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What type of tree is this?
This is a tree that I have been growing. I'm wondering if this is a mulberry, and if so, what kind?  Location is Arizona.

It's produced fruit for about 3-4 years and it grew wild in our grass and we've had 9-11 more grow its fuitt are green, then red , then juicy purple in the end

Where is the tree growing? That's essential information for species identification questions.

Arizona near Kingman

It is a mulberry.  What isn't clear from the photos, and may not be clear without a DNA analysis, is whether it's a hybrid of the native red mulberry and the white mulberry imported from Asia in the hopes of starting a silk trade in North America (white mulberry is the main food source for silk caterpillars), or whether it's distinctly a red or white.  The berries won't always indicate this, and the leaves won't always indicate this.  At this point, our red mulberry has seen sufficient habitat loss that most new mulberry trees are hybrids.

Thank you we've had 9-10 grow and they're is 2 different kinds of them. All produce fruit and the fruit is red and then mostly turn dark purple/red.

I am sure it is a Mulberry (Morus sp.). I have two of them growing in my garden. The bark, leaves and flowers look exactly like my trees. Note that the Mulberry has different male and female flowers (and off course only the female produce fruit). To be 100% sure I looked it up in Blameys' "Mediterranean wild flowers".

Looking at the landscape in your area (which suggests somewhere between west Texas and southern Oregon) it might also be a black mulberry.
Here is a snippet on black mulberries

Thank you and this is in Arizona so you're correct I want to say it's a black mulberry as well.


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How did this spider evolve to mimic exactly a human face and arms?
So I came across something terribly amazing today, that is, a video showing this species of peacock-spider, that literally, transforms into a human face waving his arms about.
What could have possibly given rise to this?
I can understand the arms waving around, but why the uncanny human-face template, complete with eyes, nose, mouth, etc.
I do not believe this to be a case of anthropomorphism on my part, (seeing what I am familiar with), because I cannot imagine any other natural case where such symmetry in a pattern would closely resemble a human face.
Would appreciate any explanation. Thanks!

I agree with @Alan Boyd, the deaths head hawk moth is another good example.

I can't see any human face on that spider.

I think this really is just a case of what you refer to in your question as anthropomorphism. We are very, very good at seeing faces. Here are some more examples.
Addendum
This site has pictures of quite a few peacock spiders, and as far as I can tell these are all the same species (The only peacock spider mentioned on Wikipedia is Maratus volans).
The remarkable thing about these images is that individual spiders seem to have very different patterns on thorax and abdomen, and many of these are much less like human faces. This seems to me to weaken the case for some sort of mimicry.
Interesting fact: seeing faces and other forms where they do not exist is a psychological phenomenon called pareidolia.

Im not so sure... I mean, yes, anthropomorphism is a relevant scenario, but some of those faces (like the samurai crab) did evolve due to Japanese fishermen throwing back what they thought looked like crabs with samurai faces, and the solution converged. I am wondering if this face on this spider evolved out of similar feedback with humans and/or other mammals?

@Mohammad, I really doubt that the kind of selection that fishermen can provide would be stable enough or even exist over enough time to drive the evolution of such a trait. Even if it were, I find it far more likely that fishermen would chose the crabs that most looked like human faces rather than discard them.

@terdon What about the example with the moths in London who changed their wing color to a darker shade when the industrial revolution covered the city in ashes? I think human activity can provide stable selection in many cases.

@Drosophila Of course it can. But not when that activity affects only the small percentage of crabs that happen to have been fished by superstitious fishermen. The ashes you mention affected the entire population. Anyway, you have to admit that none of the examples mentioned in this thread are that human-like. They might look like faces to us, but a colon and a parenthesis looks like a face to us :). This is most certainly anthropomocentrism.

@terdon Absolutely, we do see faces everywhere. But we use a colon and parenthesis because they look like a face. My whole argument is that indeed there's antroporphism, but animals take advantage of that all the time. As for that spider, it is not trying to imitate a human face in particular. Rather, having a back that looks like a scary face may help with larger animals.

And to note: this is all rather hypothetical, of course. It's hard to get a direct answer to any evolutionary/ecological question, hence there's so much debate.

Argh, phone typing anthropomocentrism = anthropomorphism

Micheal Shermer shows a few interesting examples of pareidolia in this video: http://youtu.be/8T_jwq9ph8k?t=6m25s

The samurai crab story is probably a myth, spread by Carl Sagan; discussed here and here, among other places.

Peacock spiders certainly aren't mimicking human faces, and I strongly doubt they're mimicking anything at all. As others have noted, it's the combination of a fluke, and some anthropomorphising on your part (easy to do!).
The stunning colours and 'dancing' are actually part of a courtship display, and are most likely under strong sexual selection, rather than selection for any anti-predator function. The male-limited colours are only on display during courtship, and are otherwise flattened along the abdomen. It's also worth remembering that these spiders are tiny (< 5 mm), so the only other animals that are likely to be able to resolve those patterns in any detail are similarly sized organisms with decent eyesight (i.e. female peacock spiders).
Madeline Girard is in the latter-stages of her PhD on these guys, I'd recommend shooting her an e-mail if you're really interested.

In part, the way the spider resembles a human face is due to bilateral symmetry in the body shape and coloring of the spider. Bilateral symmetry evolved early in the animal kingdom to facilitate streamlining of the body (which makes it move faster in any fluid, including air and water), formation of a central nervous system and a head. Human faces (and bodies) are also bilaterally symmetric, hence the resemblance.
Another reason, as you note, is antropomorphism - the ability of humans to see a human face in many natural shapes and colorings. Other animals, including predators probably also have this ability to see faces in nature. This allowed the spider to evolve to imitate a scary face. This is called mimicry and it helps the spider ward off predators.

Thanks drosophilia. Do you think that in this particular case, this 'face' is used to ward off bigger, (ostensibly animals) who would recognize this as a 'face' of some sort? Or do you think it is just a relic of bilateral symmetry?

Not sure. Could be both, I think, since bigger predators may inadvertently crush the spider or use it at play. The scary face could stop them from doing that.

The subtitle of the video you linked to says it is a courtship ritual.

There are 44 species of peacock spider known to date and each species has a unique pattern on the thorax. Although this patterns can often resemble human faces, the likelihood of this being is the case is almost impossible because that would mean that humans would have to be present right at the beginning and throughout the evolution of these species.
They are endemic to Australia and as you may know Australia has vast areas of Australia that have only been inhabited humans for short periods. The process of evolution take much longer than a few generations. This similarity should be seen as more of a beautiful coincidence than any sort of mimicry
source - MSc dissertation written on the fascinating little creatures

Australia has vast areas that have never been inhabited by humans? Such as...? Indigenous Australians have roamed the country for a long, long time before white folks occupied the place. And a link to your source would be helpful.

@GeorgeLilley It would be great if you could add some of these ressources. Or a link to your thesis if this is possible.

My apologies, my source is my own MSc dissertation so the infrmation is from several reliable sources.                                                                        By uninhabited I meant areas that have not been inhabited by any permanent residence, rather than roaming semi/non-permanent residence. The process of evolution takes a very long time as i'm sure you know so for these spiders to mimic human faces it would have to of had that influence for more that a few generations period.

Unfortunately it has been many years since I did this piece of work so the sources I used are not to hand.

No need for apologies! The Australian Indigenous peoples were indeed nomadic. If you could adjust your answer I'm happy to remove that downvote. Having lived in Australia with a cultural anthropologist as lifelong partner I happen to be more critical than most :) But without references and leaning on memories only the answer is under-sourced.

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Is there an animal which, when eaten by other animal, poisons the predator and gets out of it's stomach?
It was a question in one competition, but it remained unanswered and i am curious about an answer.
There was a hint: American bullfrog
but i can not find any example of this behaviour on the web.

Close is the hagfish which turns the water around it into a choking slime when it gets attacked. In this video there are a bunch of predators that almost swallow the hagfish, and then spit them out.

The closest I can think of with that hint is a Middle Eastern beetle that hunts frogs and other amphibians:

In almost 400 face-offs, the amphibians only managed to get the larvae in their mouths seven times. Even then, they soon spat out the larvae, which quickly turned on them (first video below). One toad even managed to swallow a larva, which moved inside its stomach for two hours. For some reason, the toad eventually regurgitated its catch, and the larva, apparently unharmed, killed and ate the animal that had just eaten it (second video below).

However, it's only a pseudo-fit to the clue. The beetle doesn't hunt American bullfrogs, but ones native to its area of the world.

I think your clue probably leads to this video, which shows a rough-skinned newt (Taricha granulosa) consumed by a bullfrog (Rana catesbeiana). The frog then dies and the newt exhumes itself.
This is probably less likely in most settings since selection would quickly strike a balance between the prey's defensive toxin and the predator's immunity (for instance).  This is probably more likely to occur in invasion scenarios wherein the predator is naive to the prey defense (for example).

