scale with cross-sectional area. Since volume is cubic and area is squared, weight can overcome strength unless the legs are made thicker relative to the rest of the body. Additionally, insects have less efficient circulatory systems, where hemolymph escapes from the vessels and passes directly over the tissues, being collected at the other end of the vessels and passed back through the heart.


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Why don't mammals have more than 4 limbs?
Arthropods have 6 or more limbs and arthropods with 6 limbs appear to move faster than arthropods with 8 limbs so I wonder whether this might have something to do with fast and efficient locomotion. But, this is just a guess. I wonder what the official explanation is, if it exists.

Basically because mammals and arthropods evolved separately. If we evolved from a four-legged, fish-like ancestor, then mammals never got to choose how to evolve more efficiently (if it is).

@anongoodnurse What does "efficiency" have to do with anything? If the theory that everything evolved from single-celled organisms is correct, then that argument holds little water.

@b1nary.atr0phy - how so?

Are prehensile tails not considered limbs in this case? Common definitions seem to include them as limbs, giving many mammals 5 limbs instead of 4.

I think that if mammals had 6 limbs, you could ask why don't mammals have 8 limbs. Or if they had 8 limbs, you could ask why wouldn't they have 6 limbs. Evolution had to act a certain way, and it worked in the way so that present day mammals don't have more than 4 limbs.

It is also worth considering that mammals have an upright posture and 2 extra limbs would not be helpful, they would tend to get in the way. So even is my by some anomaly such a mutation occurred it would be selected against.

Before I find myself paraphrasing multiple times, many essentially duplicate answers, to many relevant questions being asked on SB, about selection-based adaptive evolutionary explanations about observed traits. I will link this alternative answer here: http://biology.stackexchange.com/a/57315/5005, perhaps @Remi.b could consider such an answer in future answers, some form of Neutralist evolutionary perspectives... in addition to selection-based perspectives.

Number of legs in terrestrial vertebrates
Not only do mammals have four legs but actually all terrestrial vertebrates (which include mammals) have four legs. There are slight exceptions though as some lineages have lost their legs. Typically snakes have no legs anymore. Apesteguia and Zaher (2006) discuss the evolution of snakes legs reduction and report a fossil of snakes with a robust sacrum. Cetaecea (whales and friends) have lost their hind legs but we can still spot them on the skeleton. See for example the orca (killer whale, easily recognizable to its teeth) on the picture below. Pay attention to the small bones below its vertebral column at the level on the left side of the picture.
I also want to draw attention to the importance of the definition of legs. I guess that we would call something a pair of legs if it is constructed using a similar developmental pathway than current existing legs. If we are using some broader definition, then a prehensile tail as found in some new world monkeys, for example, could be considered as a leg (but only a single leg, not a pair of legs obviously). A list of animals having a prehensile tail can be found here (Wikipedia).
Did you say Natural Selection?
I think (might be wrong) that you have too selectionist a view of evolution. What I mean is that you are wondering why mammals have four legs and you're looking for an explanation of the kind "because mammal have this kind of need of locomotion and for this purpose four is the most optimal number of legs". Consider the following sentence: "If there is a need, natural selection will find a way!". This sentence is wrong! Evolution is not that easy. This false view of evolution is sometimes referred to as panselectionist.
The reality is that it is not easy to evolve such a developmental pathway as drastic as having an extra pair of legs that are well integrated into the body of the carrier of this new trait. Such an individual would need a brain, a nerve code, a heart and some other features that are adapted to have extra legs. Also, assuming such a thing came to existence it is rather complicated to imagine how it could be selected for. To go slightly further, you have to realize that there are many stochastic processes in evolution (including mutation and random variation in reproductive success) and an organism is a piece of complex machinery and is not necessarily easily transformable to some other form that would be more efficient (have higher reproductive success). Often going from one form to another may involve a "valley crossing" meaning that if several mutations are needed, intermediate forms may have low reproductive success and therefore a high amount of genetic drift (stochasticity in reproductive success) to cross such valley of low reproductive success. See shifting balance theory. Finally, even if there is selection for another trait, it may take time for the mean trait in the population to shift especially if there is only little genetic variance. A complete discussion on why the sentence "If there is a need, natural selection will find a way!" is wrong would fill up a whole book.
Gould (1979) is a classic article on the subject and is very easy to read even for a layperson.
Why 4 legs?
Terrestrial vertebrates have four legs because they evolved from a fish ancestor that had four members that were not too far from actual legs (members that could "easily" evolve into legs). This is what we call a phylogenetic signal. The explanation is as simple and basic as that. You can have a look at the diversity of terrestrial vertebrates here (click on the branches).
Number of legs in invertebrates
Arthropoda (Spiders (and other chelicerata), insects (and other hexapods), crustaceans (crabs, shrimps…) and Myriapoda (millipedes) and Trilobite as well)) evolved from a common ancestor who had a highly segmented body. From this ancestor, many groups have fused some segments. In these taxa, each pair of legs is attached to a particular segment (I don't think the segments are still visible in spiders today). In insects, for example, all 6 legs are attached to the thorax but to 3 different segments of the thorax, the pro- meso and meta-thorax (see below).
As a side note, it is interesting to know that the wings in insects did not evolve from the legs (as it is the case in birds and bats). There are two competing hypotheses for the origin of insect wings. Wings either developed from gills or from sclerite (chitine plate, the hard part of the insect). When insect first wings, they actually evolved three pairs of wings (one on each segment of the thorax). At least one pair has then been lost in all modern species. In the diptera, a second pair of wings have been lost and are replaced by halteres, particularly easy to spot in craneflies (see below picture). In millipedes, the link between segmentation and legs is even more obvious (see picture below). You can have a look at the diversity of Arthropoda here (click on the branches).
Pictures

