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Human brain is superior than till-date computers, yet why we perform poor than computer?
Scientists found storage capacity of synapses by measuring their size.
They found, on average, a synapse can hold about 4.7 bits of information.
This means that the entire human brain has a capacity of one petabyte.
This is same as about 20 million four-drawer filing cabinets filled with text.
Striving around this stuff, I have a weird doubt crawling in my mind and it goes like this: Why is it like this that a human whose brain has got a capacity to store 1 petabyte, i.e. 1 million GB, cannot fully remember even the contents and information of a simple textbook which on the maximum would not be more than 1 GB, when he has to appear in exam? Why is storage capacity not directly linked with remembering capacity?

The reason is that it doesn't make sense to compare human brain with a computer. If you do that you will always end up with these kinds of questions.

Keep in mind that scientists have consistently underestimated the storage capacity of the brain for generations. One petabyte sounds like yet another limit that'll look ridiculously small one day. 4.7 bits per synapse also sounds very low; not only do we not know how much of the bit depth of each electrical charge is translated into information, but we're still discovering new, multiple forms of charges arising from different chemical processes in each synapse. How much information is added by recurrent structures, continuous time differences in spiking and the like is all up in the air too.

@Ankur you haven't understood my question properly. I advise to you to kindly go through the question once more.

@Ankur To skeptically understand the brain's (or even any cell's) work; we must have to consider its 'computation' mechanisms at some or some step . So indeed it makes sense.

Maybe we need a RAM upgrade? :)

Three reasons:
Most of the storage capacity of the brain is used to store implicit knowledge. For example how to move your body, how to automatically recognise objects or how to hear and parse your language. These things may seem easy to you, but they require a lot of learning. Just look at how clumsy five year olds still are, they have been training how to use their body for five years straight and still skin their knees all the time.
Humans are actually able to retain huge amounts of information, both in their short term memory and in their long term memory. We know this because there are savants and hyperthymesia. It is likely that these abilities are actively suppressed in neurotypical people.
Because it is just not evolutionary adaptive to remember every detail. Intelligence depends on weeding out unnecessary information. If normal people learn huge amounts of information they often rely on memory abilities that are evolutionary adaptive, like the ability to remember a path from landmark to landmark.

Quite satisfactory!

The subconscious and unconscious processes too, should require some memory space.

To answer your question, we store information in a different way than a computer would, the storage happens in the connections in between neurons and it's not a perfect copy of what the environment presents, but rather certain features, I'll give you a classic example, read this sentence:
Tahkns for Cnotriubtng an asnewr to satck ecxahgne

You can understand the sentence even though the inner words are scrambled because it is not stored as a carbon copy, but rather as similar things attached to meaning within semantic and syntactic rules which in turn are stored as well, the recall and storage happens through a network in parallel, so the storage and the recall happens as you read it.
To give you a numerical example of how limited our brains are in terms of data as we know it, there are around 26,000,000,000 (26 billion) neurons on the Neocortex ( the number will probably go up-down in the future, but let's just use it for reference and assume it is only used for vision), your vision has 260,000,000 (26 million) cones and rods, where light is registered. If you were storing the information pixel by pixel in neurons alone, you would run out of space after just 100 frames. The synapses though  are a different matter,a conservative estimate is around 150 trillion: 150,000,000,000,000, and if you were storing perfect copies, you would run out of space after ~ 580,000 frames, or 4 movies.

This is a very good answer, +1'd for that  'classic example'

I think that it's not a store problem, but the way we access the stored information. Suppose you have a computer with 1 petabyte storage and you are asked you to find a file, that is stored somewhere. If you don't have a decent searching strategy or your files are not stored orderly, it would take you a very long time to find them.
This is why learning strategy focuses more on how to retrieve information in exams and less on how to store it.

OK, I got what you are trying to say, but what about this : I suppose that during the peak hours before the exams, one focused only on the prescribed syllabus preparation, si

So, why does he still fails to remember the complete stuff that he reads? I guess there is something very peculiar in this. What you have to say regarding this?

Well, i guess he fails either because he did not store the complete information or he cannot retrieve it all or fast enough. You have to keep in mind that just because you read something, you don't automatically remember all of it in great detail. And i think @BlindKungFuMaster 's answer adds well to this:  it's not is just not evolutionary adaptive to remember every detail.
I'd still say it's mostly about how to get what you want when you want it from your brain. Imagine it a s large library and your task is to organize it all well so you'll find the books you need fast enough.

Fail to recall is one cause... but not the only-cause. Brain doesn't capture unnecessary information. It doesn't collect at all (filters them out). http://www.bbc.co.uk/science/humanbody/mind/surveys/memory/feedback.shtml?photos=2&mbindlevel=4&mbindscore=4&numbers=9&grid=16&coin=3&stamp=3&delayed=1&sentences=6&manball1=11&manball2=12&rem1=1&rem2=2&rem3=1#6

@Heinke Hihn Even-if we well-arrange the lessons in our mind, we (normally) can't "recite" a story in exact detail (but can make a short summary of it); whereas a notepad or word-file can present that exact within moment (though the second one should be more simple and easier from computational viewpoint). This is because our brain is not at all hard-wired to do that. Whereas instead a story if you take a certain 'molecular pattern' (such as vaccine from a pathogen * ); a cell (for this * example immune cells) would easily memorize it bcoz immune cells hard-wired naturally that way.