YES:
The rough skinned newt is very poisonous and can kill frogs and climb out of them. using a cocktail of heart stopping, paralyzing toxins, it can kill a human too.
http://video.nationalgeographic.com/video/weirdest-newt
Some frogs can make their predator vomit without killing them:
http://www.cairnspost.com.au/free-from-the-jaws-of-death-frog-escapes-snakes-stomach-after-being-regurgitated/news-story/861879b553964ec75866dd6ae354a5bd
And the Epomis Larvea make a frog attack them and then bite  it on the head, poison it and eat it, probably alive. https://www.youtube.com/watch?v=0y1FPm5WNVc
Some beetles can literally chew their way out of a venus fly trap using their mandibles, although perhaps that's less common in the wild. https://i.sstatic.net/lpY63.jpg ... other pages on that topic http://www.flytrapcare.com/phpBB3/holes-in-my-plants-t28144.html http://www.flytrapcare.com/phpBB3/earwigs-giving-my-plants-problems-t6041.html
this is the beetle that i confusedly watch eat its way completely out of the plant. they don't do that on tv! it took 2 days to escape.
http://www.naturespot.org.uk/species/common-red-soldier-beetle

I hadn't thought about this situation in plant carnivores, but that is an interesting consideration. Can you please add references for your last two statements?

ok i added some references.

Thanks @comprehensible That toad video is pretty incredible! I don't mean to be pedantic, but the photo of the fly trap isn't really evidence of your claim. Is there a reference that shows this happens and that it only happens outside the plant's natural range?

It's possible that a venus fly trap can get chewed by a beetle/ant within it's original habitat. What i meant to say is that... when i was a kid I had a venus fly trap once and gave it a common small beetle from the garden, because it had to eat something. it was a small beetle and the beetle completely ate a hole in the plant and managed to escape. It was a common red soldier beetle. ill add the references. I just thought it was fun info about the venus fly trap, difficult to know for sure about behaviour in the wild. thanks

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Carotenoid biosynthesis in yeast
Does Budding Yeast Sacchromyces cerevisiae produces significant amount of carotenoids?
Have anybody estimated the ratio of flux going in branches 1. Cholesterol synthesis(via squalene)
2. Coenzyme Q6 and 3. Dolichols Glycoprotein and others from the branch point of Farnesyl diphosphate.
Here is the kegg pathway
http://www.genome.jp/kegg-bin/show_pathway?map00900
I also have pathway formatted but couldn't upload.

The enzyme phytoene synthase is the first committed step in carotenoid biosynthesis. Saccharomyces cerevisiae doesn't have this enzyme, nor does it have the rest of the relevant pathway. Other yeasts such as Rhodotorula spp and Phaffia rhodozyma can make carotenoids.
However, carotenoid biosynthesis has been engineered into S. cerevisiae.

what about the distribution of fluxex from Farnesyl


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Prenatal Marketing
This is for a short story idea.
Is it possible to modify the DNA of a child to make their metabolism more susceptible (physical response, addiction, etc) to a certain type of chemical i.e. a chemical present in a fictional food. The idea being that their DNA is modified when in the womb (or before) and when they grow older (think teenager) they become addicted to said product.
This could be before conception, during pregnancy or after birth. What ways, in the future, could we go about doing this? Maybe chemical mutagens (http://en.wikipedia.org/wiki/Mutagen) or site-directed mutagenesis (http://en.wikipedia.org/wiki/Site-directed_mutagenesis)? Gene therapy?
Or is there a way to alter the regulation of the physiological processes in the human body to make someone become easily addicted to a particular product?
I'm looking to have this aspect of the story as scientifically accurate as possible so I can examine the ethical questions around it within the story.

Also, as an alternative I've been suggested Epigenetics. Suggestions?

To extend with a theoretical way such a method might be possible (though I really hope this will never work or be done!) This is essentially a gene-therapy approach.

Are you talking about psychological addiction (needing it to avoid running crazy), or physical dependence (needing it to avoid health complications)? The latter could be achieved in a cruel way for example by engineering vital genes of enzymes involved in cell metabolism in such a way that they require your substance of choice as a cofactor to work. The former would first require the identification of some genetic basis of psychological addiction. Though for science fiction you could stay vague (because scientific knowledge is vague) and say that the metabolism of their substance is genetically modified in such a way that it overstimulates reward pathways. This would not make them addicted, but rather susceptible to addiction after little exposure.
One of these methods will require altering an existing gene, the other may require inserting a new gene for a new enzyme, or altering the gene of an existing enzyme. The modification will have to be made at the very earliest stages of embryonic development to ensure that all cells carry the modification later. If in-vitro fertilisation is performed, this can be done before inserting the embryo into the mother's womb. In a normal pergnancy, there is a problem as the developing embryo does not become accessible from the mother's blood vessels until several days into development, when there is already a considerable number of cells. You could claim that a virus was modified in a way that it would be able to cross endometrial tissue and enter the embryo. If you want to go more "fancy" high-tech (even though successfully engineering such a virus would already be very high-tech), they could use a nanoparticle, for example made of silicon, gold, or pure carbon.
Whichever method you choose, they could use said delivery method to carry a short stretch of DNA with the desired gene and machinery to recombine it into the embryonic cells' genomes, either exchanging the old gene for a new, engineered one, or simple inserting their own gene.
As for how they manufactured their own new gene or version of a gene, this could be achieved by site-directed mutagenesis

As fiction this is a reasonable premise, but at this point you are talking about what is called Gene Therapy - intentionally modifying or adding the sequence of a functional gene to change a deficiency of the subject.
Gene therapy is a persistent goal of research, but it has only recent been executed - changing the DNA of cells in a living human being.  There have been some scary and unpredictable side effects of gene therapy.  In the mid 1990s an 18 year old boy developed multiple organ failure as the result of gene therapy to cure a genetic digestive deficiency.
This article describes a retrovirally mediated gene therapy to treat X-linked severe combined immunodeficiency (SCID) in 2003.   SCID patients (also known as bubble boy disease) have a single defective gene (yc) on their one X chromosome and the varicella–zoster virus infection inserted a functional copy into the patients.  Three of the four subjects responded well and at 3 years seemed to be effectively cured, but a fourth developed acute lymphocytic leukemia.
Most of the gene therapy projects continue to happen in mice, but there has been some encouraging progress recently, the devil is in the details as to how gene therapy would work.
Here is a decent feed of gene therapy goings on.
If and when gene therapy is safe and precise enough to use, then it could change a lot of characteristics in human beings - just about anything that genes do could be modified or modulated.


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How and when did sex evolve?
As I know evolution comes bit by bit mutation by mutation
How sex evolved which requires a major change in at least two individuals one to become male and one to become female ?
When that happened as we can see sex in all animals and most plants?

possibly of interest: http://biology.stackexchange.com/questions/15990/how-did-the-first-sexual-animal-come-to-exist/16014#16014

If you're interested in a deep exploration of the subject at a more readable level than articles in PubMed, I strongly recommend this book:
http://www.amazon.com/Power-Sex-Suicide-Mitochondria-Meaning/dp/0199205647

Sex (depending on how you define it), evolved very early (more than a billion years ago). Even species like yeast have a type of "sex" (see below).
Also, this doesn't mean there is necessarily a big difference between the two sexes.
The yeast Saccharomyces cerevisiae, for example, also has two "sexes", called mating types. One is called alpha and the other is called a. They can only mate if they have different mating types, so it is analogous in a way to mammalian sex. However, the genetic difference between these two types is tiny. There's a specific location in the genome that's called the MAT locus. This location can have either an alpha sequence or an a sequence, an that will determine the sex. The rest of the genome will be the same between sexes.
So it really doesn't seem like it is a huge evolutionary step to go from no sex to some simple version of sex.
See more details about yeast mating here.
Also see this wikipedia article on the evolution of sexual reproduction.

@TheLastWord yes, the name is the letter a.

The oldest evidence we have of sex comes from the fossil record which shows it was present more than one billion years ago - it could be even longer (it would be naive to think we have found all fossils or that all organisms that ever existed became fossilized). Sexual reproduction introduces potential benefits because it allows recombination meaning useful gene combinations are created more regularly and deleterious mutations are lost more efficiently (see Muller's Ratchet).
It is thought that sexual reproduction first occurred in single celled eukaryotes. In bacteria it has been shown that stress can induce the process of transformation. Transformation is a sex-like process in bacteria where one bacterial cell takes DNA from a donor bacterial cell and incorporates it in to it's own cell, it could help to repair DNA damage caused by stress. Transformation could represent one early form of sex.
It is difficult to put a timeline on it because it can only be seen from fossil data. But from early primitive haploid organisms we would need the evolution of diploidy, some sex-determining mechanisms, anisogamy, and reproductive physiology for basic recognisable sexes. From transformation you could get early eukaryotes that take up extra copies of genes from donors, leading to primitive diploidy.
To put down some unsupported thoughts (because this question is very hard to answer - there is no really firm consensus)... Once diploidy (having more than one copy of a section of DNA) is established it may be possible to form some gamete type functions, and anisogamy, where donors can more actively package, send, and receive large sections of DNA. From there anisogamy could encourage the specialization of gamete cells more similar to what we are familiar with (eggs and sperm). One likely next step would be through hermaphroditism - the ability to be produce both gamete types simultaneously or sequentially. Then some individuals would specialize in being one or the other (sex-determination). Continued evolution would lead to more distinct male and female phenotypes.


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Can the retina emit light?
The retina is light sensor, which converts light to an electrical signal.  LEDs can both emit and receive light. Similarly, is it possible to apply electricity to retina to generate light?
Simply put, in theory, can humans emit electromagnetic waves from their eyes?