Update 1
Asking how likely it is for a given population to evolve a given trait is extremely hard to answer. There are two main issues: 1) a definition of the question issue and 2) a knowledge issue. When asking for a probability one always needs to state the a priori knowledge. If everything is known a priori, then there is nothing stochastic (outside quantum physics). So to answer the question one has to decide what we take for granted and what we don't. The second issue is a knowledge issue. We are far from having enough knowledge in protein biophysics (and many other fields)  to answer that question. There are so many parameters to take into account. I would expect that creating a third pair of legs would need major changes and therefore one mutation will never be enough in order to develop a third pair of legs. But, no I cannot cite you any reference for this, I am just guessing!
Following the wings example in insects. Insects have had three pairs of wings. While some mutation(s) prevented the expression of the third (the first actually) pair many of the genetic information for this third pair remain in the genotype of insects as they still use it for the two other pairs. Taking advantage of that, Membracidae (treehoppers) developed some features using a similar biochemical pathway than the one used to develop wings. Those structures are used as protection or batesian mimicry.
Update 2
Let's imagine that an extremely unlikely series of mutations occur that create some rodent with 6-legs. Let's imagine this rodent with six legs has a larger heart in order to pump blood to these extra legs and it has a brain that is adapted to using six legs and some changes in its nerve cord so that it can control its 3rd pair of legs. Will this rodent have higher reproductive success than other individuals in the population? Well… let's imagine that with its six legs, it can run faster or whatever and has a very high fitness. How would the offspring of a six-leg mother (or father) and a four-leg father (or mother) look like? Will it be able to reproduce? See the issue is that it is hard for such trait to come to existence because 1) it needs many steps (mutations) and 2) it is hard to imagine how it could be selected for. For those reasons, there exist no vertebrates with 6 fully functional legs.
Well, let's assume it does and in consequence, after 200 generations or so, the whole population is only made of 6-legged individuals. Maybe the species got extinct then and no fossil record has ever been found. This is possible. It is not because something has existed that we necessarily find something in the fossil record.

"all terrestrial vertebrates have four legs". What about snakes? Are they an exceptional exception, or somehow not counted on this?

@BoppreH Good point! Snake lost their legs. I'll give a word about cetacean as well which back legs are only visible on some small bones in the skeleton. If you can think of other exceptions, please let me know.

@Remi.b - I like your edit, but will maintain that there has never been such a creature. The mutations required would take many, many millions of years to produce such a creature, and the body plan would have descendants for far more than 200 generations. Fossils will never be found because it never happened. There is a reason all vertebrates have the same body plan - that's what crawled out of the ocean onto land, and populated the earth and (for some) then back. It's almost as bad as asking why we didn't evolve a set of wings on our backs to escape predation and amke is better hunters.

@anongoodnurse: Depending on your definitions, conjoined twins might provide a counterexample to your assertion.  And of course, some mammals have evolved wings, so it seems reasonable to ask why our particular species did not.

@NateEldredge - you're not reading my comments properly. Conjoined twins are a developmental, not genetic, defect, and bat wings are not from a third pair of limbs.

Nate I encourage you to lookup pictures of bat skeletons. Their skeleton looks like a person with really big hands, because that's basically what bat wings ARE: really long fingers with skin stretched between them. In fact, bats are one of the best illustrations of how all mammals evolved from a common ancestor and thus have basically the same body structure (ie. the answer to this question).

@anongoodnurse a mutation in the Hox genes can cause formation of additional limb buds

I thought I did acknowledge that extra limbs can form, but they are not usually fully functional. For a fully functional six-limbed vertebrate to form would take an enormous number of mutations.

Regarding update 2: A more likely scenario would probably be development of ornamental limbs (maybe due to sexual selection) which then become more and more functional.

I think having an additional limb isn't that rare in mammals. Having one which is usable to a degree that it increases fitness (i.e. chances of reproduction) is apparently much rarer. People who solder or cook for a living would love to have another arm... @anongoodnurse: Beauty is in the eye of the beholder; what some call a "defect in embryonic development" may be an enhancement to others. And don't tell me embryonic development is not dependent on the genes...