No. More importantly, if the retina was emitting light you'd almost certainly saturate the photoreceptors with the emitted light, making it impossible to see anything, so what's the point?

@user137 I just think if retina could emit em wave in the same manner as LED, It would emit longer wavelength, maybe infrared, so not the same wavelength it could absorb. And it could be possible if we could control and practice it tobe useful with electronics device. Or have some hypotheses about superpower like mind reading or telepathy

@user137 but The main point is I want to know mecanic of absorption and energy conversion of retina that is it the same as LED or not. If it is then we could grow organic LED with bioengineering

Close voter and skeptics: this is a great question. Ever heard of otoacoustic emissions?  Ever thought about the physics between photon absorption and relaxation generating fluorescence?

It is very interesting but it's making no attempt to understand the biology of the problem, I'm going to close vote but would retract/reopen if the user makes it more biologically focused.

I'm voting to close this question as off-topic because it needs to explicity seek understanding of the biological considerations.

Even if it were possible to make the photoreceptors emit light at some wavelength, I imagine the efficiency would be so low that getting any appreciable energy out would require a huge amount of energy in. Of course, everything emits photons when you get it hot enough.

LEDs do not absorb light; a photodiode does.

@user137 - first you guess any photo emittance would swamp the retina and then you guess the efficiency would be too low to occur anyway? Criticizing questions is OK, shooting at them randomly with unfounded arguments is not.

The two close reasons so far are Primarily Opinion Based and "off-topic because it needs to explicity seek understanding of the biological considerations." Addressing the first, how is it POB? It either happens or it doesn't. Addressing the second, it might be addressed in this meta question. It seems that @user137 might benefit from seeking to understand biological considerations.

@anongoodnurse I retracted, but based on the way the question is written, it is asking if humans can emit light if electricity is applied to the retina. As I  don't think that there has been an experiment expressly that has been conducted to apply electricity to the human retina to the point at which it emits light, then an answer to that question would be opinion based, even if you are drawing on information based on the research that you have referenced; that the retina can absorb blue light and emit yellow light. You provided a really good answer, but is an answer to a different question.

I think either you or @Christiaan should consider an edit to the question to bring it in line with the answer. Given that autofluorescences is definitely a plausible phenomena for which there is evidence for.

Yes, you can grow organic LEDs @Thaina, that is entirely possible. You might as well call human fabrication of LEDs 'growing '  LEDs, but I think I see the actual question you were after...;) Cool thought.

@AMR - "You provided... an answer to a different question." Yes, I think you're right. Some is due to not knowing anything about LEDs, another to misinterpretation of electricity (I was thinking of electromagnetic waves). But the titular question remains, and that's what I answered. :-/ But I agree; it's not an answer that addresses the spirit of the question.

I still maintain that there is no attempt to illicit a biological answer, there is no evidence that the user has even considered the physical properties of the retina

The retina is already constantly emitting electromagnetic waves. It emits infrared light.

Please allow me to start by saying I know nothing about LEDs, so my answer isn't going to address your analogy. I'm also going to keep it more simple.

Can the retina emit light?

Yes. The retina is able to give off light in the form of fluorescence. Since fluorescence is the emission of light by a substance (granted that substance must first absorbed light or other electromagnetic radiation of a different wavelength.)

“We can use autofluorescence emission to image the retina and see certain features of it,” said Dr. Sparrow, the Anthony Donn Professor of Ophthalmic Science in the departments of Ophthalmology, and Pathology & Cell Biology. ...Most objects in the environment are visible because they reflect, as opposed to emit, light. However, the retina—which exists within the eye’s back wall, known as the fundus—can generate its own fluorescence.

The cells of the deepest layer of the retina, called the retinal pigment epithelium (RPE), contain fluorescent compounds, which when excited by blue light emit a yellow fluorescence.
This ability changes with age, disease, etc.

Excessive accumulation of lipofuscin granules in the lysosomal compartment of retinal pigment epithelium cells represents a common downstream pathogenetic pathway in various hereditary and complex retinal diseases, including age-related macular degeneration.

Lipofuscin is one of several fluorophores in the RPE. Different fluorophores may be related to different damage to the eye.

A major hydrophobic component of RPE lipofuscin is the fluorophore A2E... Given that A2E strongly absorbs in the blue region of the spectrum, together with the known susceptibility of RPE to blue light damage, we undertook to investigate A2E as a fluorophore involved in blue light toxicity.

Science Insight: Using the Retina’s Natural Fluorescent Light to Measure and Treat Disease
FUNDUS AUTOFLUORESCENCE IMAGING: Review and Perspectives
The Lipofuscin Fluorophore A2E Mediates Blue Light–Induced Damage to Retinal Pigmented Epithelial Cells

Thanks for your answer. But the main point I mention LED is because it is photovoltaic, conversion between electricity and electromagnetic wave. The point is photovoltaic will absorb wave to generate electric current. And it is reversible material that if apply electric current it will emit light. So I wonder if the mechanic of light absorbtion to convert light energy to electric signal of retina is photovoltaic then it could reversible by retina material emit light when apply cirrent

Still your answer amaze me that retina is also fluorescence emitting yellow light. So maybe human always see blue light with a bit of yellow, never see true blue, or even any true color if other cell fluorescing other light too

@Thaina To specifically address the idea of using electricity to make photoreceptors "work in reverse" and emit light, we have to look at how photoreceptors work. A photon hits a chemical in the receptor, causing it to absorb energy and change shape. This triggers a series of proteins to signal each other and eventually close sodium and calcium channels. With those channels closed, the cell becomes hyperpolarized. While this is described in terms of electric charge, it is not the same as semiconductors like LEDs.

I think is an simple yet very applicable answer here.
Anything with a temperature will emit photons via thermal radiation.

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Key points of Wagner's theory of innovation
What are the key points of Andreas Wagner's "theory of innovation" from his book The Origins of Evolutionary Innovations?
Specifically:

What is new in his theory?
What problems in evolutionary theory does it address*?

Wagner does not propose any new theory. He uses the word innovation to mean evolutionary adaptations that manifest qualitatively different traits. In fact, he has himself not defined it properly in the mentioned book. This is what he has written about the term innovation:

It may be difficult to define rigorously what an evolutionary
  innovation is [538,616]. However, these and countless other examples
  show that it is usually easy to recognize: a new feature that endows
  its bearer with qualitatively new, often game changing abilities.
  These may not only mean the difference between life and death in a
  given environment (just think of biosynthetic abilities), they may
  also create broad platforms for future innovations, as did innovations
  of photosynthesis and of complex nervous systems.

However the examples he cites in the introduction are not as obvious as he says. Lets say the evolution of nervous system. The innovation that would have led to evolution of nervous system could have been the evolution of electrically excitable cells.
Actually, throughout the introduction he does not actually clarify the meaning of innovation. In page-3 he does list some features of innovation but it is all still vague. Without a rigorous definition nothing is easy to recognize and classify (especially in theoretical terms).
I do not have the book and cannot look through the entirety of it. However, based on what I have read in some of his papers I can comment something about what he possibly means by innovation.
In certain dynamical systems, some parameter changes can lead to qualitative differences in the output (bifurcations). Steven Strogatz's book on Non-linear Dynamics and Chaos is a nice and easy read on this topic.
If you look at some of Wagner's research papers, you would understand this idea better. Some of these papers are about how some parameter changes can affect the overall outcome (which may be drastic). For example, in this paper the authors talk about how differences in cell division rates can affect the outcome of a cell differentiation event.
He also talks about metabolic innovations which refer to changes in metabolic reactions and network leading to new products/optimized growth etc. Details of this can be found in his lab's papers on Metabolic Flux Balance Analysis.
There is nothing new or drastically different about all of this. This is just an addition that was unknown during Darwin's time. All that he says is still quite in agreement with the current evolutionary theory. (But personally, I find the opening of the book too vague).
As far as empirical corroboration is concerned, you may have a look at his lab's research papers.

What is new in his theory? What problems in evolutionary theory does it address?

No major problems really. The problem he is claiming, or at least how it is portrayed, doesn't really exist. To borrow from my answer to your since closed question (see that answer for more):

"Wagner appears to suggest that Darwin's theory relies on novel mutation arriving after selection changes, which it does not.."

Put simply, selection acts on genetic variation. Novel selection can occur through two principle routes: acting on standing genetic variation or novel mutations. In the case of standing genetic variation, variants exist in a population and then the adaptive landscape changes, introducing selection (fitness differences) between the variants. In the case of novel mutations, there is a standing potential for fitness differences but there is no genetic variation underlying the trait, until a mutation arises.

Side note: examples of how standing genetic variation and novel mutation affect adaptation
Imagine that there is standing genetic variation for heat tolerance, but this variation is outside the normal range of temperatures (allele 1 allows tolerance of up to 30 C, allele 2 allows tolerance of up to 40 C, but the environment never exceeds 20 C). There may then be a shift in the environment which means that it sometimes exceeds 30 C. This means selection suddenly acts on the previously neutral standing genetic variation. It is not a new idea that previously neutral genetic variation can come under selection.

"Alternatively, a pre-existing neutral allele can drift to intermediate frequency and can later become advantageous when selection pressures change owing to environmental change or to colonization of a new habitat."

Conversely, imagine that higher sperm motility would increase reproductive output, but there is no genetic variance for sperm motility. In this case there is no selection on sperm motility (selection occurs only when there is genetic covariance with fitness), but if a novel mutation arises which does affect sperm motility, suddenly we have selection.

What Wagner's idea does suggest is that, because genes act in interacting networks (see epistasis), previously neutral standing genetic variation can be brought in to play for selection. If novel mutations arise in one gene that allow standing genetic variation in another interacting gene to affect fitness then selection acts on both loci. It's not so much a problem he is dealing with, just an additional idea of how genetic variation can accumulate in populations and allow rapid adaptation. It is this idea of harbouring genetic variation that can be brought in to play that is the novelty of the work.

"Wagner has emphasized how epistasis – interactions among genes that shape the adaptive consequences of mutations – allows neutral variation to modulate the effects of other mutations, producing a vast range of possible mutant phenotypes that may lead to an adaptive innovation."


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Why are fingerprints different even in identical twins?
Why are fingerprints different from person to person? It can't be genetics. Even identical twins has different sets of fingerprints. What is the deciding factor that form and shape our fingerprints?


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Why isn't the upper limit of pain lower in humans?
From what I understand, pain is an useful mechanism that signals us that something is not quite right with our body (in particular, we're under attack). It's good - it alert us and tells us that we got to do something (stop the threat, or run away, etc). From Wikipedia:

Pain motivates the individual to withdraw from damaging situations, to
  protect a damaged body part while it heals, and to avoid similar
  experiences in the future.

However, there are damages that cause too much pain. If you are stabbed in a particular place, you will most likely have so much pain that you simply can't fight back or run away. The shock makes it incredibly hard to do something or even think properly.
So my question is: is there a reason why pain can elevate to such high levels? I'm just assuming that if we had some sort of hard limit on the amount of pain we receive, we could perform better in several dangerous situations. In other words: instead of hurting so much that we can't even think properly, it hurts enough to let us know we are in grave danger but still capable of assess the situation and perhaps even act accordingly.
Obviously some physical damages will render you unable to act anyway. Like, damages on the spine that may cause your limbs to malfunction. But I mean damages such as a large open wound on the abdomen: if that didn't hurt so much, I'd imagine you could probably stand up and run away (you'd probably bleed out but at least you'll have a chance to escape the threat).
My guess is that it "cannot be helped". Pain are signals from different parts of the body to the brain, and once a signal is sent, the brain has no choice but to process it accordingly.

There is no hard upper limit, but there is a soft (dynamic) upper limit. An injury that will result in you being paralyzed with pain would be almost unnoticeable if you are in shock.

You are assuming that fighting back with a bad wound would be more useful than dropping to the ground. That is not always the case.
Dropping to the ground and ceasing activity is very adaptive in almost any situation involving potentially significant blood loss. Becoming prone or supine prevents loss of consciousness, the most critical aspect of survival. Decreased movement is also likely to decrease the rate of blood loss (though not in as significant a manner as consciousness).
Certainly with a significant abdominal wound, running would increase cardiac output, which would increase bleeding. Is running from a traumatic event advantageous if you pass out before escaping? On the other hand, lying prone and holding the wound (instinctive) may reduce bleeding and prolong consciousness and life.
What "cannot be helped" (like withdrawing a hand from a flame) is usually advantageous.
An infant's cry changes during circumcision (an involuntary reaction to pain). The cry in turn naturally produces a visceral reaction in nearby adults that compels action (causes a state of strong sympathetic nervous system activation.) The adult either avoids the cry by trying to distance themself, or responds by coming to the infant's cry.
The infant cannot help changing the intensity of the cry with intense pain. If a "certain level of pain" was as far as one could feel, the baby might not elicit the sense of urgency in adults which it does.
Newborn pain cries and vagal tone: parallel changes in response to circumcision.
ASSESSMENT OF INFANT CRY: ACOUSTIC CRY ANALYSIS AND PARENTAL PERCEPTION

The upper pain limit is far above the the worst cry though. I suspect from reports on runaway pain disasters that cutting it in half would make no difference.

@Joshua - I'm not sure what "runaway pain disasters" are, and as someone who worked in an emergency department wherein pain management is a necessary skill, it seems I should know about runaway pain disasters. I agree, though, that there is pain in excess of our ability to express it, but, again, as an ED doc for many years, I have only seen it a few times. What can't be expressed as words (or cussing) is expressed in body language, and there is only one time that the pain seemed so great it was truly inexpressible. It was hellish for me, too, watching and trying to treat that.

I wondered how I might answer, and then much later I remembered how a dog has a much lower pain awareness or a much higher pain tolerance. I've never seen the human having too much fun to let us see if the mouth bleed is a problem, but the dog sure wanted to play despite the mouth bleed from what we could only think was a thorn. But if that's all the pain experience a dog needs (which doesn't have a good enough head to know what needs treating otherwise) than why do humans need so much more pain experience?


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What are limitations on the number of objects the eye determine at a glance?
Take two people Sam (average human) and Jack.
Jack says to Sam "I'm going to show you some skittles (or other object) and I want you to tell me as quick as you can how many I'm holding." He opens his hands and there are three. Sam can instantly tell there are three. Then Jack shows five to Sam, who takes a little longer, as he knows there are around 4/5 but can't tell so has to count.
As the number of skittles increases, Sam takes longer and longer to answer to the point where he needs to count the skittles one at a time to be sure, and sometimes to even recount them.
Why is it that we can instantly if we are looking at three maybe four objects but any more than this we cant? It gets harder and harder to estimate?

The answer to this question is complicated, but assume it's not for the moment. The easy answer is that our eyes can detect patterns we're familiar with and "produce" an answer in the form of a number. Unfamiliar patterns do not produce this 'number'.
Take a die. We are immediately aware of the number of dots in the typical arrangement of one to six. We need expend no counting to do so. If the skittles are arranged in the familiar die pattern, we will have no problem knowing if there are 4 or 6 skittles.
Given a pair of dice, any gambler can tell you what number any two faces adds up to without counting the spots. Do it long enough, and your brain is on auto-recognize. In your example, if Sam is a gambler, and the skittles are arranged like the spots on two dice, again, no problem telling between 2-12 skittles.
If you arrange things in a comfortable pattern, this can go on into the hundreds.

The above was easily recognized by you as nine, I presume.

Someone good with pattern recognition will know that the above left is 25 dots. However, they will not know that there are 25 dots in the above right.
So, the easy answer is that the eye can grasp high numbers of things if they are presented in a familiar pattern. The normal mind, however, is not able to do so with higher numbers arranged in a random pattern. And, random is how most things present themselves. So, we need to count.

While this is interesting, this sounds like pure conjecture. Do you have sources for this information?

@gravityassist - I hope you realize that by eyes, I don't mean the retina.

I didn't make that assumption. I just wanted op to have that information.  Still doesn't change the fact that you have no sources to back up your answer.

Ahh so its not neccesarily amount of objects but the pattern they are arranged?

This question appears to be related and the top answer lists a number of sources:
https://psychology.stackexchange.com/questions/3475/what-is-the-maximum-number-of-objects-an-average-human-being-can-recognize-at-on
Summed up, the average human can apparently recognize the exact number of up to 3-4 items almost instantly, but for anything above that either needs a counting mechanism that somewhat linearly grows with amount of items (which for 4-8ish can still be super fast, so you wouldn't necessarily notice the difference yourself) or there needs to be a familiar pattern which helps you determine the number more quickly.

I have modified your answer, in particular substituting number for amount. Amount should only be used for non-countable objects in English, which in this specific instance is particularly pertinent. As an aide memoire — "amount of  sugar (non-countable), number of lumps (countable)".


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Boundary of a cell and its membrane - position definition and jargon problem
Can extracellular be extramembrane/intramembrane?
Definition of Extracellular here:

Extracellular matrix: The extracellular matrix is a complex network of material such as proteins and polysaccharides that are secreted locally by cells and remain closely associated with them to provide structural, adhesive and biochemical signalling support.

Another definition here:

The extracellular space is the space outside of the cell membrane but part of a multicellular organism. The term is typically used for a secreted protein that remains associated with the cell, e.g. as part of the extracellular matrix. It is not used for a protein that is secreted into the blood stream (or other body fluids) of eukaryotic, multicellular organisms, such as insulin or fibroblast growth factors.

Not really helpful in clarifying. On Google, various sources tend to give rather conflicting definitions.
This is one definition of Extramembrane found here:

In this study, we find that over 60% of the extramembrane domains were structurally related to proteins of known structure.
There's no definition or figure of what makes up extramembrane, yet it's been used over in journals.

Consider following scenario in terms of domains of integral proteins, membrane proteins, for e.g. loop-1 of A-protein is inside cell but outside membrane(?), helix-1 is inside membrane but outside cell(?), loop-2 is outside cell and outside membrane.
Can we refer to loop-1 as extramembrane and intracellular since it's not within membrane but within the cell? What is the correct reference to this domain?
Can we refer to helix-1 as intracellular (as well as transmembrane)?
Can we refer to loop-2 as extramembrane? extracellular?
What is the corrent way to refer to these 3 positions?
Asking this question becasue there's a real dilemma around holding an accurate understaing understanding and definitions of cell components references/positions and use of the above jargon.