While I understand the answer, the final conclusion "Terrestrial vertebrates have four legs because they evolved from a fish ancestor that had four members that were not too far from actual legs", seems to imply that all vertebrates evolved from a common ancestor species. -- Isn't that highly unlikely? If the traits of vertebrates are "positive", wouldn't parallel evolution take place? Why did only 4 legged "proto vertebrates" evolve to have a spinal chord?

Vertebrates (Vertebrata) is a monophyletic taxon (see this post for intro to phylogenetics; see here on tolweb for the node vertebrata). In other words, all vertebrates share a common ancestor who already was a vertebrate and not descendant of this ancestor is not a vertebrate. It does not mean that there are not non-vertebrates that evolve some kind of a skeleton, such as insects with their exoskeleton.

I also think its worth pointing out those vertebrates who have evolved extra limbs. For mammals, this usually comes in the form of an additional prehensile limb, either the tail or the nose, but we have at least one example of a vertebrate evolving wings as well - had it and its ancestors not gone extinct, it's easy to imagine how Weigeltisauridae (notable Coelurosauravus) would have had an evolutionary path towards a six limbed animal like a dragon. They managed to evolve a couple dozen extra bones for their wings!

@GlyphGryph those are not new bones, they are repurposed gastralia, you might want to look at Drepanosaurus instad which has a claw on its tail for grip.

the brain and spine and heart should not be an issue, all are plastic enough to accomidate new limbs. Monkeys can learn ot control a thrid robotic arm in a matter of weeks, if it developed with said limb it should have no problem. making the limbs functional is harder and relies on bone and msucle anatomy. and evolution will not favor nonfunctional limbs.

I think I might interpret your question as asking, not just why don't mammals have more than four limbs, but why arthropods have more variety.  Insects have six, but others have eight, ten, or more.
Partly there are just many more species of arthropods.  80% of animal species are some sort of arthropod, and some lineages of arthropods are distantly related to each other because arthropods as a group have existed since the Cambrian period.  With so many more species, it's no surprise that they've managed to tack on some extra variety.
Although it might seem that insects and spiders are more closely related than, say, humans and fish, the reverse is actually true.  In fact, insects split off from other arthropods at approximately the same time that fish were diversifying into the three main lineages that would eventually become cartilaginous fish (sharks & rays), ray-finned ("regular") fish, and lobe-finned fish (coelacanths and lungfish).  All of these things happened at approximately the same time, geologically speaking, at around 400 million years ago.  Some ancient lungfish crawled up onto land a short while after, giving rise to land animals.  So in light of this, it's not really surprising that arthropods would have so much diversity in body plan - you don't look much like a leafy sea dragon (I hope).
But perhaps another way of looking at it is in the difficulty involved in adapting the body plans of these different types of animals.  Arthropods have segmented bodies.  In some arthropods, especially the myriapoda (centipedes, millipedes and so on), there's a pretty straightforward arrangement of one segment to one pair of legs (excluding the head).  Vertebrates have a segmented body plan too, but our segments aren't quite so well-separated.  In vertebrates, a "segment" is approximately equal to one vertebra.  So since vertebrates aren't in the habit of attaching a pair of legs to each vertebra, it's harder to grow more legs.  Instead, vertebrates have internal skeletons, with the familiar hips and shoulders in land animals.  Vertebrates do have good luck adapting the internal structure when they need to.  Most use the traditional four-leg layout, but humans, birds, whales, and snakes have all made pretty significant changes to it.  But internally, it's still the familiar hips and shoulders - even snakes still have the necessary bones.  Given another few hundred million years, they might disappear entirely, but it seems like the basic bone structure is tough to change.  Who knows, in a hundred million years, the far future descendants of snakes might end up with legs again, and grow six or eight instead of four!
So, overall, I'd say that the two main reasons are that the arthropod body plan is just a little more flexible due to its higher degree of modularity, and that different kinds of arthropods are actually more distantly related than you might expect.

needs references

Here is a more morphologic, less genetic answer:
According to Sansom 2013, the 2 sets of paired appandages (shoulder and pelvic) was set in stone when agnathans transitioned into gnathostomes (ie. when the first vertebrate organisms began to evolve jaws, an anatomic change that allows for classification of different stages of history found in the fossil record). They found variations where an agnathan had a paired set of anal fins (sort of the 3rd set of paired appendage, since anal fins are typically unpaired).
Now, moving forward millions of years, the Sarcopterygii (lobe fin fish) evolved into the tetrapods (4 limbed land vertebrate including amphibians, reptiles, birds, and mammals), this pattern (2 sets of paired limbs) became immutable, though much less fundamental variation throughout the phylogenesis of the various tetrapods.
Sansom RS,Gabbott SE, Purnell MA. 2013 Unusual anal fin in a Devonian jawless vertebrate reveals complex origins of paired appendages. Biol Lett 9: 20130002.