Neither of those definitions are definitions of "extracellular". One is "extracellular matrix" one is "extracellular space". I think overall you're not really asking a very goal-directed question, what's the problem to solve here? Can you give a specific example where conflicting terminology is used in different places?

@BryanKrause goal is to know clearly what defines extramembrane and extracellular of a cell, membrane, that consists membrane proteins. e.g. a figure/image showing exactly what comprise of these definitions.

They are adjectives that mean "outside a membrane" and "outside a cell". Do you know an example where these terms are used inconsistently based on those meanings?

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


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Do plants use only solar energy or can they get energy from other forms of light?
Plants use energy from sun. Is it just sun's light energy or any form of light (like light from a tube light) can excite electrons and initiate photosynthesis.
This actually sounds a bit idiotic but in Campbell Biology 10th ed. there is a line in Ch 4. "Plants use solar energy to convert atmospheric CO2 to molecules of life...."
If it is due to sun, then how does plant know which light is from sun and which is not?

Plants use any light of the proper wavelengths. The sun provides a lot of light, but think of covert/indoor plant growing: the right bulbs (and enough of them) allow the plants to grow strong.

@anongoodnurse I think, you could make an answer out of your comment.

@Remi.b - I don't mean to sound unkind to the OP, but I think it's pretty common knowledge.

I don't think we should refuse questions because it feels too introductory to us. When not knowing the answer to such question, it might actually be hard to look for it so I don't think it shows lack of effort. I'll just answer it using your comment if you don't mind.

As per @anongoodnurse comment:
Plants use any light of the proper wavelengths. Typically the available light to plants is the sun but if you place a plant indoor under a fair amount of light bulbs that produce light at similar wavelength that the sun, there is no reason for the plant to even notice the light is different that the sun light and the plant will grow just normally.


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What specific interaction between methylphenidate and quetiapine causes toxicity concerns?
A number of reputable sources on drug interactions posit a potential interaction between methylphenidate and quetiapine, described on Medscape as follows:

quetiapine increases toxicity of methylphenidate by pharmacodynamic antagonism

I'm trying to understand the pharmacodynamics of this supposed interaction, and where the elevated toxicity concerns come from. I've been unable to find a direct source for it that describes the exact mechanism of toxicity.
I'm coming at this without a whole lot of background in the topic, but I do understand the basics of binding profiles, dissociation constants, agonists/antagonists, binding affinity, etc., which has at least allowed me to do a bit of preliminary digging. This is what I came up with, based on the reading I've done so far:
Quetiapine's binding profile differs from its primary active metabolite, norquetiapine. Both have a fairly long list of receptors to which they can bind: SERT, NET, 5-HT receptors, α receptors, σ receptors, dopamine receptors, histamine receptors, and muscarinic acetylcholine receptors.
The most frequently theorised hepatotoxicity concern for methylphenidate apparently involves an interaction with β-adrenergic agonists. However, quetiapine does not appear to have any particular binding affinity for β1 or β2, and the description above says antagonism rather than agonism.
Methylphenidate mostly affects DAT and NET, along with a couple of 5-HT receptors.
5-HT1A seems unlikely to be involved, since methylphenidate has a fairly low binding affinity for it, and quetiapine / norquetiapine are agonists.
Quetiapine is an antagonist for 5-HT2B, but only dexmethylphenidate is known to have any affect on 5-HT2B, and even then it doesn't appear to have a particularly strong binding affinity.
Quetiapine, unsurprisingly, has a strong effect on SERT. Levomethylphenidate has a mild effect on SERT, but other forms are not known to (both Ki and IC50 exceeding 10000).
This left me with the most likely interaction: methylphenidate is an NDRI, so it fairly strongly blocks the norepinephrine transporter (NET), and norquetiapine also has a strong blocking effect on NET. This seems like a strong candidate for being the source of concern - they're both antagonists on the same receptor. Two drugs blocking the same receptor is usually a recipe for problems.
Reading more of the literature, it seems like α2A probably also plays a role here. From what I've read it controls norepinephrine production in a negative manner, since it's an autoreceptor. If inhibited, it may increase the amount of norepinephrine in the brain. Quetiapine is an α2A antagonist, so that's a secondary mechanism by which quetiapine would affect norepinephrine levels. α2B and α2C may also be involved here but I couldn't follow the literature well enough to figure that part out.
This is where I start to lose track of things. What I suspect the interaction is referring to is that both drugs increase norepinephrine through one or more mechanisms (e.g. by inhibiting reuptake and/or increasing production) leading to a potential scenario where a person who takes both drugs may end up having far too much norepinephrine. However, it isn't clear to me where the toxicity comes from. The symptoms of excess norepinephrine mimic that of stress, which can lead to increased blood pressure, but it seems odd to refer to that as "[increasing the] toxicity of methylphenidate"  - that phrasing implies that some aspect of methylphenidate is already inherently toxic, and that quetiapine somehow specifically amplifies that. I'm struggling to reconcile that with my understanding of the pharmacodynamics. It also seems odd, to me at least, to refer to those symptoms as "toxicity". I guess it's technically correct, in the sense that anything that damages an organism is toxic, but it seems like a stretch.
Can someone provide a clearer explanation of this theorised toxicity? Am I missing something obvious? Is my (admittedly armchair) analysis fairly close, or am I way off?
 Medscape reference: quetiapine (Rx) or Methylphenidate. Both have identical statements.

Could you cite some of those reputable sources? It’ll help other people give a good answer. Thanks!

Medscape and Drugbank were the primary two. WebMD's interaction checker repeats the same interaction description as Medscape, although I wouldn't necessarily consider that to be quite as reputable. NICE BNF didn't list an interaction, but that list doesn't tend to include less severe interactions when they're only theorised.

Something potentially relevant that I just spotted: Drugbank mentions increased seizure potential from methylphenidate use, but doesn't have many details. Their page for bupropion, on the other hand, goes into more detail. However, that only serves to confuse me further - it states that norepinephrine has anticonvulsant properties, then goes on to say that bupropion (and, by inference, NDRIs in general) are thought to have proconvulsant properties that arise from their norepinephrine reuptake inhibition. That seems backwards to me.

If you're going to quote something, you need to reference the specific source of that quote. In this case you should do that with an [edit]. Ideally other specific information should also be tied directly to a specific source with a reference for that specific item.

You're already ahead of the curve on your research into this question. Doing a quick Google Scholar check (after the usual drug info/interaction sites), I haven't found the exact antagonist mechanism of quitiapine. I suspect you might need a PharmD to answer this. I'm not sure the problem is hepatotoxicity; are you? What, exactly, is your concern? I would have guessed (I'm not a pharmacologist) the interaction referred to is an increase the adrenergic property of methylphenidate, but I don't know. Please edit to make clear your concern.

Also, if this is a personal thing - as in, you're taking both meds (no judgement here) - this is the wrong place to get your information. You should be talking to your pharmacist/pharmacologist or your psychiatrist; I'd recommend a PharmD. If your primary doc put you on the combo, forget about asking them (I'm a doc, so I can say that with confidence.) The Pharmacist can give you an idea of the incidence/severity of interactions; the PharmD can give you the pharmacodynamics as well.

@BryanKrause It wasn't possible to directly link to the interactions on those websites. The search function is implemented through in-page XHRs and didn't give me a unique URL. Hence the lack of a direct cite.

@anongoodnurse I appreciate the concern, but I'm not asking for personal medical advice. I am taking both medications, but due to the dosages and dose timings the pharmacokinetics add up to a very minimal crossover, and both my doctor and pharmacist are OK with it. I asked the question out of curiosity and a desire to better understand the relevant pharmacology; I don't think it'll ever affect me personally.

@anongoodnurse Re: "I'm not sure the problem is hepatotoxicity; are you?" - No, I'm not sure it's hepatotoxicity. I suspect it's not. My current best guess is they're concerned about a scenario akin to serotonin syndrome but with norepinephrine instead, with seizures as a potential primary complaint. But I've been unable to discover a good source for this, although, admittedly, likely in no small part due to my lack of formal training in this field.

Drugs.com doesn't display any interaction between methylphenidate and quetiapine. You should be sceptical while reading articles and drug instructions. Sometimes the things people write there are nothing more than guesses and loose thinking, and you can debate them (even the claim that quetiapine is useful for "schizophrenia" is debatable).

quetiapine increases toxicity of methylphenidate by pharmacodynamic antagonism

Pharmacodynamics refers to the study of drug actions, for example the affinity for different receptors is pharmacodynamics. In contrast, pharmacokinetics is concerned with the fate of a drug: how does it spread/how is it distributed after administration, how is it metabolized.
An antagonist is something that blocks/reduces the effect of a drug/ligand.
By stating "pharmacodynamic antagonism" we can infer that there is not a pharmacokinetic concern. A pharmacokinetic interaction could include, say, drug A impacts the absorption of another drug B: that could lead to lower or higher concentrations of B when co-administered with A rather than alone. It could involve interference with the metabolism of the drug, like by inhibiting or activating liver enzymes, causing more or less of B to be in an active form for longer/short periods of time.
Okay, so how can pharmacodynamic antagonism increase toxicity? That seems to be the primary question here. How can blocking the effect of a drug make it more toxic, without having any pharmacokinetic effects?
First, it seems like this Medscape reported interaction is mostly a theoretical one. I do not see reports of this being a substantial interaction of concern, and Medscape gives it a rather low "monitor closely" guideline.
I believe the concern they are raising is that because quetiapine may reduce the effectiveness of methylphenidate, higher doses of methylphenidate may be necessary to get the same effect. That could increase the potential for hepatotoxicity, particularly in combination with other drugs. I think this warning is meant to advise providers to think about this and consider all the combination of drugs given.
It's difficult to build a database of all possible higher-order combinations of concern, and that's why this sort of information is meant to be interpreted by a physician (particularly a primary care doctor who acts as a central point of care) or pharmacist to decide what level of concern is relevant for each specific individual case.

i'm absolutely surprise that in the most supposedly famous forum about biology sciences, that no one knows what pharmacodynamic antagonism means... with all the respect, (and for god sake..) its right on the name they are antagonic: one is an antipsychotic the other is a CNS stimulant.. thats the problem, they have opposite mechanisms of actions and thus the side effects (or toxicity.. like medscape calls it,, drugbank says side effects.. who cares honestly they are antagonic and thats the problem)

Think I should first start by mentioning that I am not a physician nor I am trained to make any clinical or diagnostic reasoning.  With that in mind, let me try my best to clarify most part of the question.

regarding a somewhat theoretical point of view, pharmacodynamic interactions

are those in which drugs influence each other’s effects directly source

drug to drug interactions often are classified as synergistic, additive, or antagonistic in nature reference
and thus when the effect of one drug is impeded by another, the effects of these drugs are antagonistic
Back to the point,
methylphenidate, in a nutshell, acts by blocking the reuptake of dopamine and noradrenaline which leads to the increasing levels of dopamine and noradrenaline in the synaptic cleft
on the other hand, quetiapine (is almost the opposite) a second generation antipsychotic has antagonist actions on 5-HT2A/D2 receptors (serotonin receptor/dopaminergic receptor) but are also partial agonists at 5-HT1A receptors (another serotonin receptor).
as I've mentioned quetiapine is a second generation antipsychotic (which is still, at present time, synonym for "not so clean drugs", what I mean by that is that they bind to almost everything that is receptor.. ) and thus the other receptors that you have mentioned (H1 and alpha 1 antagonism) are linked to side effects source
as one can see

This table shows Ki values for quetiapine at different neurotransmitter receptors. Ki is inversely proportional to affinity. This means that high Ki numbers suggest low affinity at a given receptor, while low Ki numbers are associated with high affinity.

they like to bind.. (a lot..) and thus the side effects.

Now, once established some background, lets go to the main part of the question: Why some literature reports toxicity interactions between the two?
in fact drugbank.com also reports similar

The risk or severity of adverse effects can be increased when Quetiapine is combined with Methylphenidate. Drug Interactions section

that has to do with the pharmacodynamic properties of both, since one has the opposite mechanism of action of the other (pharmacodynamic antagonism) it is expected to notice some increase of side effects.

Finally I would like to address, once again, to the fact that I'm not a physician and that therapeutically it has been reported with some relative success the combination of those two drugs

Conclusion: Quetiapine addition to methylphenidate was effective in reducing ADHD and aggression in individuals who did not respond sufficiently (based on CGI-S, RAAPP, and ADHD-RS-I criteria for significant improvement) to OROS methylphenidate alone at a 54-mg/day dose. study

The quote is under methylphenidate on this page: https://reference.medscape.com/drug/seroquel-xr-quetiapine-342984 - "quetiapine increases toxicity of methylphenidate by pharmacodynamic antagonism. Use Caution/Monitor. Closely monitor for signs of altered clinical response to either methylphenidate or an antipsychotic when using these drugs in combination"

founded, my apologies, couldn't find the reference at time. I'll edited my answer.

nevertheless, what i wrote remains true and applicable to the subject; toxicity in that sense regards to the fact that since one drug is antagonizing the other mechanism of action thus leaving adverse effects as major result for the organism, that's the meaning of toxicity in this context. there's no CYP450 interaction (which means that an increase of the steady state concentration of one of the drugs will not happen) nor toxicity due to pharmacokynetic factors such as metabolization.. hence the main meaning of that phrase contextualized is that side effects can be increased

I've upvoted your answer, but the last part was disturbing. Sure quetiapine "was effective in reducing ADHD and aggression", because it makes you sleepy and apathetic. It's ridiculous to claim that it "treats" ADHD.


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Why are both glucagon and cortisol released in hypoglycemia?
Cortisol is released in response to prolonged stresses; one situation when cortisol is released is when blood glucose level is low. In this situation cortisol acts on adipose tissue promoting fatty acid mobilization, and also promotes gluconeogenesis by degrading muscle proteins and converting them into pyruvate. Cortisol also stimulates gluconeogenesis by increasing the expression of PEP Carboxykinase the enzyme of gluconeogenensis pathway promoting the TCA Cycle intermediates or Oxaloacetate to convert into Phosphoenolpyruvate and promoting gluconeogenesis to balance the blood glucose level.
These are the same effects produced by glucagon to increase the blood glucose level when it is low.
My question then is what is the need for release of Cortisol? Also, if its release is important to control other pathways I haven't mentioned here, then why does cortisol produce the same effects as glucagon? Why is glucagon alone not enough to maintain blood glucose level?

Since the ability to utilize glucose for energy is necessary for life (look at the effect of hypoglycemia on brain function, for example), it makes sense that the regulation of serum glucose concentration would have a number of pathways, that is, redundancy helps to ensure continued proper function should one of the regulatory mechanisms fail.
Glucagon is considered the main physiological response to hypoglycemia; however, epinephrine, growth hormone, and cortisol - in that order - and very probably other factors yet to be named/elucidated also help to increase plasma glucose when it drops.
This kind of redundancy is very common. Cortisol, epinephrine and growth hormone all have other effects on tissue unrelated to glucose as well.
Glucose Counterregulatory Responses to Hypoglycemia


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What impacts penetrance of Huntington's disease?
From Principles of Life by H. Craig Heller, David E. Sadava, Mary V. Price:

From what I understand, Huntington's disease exhibits varying degrees of penetrance depending on how many times the mutation is found in the person's genome. Penetrance is nearly complete if the incorrect base pair sequence is found over a certain number of times.
My question is what affects penetrance? Is it exclusively environmental?

and your question is?

It's in the title.

I also don't understand your question. That definition of penetrance says nothing about the environment.

To me, it seems like you are arguing against the "exclusively environmental" idea in the section on Huntingtons. What makes you think/ask that it is exclusively environmental? The short answer to the title Q is No - the genetic background (genes at other loci) can for instance affect penetrance. You should also include a reference to the book you've scanned.

Also, penetrance is a property of a population, not an individual.

HD is a late onset disease. The effects are not usually apparent until some threshold is reached.

@WYSIWYG - ~10% of patients have onset in their childhood (as young as 2) and teens. The majority develop their obvious symptoms in their 30's and 40's (some believe the earlier symptoms are largely overlooked) and only 10% develop the disease after 55. If you had the mutation, I doubt you would call it late onset.

It is "considered" a late onset disease; most affected individuals reach reproductive maturity before manifesting the symptoms. I don't think 10% patients develop the symptoms in childhood. See here

@WYSIWYG - it is considered adult onset. As to percent of juvenile onset, see here, here and here.

@anongoodnurse - Okay I see the difference. I had been using the term late onset to mean post sexual maturity (as I heard around).

Penetrance describes the frequency of a gene's expression:

Penetrance refers to the proportion of people with a particular genetic change (such as a mutation in a specific gene) who exhibit signs and symptoms of a genetic disorder. (Genetics Home Reference nih.gov)

More specifically:

[P]enetrance is defined as the percentage of individuals with a given genotype who exhibit the phenotype associated with that genotype. For example, an organism may have a particular genotype but may not express the corresponding phenotype, because of modifiers, epistatic genes, or suppressors in the rest of the genome or because of a modifying effect of the environment.

Note that the environment is only one factor affecting the expression of an allele.
Retinoblastoma and achondroplasia are often referred to in discussions about penetrance.
Retinoblastoma is caused by mutations in the Rb gene. Not all people who carry this mutation suffer from retinoblastoma (about 90% do). There are numerous inherited diseases (including cancers) in which the same mutation is not expressed in all the individuals who carry it. Achondroplasia, on the other hand, has 100% penetrance: every person with the specific point mutation in the fibroblast growth factor receptor 3 gene always has abnormal bone growth and dwarfism.
Huntingtons is a little different in that patients with 36 to 41 HD CAG repeats exhibit reduced penetrance; that is, some may not develop HD in their lifetime; however 100% of those with the mutation produce the abnormal/polyQ/polyglutamine-enlarged huntingtin. The age of onset is dependent on number of repeats but is affected by other modifiers (both genetic and environmental); this becomes less obvious in individuals with higher repeats sizes (e.g. greater than 44).
Huntington's is not a genotype affected only by environment.
 Genetics in Medicine
 A new model for prediction of the age of onset and penetrance for Huntington’s disease based on CAG length

however 100% of those with the mutation produce huntingtin.: Everyone produces huntingtin however its exact function is unknown. HD patients produce the Polyglutamine expanded one.


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How do cellular waste products enter arterial blood?
I recently learned that blood in renal arteries contains waste materials, which is filtered via nephrons in the kidneys.
My question is, how are these waste materials getting into the arterial blood? I believe arterial blood is pure and devoid of waste (since all the waste from cells and tissues must enter veins).

there's numerous "waste" products that are continuously produced via metabolism - like urea and ammonium - these are continuously excreted in the urine or eliminated in the feces - they are present in the entire circulation

Arterial blood isn't "pure". It is simply in one part of a complex circuit which carries varying degrees of oxygen, nutrients, and waste products, etc., to varyious parts of the circuit.

...how are these waste materials getting into the arterial blood?

The most simple and direct (but teleological) answer to this is that toxins need to get into arterial blood to ever get to the kidneys to be filtered. The arteries carry blood to every part of the body, detoxifying organs included. Veins carry blood away. If there were no waste products in arterial blood, the kidney would be superfluous.
Waste is produced in all tissue. Blood carries oxygen and nutrients to the tissue (where some of it is used), and via the venous side (all over the body) blood carries the waste products (as well as unused oxygen and nutrients) away toward the heart. The blood carrying waste products collects in increasingly larger veins until it is dumped into the right side of the heart and pumped into the lungs, where a major waste product (CO2) is partially removed. Things that need to be removed by the kidney are all still there. Blood carrying these toxic products is dumped into the left side of the heart, and thus enter the arterial blood supply. The kidney then can remove waste products partially or completely when it reaches them.

Good grief. Now that I have 10K, I can see how unnecessary my answer was. :-(

That was helpful.


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Name (and meaning of the absence) of the white semicircle at the base of the fingernail?
At the base of fingernail, there is a white semicircle (see on the first picture). But sometimes there isn't one.

My questions are: what is this white semicircle on the fingernail, and what causes it? What is the explanation when there it isn't on all of the fingernails (see on the second picture)?

The lighter crescent-shaped part at the base of the nail is called the lunula. It is a normal part of the nail matrix, and indicates nail growth. The faster your fingernails grow, the more obvious the lunula.

Absence of the lunula without any other abnormalities of the nail is not uncommon, and while it can indicate anemia or malnutrition, it is often found normally, and with aging. In this case, careful inspection of all the nails will usually reveal a lunula on the thumbs and the fingers closest to the thumb, but a very small or absent lunula on the other fingers.
In your picture, there is clearly a lunula on the middle finger, and, I suspect, a larger one on the index finger, and a relatively normal one on the thumb. This is not a finding of great concern in the absence of other pathology.

The lunula: The small, whitish, half-moon shape that you sometime see at the bottom of your nails is called the lunula(pronounced loon-yoo-la). It's actually part of the matrix. You might be able to see it only on your thumbs, or maybe not at all. Don't worry if you can't see a lunula on any of your fingers. It's no big deal. It's there, just under your skin.

Examining the Fingernails When Evaluating Presenting Symptoms in Elderly Patients
Examining the Fingernails
Nails


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Can canines communicate with each other using gaze direction?
After researching why humans have white scleras when most primates have dark scleras, I stumbled upon the cooperative eye hypothesis. It proposed that white scleras may have evolved on behalf that it is an effective form of communication in that it makes the iris stand out and enables another to clearly see where the eye is looking so as to read expressions.
I noticed that dogs, which also have white scleras, use eye direction periodically for expression. Does the cooperative eye hypothesis apply to canines as well? If not, then for what reason might dogs utilize eye movement as they seem to do? Might such a thing be learned behavior?

It is hypothesized that the starkness of white sclera against darker colors of the pupil and iris is a unique mutation in primates that have become prevalent in human beings because it enhanced our ability to communicate with other humans and animals, including dogs, by more clearly communicating where we are looking.

However, it has not yet been established that dogs use this communication with each other, communicating more commonly with other means such as body language, head direction, vocalizations, etc. Some dogs, especially domesticated ones, do have white sclera and it is proposed that this is due to unintentional selection by humans who have a preference for such features.

What is extremely fascinating is that this 'mutation' occasionally occurs in chimpanzees and apes, too, but has not become prevalent in their respective populations.

Sources:

Secret Life of Dogs- BBC Film
Do the Eye Have It?-Academia
Common feature in domesticated dogs-CARTA
Juvenile features-NIH

"it has been observed that dogs do not use this as communication with each other" I saw no evidence of this in your cited papers. Can you provide support for this claim? That is, after all, the OP's question.

His original question asked if the cooperative eye hypothesis applied to canines.

I'll clarify what I meant to say.

A new study published in the journal PLoS One compared facial characteristics, gazing behaviors, and sociality of 26 different canid species (including wolves, bush dogs, and Arctic foxes). The researchers found that animals with eyes and facial features that are easier to discern are more likely to live and hunt socially. (One of the authors, S. Kohshima, has studied the morphology of the human eye, its adaptive meaning, and has done comparative studies on external morphology of the primate eye.)
In this paper, the authors identified three face-eye types based on four contrast indices: the A-type, in which both pupil position in the eye outline and eye position in the face were conspicuous (11 species, including wolves and coyotes); the B-type, in which only eye position on the face was conspicuous (9 species, including the Fennec fox and jackals); and the C-type, in which both the pupil and eye position were inconspicuous (6 species, including the bush dog and the African wild dog).

They compared group living vs. solo/pair living, group hunting vs. solo hunting, gaze duration and other parameters. Citing supporting evidence from other authors as well, they found that in species engaging in group living, 8 of 10 study species exhibit A-type faces. African wild dogs (C-type) use their white-tipped tails as visual signals, and like dingos, use vocalization, suggesting a developed acoustic communication. In contrast, gray wolves made almost no sound even during play or fighting but had more gazing behavior in more postures. Therefore, species with B- or C-type faces that in engage group living may use acoustic and/or other visual signals instead of the gaze signal as their primary means of communication (as is true for wolves and dogs). The enhanced gaze-signal of the A-type face could be disadvantageous during hunting, as prey animals could use the gaze signal to realize that they have been targeted by the predator and then prepare to escape. A-type faces were more common, then, in group hunting, where solo hunters were more commonly B or C-type faces.
In gray wolves, the gazing behavior (0.5s on average to humans, 3.32s average with up to 38s maximum with other wolves), termed conspecific with others of the same species, suggest that the gaze signal of gray wolves is mainly used for communication among conspecifics.

These results suggest that the facial color pattern of canid species is related to their gaze communication and that canids with A-type faces, especially gray wolves, use the gaze signal in conspecific communication... Our comparison of face morphology and gazing behavior among canid species highlighted the gaze-signal communication in species with A-type faces, especially gray wolves, and provided a novel perspective for studies on their communication and morphology.
Could the cooperative eye hypothesis apply to dogs as well? If not, then for what reason might dogs utilize eye movement as they seem to do?

Yes. (By the way, many dogs have white sclera.) The difficulty is that dogs are usually raised alone with humans and can lose the ability to "read" other dogs. One study, however, examined the behavior of dogs with human social cues (such as gazing) and conspecific (other dog) social cues. (Primates have been found to respond to conspecific social cues more than human gaze/pointing.) When the informant in this study (the one giving the cues) was an unfamiliar human, dogs responded well to gaze and gaze/pointing. However, when the informant was an unfamiliar dog (tethered, standing still, no human around to look at), the dogs were also able to follow the gaze of the informant dog, even when the body pointed elsewhere. Furthermore,

This skill with conspecifics is somewhat surprising because many of these domestic dogs had had only limited experience with other dogs. Indeed, the one intriguing developmental finding was that the 6-month old juvenile was only able to use cues produced by conspecifics, whereas two 4-year olds (the oldest in the sample) were only able to use human cues. ...it does suggest the hypothesis that many dogs are able to use conspecific gaze cues from early in life without extensive experience with conspecifics, and then ontogenetically, they extend this ability to humans (to some degree on the basis of similarities in human and dog facial features) as they interact with them - perhaps in some cases to the point that they lose their ability with conspecifics.

If more studies focused on conspcific cues among dogs instead of focusing on their interactions with humans, I think this behavior would be borne out and would be readily established.
A Comparison of Facial Color Pattern and Gazing Behavior in Canid Species Suggests Gaze Communication in Gray Wolves (Canis lupus)
Development of Gaze Following Abilities in Wolves (Canis Lupus) (interesting video)
Domestic Dogs (Canis familiaris) Use Human and Conspecific Social Cues to Locate Hidden Food
A Review of Domestic Dogs' (Canis Familiaris) Human-Like Behaviors: Or Why Behavior Analysts Should Stop Worrying and Love Their Dogs (just a cool paper)


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Book recomendation: cell cycle regulation
I aim to study cell cycle regulation, can some of you suggest a good book or website that systematically explains the topic.
It should include-

Detailed account of Cyclin and cdks involved in different stages of cell cycle
Spindle assembly checkpoint
DNA damage checkpoint
Special roles of Rb and p53 proteins in cell cycle regulation

A) Useless title, again. B) For book recommendations you need to specify with detail what the book should include detail on and why "obvious" choice are unsuitable - as it stands its far to broad/will illicit primarily opinion based answers

Robust texts covering such 4 listed points with rigour include the following selection:

Molecular Biology of the Cell
Molecular Cell Biology
Cell Cycle Regulation
The Cell Cycle Principles of Control.

& even a review of the latter here.
HTH

Start with "Cell Biology" by Gerald Karp (Wiley). You can then move onto "Molecular Biology of the Cell" by Bruce Alberts and Alexander Johnson (Garland Science).


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What are silent carrier traits?
I couldn't find a definition but I have come to know the following from google search:

People who are carriers of a thalassemia gene show no thalassemia symptoms and might not know they're carriers.

So is thalassemia a "silent carrier trait"?

How many times do I have to tell you that you should not ask a question about the definition of a term that is not really a standard term? There are no "definitions" for terms like these; they are just contextual and anyone who understands English language would figure out what these terms mean. You did the same in your other question on "Why is tRNA called an adaptor molecule".

Thalassemia is a recessive trait. That means individuals with only one copy of the allele (Heterozygotes) have the "normal" phenotype (they don't have Thalassemia).
If an individual is homozygous for the recessive allele they will have Thalassemia.
Heterozygotes are often referred to as carriers as they can transmit the allele to their offspring, but do not themselves express the trait.
"Silent carrier trait" is quite unusual terminology, just call it a recessive trait.


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Linear and Circular DNA
So school has taught us that eukaryotes have DNA that is linear and inside of a membrane - called the nucleus. And that prokaryotes have circular DNA that is free floating inside of the cell.
We also know the pros and cons of both linear and circular DNA.

Are there organisms with circular DNA that also have a cell nucleus?
Are there organisms with linear DNA that is also free-floating within the cell?

generally prokaryotic cel contain circular DNA with exception like agrobacterium tumefaciens that contain 3 circular & one linear DNA.

Yes there are prokaryotes with linear chromosomes (especially archaea). Eukayotic chromosomes are almost always linear but this, study reports that yeasts with a loss of function mutation in the ATM homolog genes TEL1 and rad3, form circular chromosomes as a consequence of lack of telomeres. Upon prolonged culture these yeasts were found to undergo mitosis but not meiosis.

Strictly speaking, all nucleated (eukaryotic) cells contain linear DNA. In addition to the nucleus, the mitochondria (which break down food molecules and create chemical energy) and chloroplasts (which facilitate photosynthesis) also have small stores of their own DNA and this DNA is circular. This adds weight to the hypothesis that these organelles were once prokaryotic cells that came to exist in symbiosis with early eukaryotes.
There is also cytoplasmic DNA free-floating in eukaryotic cells. These are also circular and normally contain short copies of chromosomal DNA sequences. Their function is not well understood.
In prokaryotes, some species of spirochaetes and bacteria have been found with linear chromosomes. In addition, prokayrotes contain extra-chromosomal DNA called plasmids. Bacteria are able to pass plasmids from one to another and express the genes on them: this is an important source of the spread of antibiotic resistance genes through bacterial populations. Plasmids are also normally circular, but linear structures also exist.
References:

Cohen, Sarit; Andreas Houben; Daniel Segal (2008). "Extrachromosomal circular DNA derived from tandemly repeated genomic sequences in plants". The Plant Journal 53 (6): 1027–1034.
Hinnebusch J; Tilly K (1993). "Linear plasmids and chromosomes in bacteria". Molecular Microbiology. 10(5):917-22
Finbarr Hayes (2003). "Chapter 1 - The Function and Organization of Plasmids".

"There is also cytoplasmic DNA free-floating in eukaryotic cells." Is this stated in one of your references? I'm having a hard time tracking it down.


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What traits make mountain goats so well adapted to mountain living?
I've never really understood how mountain goats manage to survive so well in mountainous regions. I've seen them scale almost sheer cliff faces with apparent ease, and they can almost sprint vertically downwards without losing their balance.
How do they manage to do this? I can't see any discernible characteristics that would make them able to achieve this particularly well. For example, snow leopards achieve similar feats, but they have incredibly long tails and large paws to help with balance and agility, yet the skinny legs and hooves of mountain goats seem largely unfit for this purpose.
What adaptations do mountain goats have that allow them to survive in mountainous regions, and how do they work?
I'm hoping mostly for information on how they perform such feats of agility as to move around on very precarious outcroppings and such, but am also interested to hear about any other qualities that they may have to deal with the other mountain conditions (altitude/ cold etc.).

Pretty sure this answers it: https://en.wikipedia.org/wiki/Mountain_goat

@Minnow That has a good overview of which features allow it to live in the mountains, but it doesn't really go into the detail of how those adaptations work in order to allow it better chances of survival.

Are you sure?  "The mountain goat's feet are well-suited for climbing steep, rocky slopes with pitches exceeding 60°, with inner pads that provide traction and cloven hooves that can spread apart. The tips of their feet have sharp dewclaws that keep them from slipping."

@Minnow Dogs have inner pads for traction on their feet too, as well as dewclaws, however they don't live on the sides of mountains. And it doesn't go into any detail whatsoever about how cloven hooves help them to traverse such inhospitable terrain. I'm looking for more specific answers, such as: How do they have such good balance? How can they determine which outcroppings will be stable/ large enough to stand on? Does their eyesight help them to do this, or is it learned from parents? I wanted to keep it reasonably broad, as I'm looking for any and all ways they survive on mountains.

+1  I relent.  you want to know more about mountain goat adaption! :)

@DavidBlomstrom If that was posted as an answer I'd happily accept it.

Mountain goats belong to the subfamily Caprinae, or goat-antelopes. The higher family is the Bovidae (cloven-hoofed mammals).
Now members of Caprinae are pretty stocky in their build and have thicker fur both of which help them survive in the higher altitude. Their ability to scale/descend sheer cliffs with such agility comes down to their cloven hooves. Their hooves enable them to grasp onto the the face of the mountain in areas other animals could not as well as shift direction very quickly. Despite the fact that cloven-hooves are not unique to mountain goats or other members of Caprinae it is a trait essential for them to be able to inhabit those harsh environments.
Nubian Ibexes (also a member of subfamily Caprinae) are experts at climbing as well; one of the best Caprinae members in my opinion. Nubian Ibex baby and fox


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Variant VCF: AD vs DP?
In my VCF file from GATK, I have the following definitions for AD and DP.
AD - Allelic depths for the ref and alt alleles in the order listed
DP - Approximate read depth (reads with MQ=255 or with bad mates are filtered

I don't understand the definitions, can anybody explain in a less technical way?
From what I can read, AD gives the number of reads spanning the reference and variant allele. But what does DP mean? This doesn't look like the total number of reads spanning a variant, so what is this? How does this different to AD?

DP is the total number of read bases spanning a particular position. If you add up the different AD, you should get a number close to DP, the difference being merely in how the reads are filtered in either set of numbers.


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How to solve the problem of 2 melt peaks in real time PCR?
I am facing a problem in my real time experiment. After standardizing the annealing temperature by semi-quantitative PCR, I did real time for my gene of interest. In one of my samples, I got 2 peaks in the melt curve. Thinking it would be non-specificity, I tried by increasing the temperature further by 3 degrees. But still found 2 peaks in the same sample. I ran the product in a gel and found one blazing band and below it another distinct band. Is it still non-specificity or I am starting to think it could be an isoform? Also, in the same sample, with respect to control, protein expression is increasing whereas when I analyzed my real time, the RNA levels are coming low. Please provide your inputs.
See an image of the melting curve below. The red ones are melt peaks of my gene of interest. Green is of housekeeping gene. There are only 2 samples that show two peaks.

What is the size of the band corresponding to the first peak (I suspect that it should be around 100bp. What is the GC% of your primer?). You may try reducing primer concentration and run the PCR again (for all samples). I cannot be sure if it is an isoform. Try extracting it from the gel and doing a Sanger sequencing. Did you run the RNAs on gel to check integrity? You may try doing that too. The other band can also be because of a degradation product.

Regarding protein expression not correlating with RNA expression- that can be quite complex. You may compare this case with other samples which are supposed to show the same biological effect.


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Is complete genetic linkage possible?
Linkage is the tendency of genes on the same chromosome to remain together during the process of inheritance. Is it possible that two genes will remain linked generation after generation without any crossing over between them? Can anyone give an example?

Complete genetic linkage does occur in some cases.
Most of the Y chromosome (present as a single copy in males of many species) does not recombine with the X chromosome. Any genes in this non-recombining region, the "male specific Y" (which is 95% of the Y), will be "completely linked", in other words, they cannot be broken apart by recombination and are inherited as a single unit.

Non-recombining region of the Y marked as NRY from this paper.
The closer two genes are, the higher the general tendency for them to be co-inherited. When co-inheritance is non-random the genes are in linkage disequilibrium. The genetic linkage between genes is measured in centimorgans.
I'm not aware of any completely linked genes in recombining parts of the genome. By definition there is some distance between two linked genes (otherwise it's one pleiotropic gene). Therefore, if recombination is possible, then it is possible for them to become unlinked at some frequency, even if that frequency is extremely small (I could be wrong though, but scholar searches have given me nothing). There are, however, cases of very tight linkage between genes (1, 2, 3).
Note that factors other than genetic linkage can affect linkage disequilibrium.