Yup you are on a right question.
This concept is already well known as Turing Test, named after famous mathematician A. M. Turing. You might notice that if you ever read about CAPTCHA values.
Human and all other living beings (including a cell) can do some very complicated things. We do very complicated tasks at our day to day life, may it be chatting with your friends about random topics, finding a similarity between today's soft weather with trees waving in breeze with  a similar one 2 years ago, or to understand and elaborately explain the meaning of 'rolling stone gathers no moss', or to be able to tell a short summary of a long story.  or writing a poem. Or to 'create' new paintings.
Yes skeptically, all these tasks can be done with help of computer; but it will take huge algorithms and hardwares. These tasks are troublesome for a computer, but easy and 'simple art' (so-called) for us.
But what is difficult to most of us; such as to calculate a huge mathematical problem within instant; or to recite the sentences of a huge novel in exact ditto, or to serve some tasks in an exact routine; etc. is very easy for a computer, and takes much smaller algorithms and hardware-advancements.
Turing-tests try to provide tasks, those are easier to human (or perhaps animals), but tougher for a computer. It could be said, The better a Turing-test, the more it easier to human than computer.
But Why that difference? plausibly we're evolved in a way to perform some highly complicated tasks that we perceive as apparently "simple". We are (mostly) naturally talented on them. But we're not hard-wired for some 'real' simple tasks so we defeat in front of computer.


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What makes us "tired" in the gym that forces us to rest?
If I'm doing push ups or any other of gym exercise, I can do 10 in a row, but each one I do I feel more "tired", but if I rest for 5 minutes, I'm much "full of energy". Please explain me exactly what is different in my muscles chemistry.
I read that lactic acid overproduction is possibly linked.

I think you refer to the Muscle fatigue:

A state of exhaustion or loss of strength and/or muscle endurance following strenuous activity associated with the accumulation of lactic acid in muscles. (Source)

So yeah, you're right about the lactic acid overproduction :)
How Muscle Fatigue Works ?
During short term (anaerobic) exercise, ATP and creatine phosphate (CP) are used up within the first 7 seconds of training. This signals the metabolism of glycogen to produce energy for your body. This process is known as glycolysis.
During glycolysis, glycogen (muscle sugar) is broken down to produce more CP. The breakdown of CP releases energy, which catalyzes a reaction to produce ATP. The production of more ATP allows movement of the muscle to continue.
Lactic acid is a product of glycolysis created by the breaking down of pyruvate.
Lactic acid is then disassociated to produce lactate. When lactic acid (C3H6O3) releases a hydrogen ion (H+), the remaining compound binds to a sodium ion (Na+) or a potassium ion (K+) to form a salt. It is this salt that is lactate.
Now the cell contains a lactate compound and a free H+ for each compound of lactic acid that is produced. It is this increase in cellular H+ that causes the pH to decrease, becoming more acidic. The acid in the muscle causes the fibers' calcium-binding capacity to decrease, thus limiting muscle contraction. This is the cause of muscle fatigue.

So the muscle Fatigue occurs when the muscle experiences a reduction in its ability to produce force and accomplish the desired movement.
Short term fatigue (failure to lift a heavy weight, do more push-ups, etc.) is different than long term fatigue such as as a marathon run, a 100 mile bicycle ride, or a full-day hike through the Rocky Mountains of Colorado.
Muscles become fatigued during high intensity exercise, most notably that the demand for oxygen can be greater than the supply. The blood flow to the muscle can be reduced because of :

muscles intensely contracting can reduce blood flow and thus oxygen availability, or
the muscle is simply working so intensely that there literally is not enough oxygen to meet demand (a sprint at top speed).

The factors that explain fatigue are complex and after more than 100 years of investigation are still a topic of active research, you can check those articles for more informatoins :

Experiment: EMGs during Muscle Fatigue
All About Muscle Fatigue
Skeletal Muscle Fatigue: Cellular Mechanisms

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Why aren't cat hybrids common?
Why aren't hybrids of different species of felinae (say, hybrid of domestic cat with manul, cheetah, ocelot, puma or panther) widespread? Why were they not artifically created?

I'm not sure why you say cat hybrids are not common. Savannah cats spring to mind. Generally speaking animal hybrids aren't common, because they often have to be produced through unnatural methods. See Felid hybrid for a number of examples. It is true that there have not been reported successful hybrids of Felinae and Pantherinae, but I doubt it is not for lack of trying...

In fact I first read about savannah cat, than read that article about hybrids, noticed the hybrid of puma (felinae) and leopard (panthera) and thought that if such species far away from each other on the dendrogram (the one in the first answer) have hybrid, there may be other hybrids of felinae and panthera. So I wondered why there is no so many diverse artifical hybrids.

@KOLANICH I hadn't heard of the pumapard when I answered, so I added an edit mentioning it. It doesn't appear to have been genetically robust, and at least some people have questioned whether it was a leopard-puma hybrid at all, but I can't find any reputable sources on it. It appears to have been sterile. In general such hybrids are not impossible, but at best unlikely, and as I said in my answer their existence is more surprising than nonexistence of others.

In order to form a hybrid, substantial genetic similarity between the organisms is required. To understand why, the successful formation of a zygote from the gametes of the two parents (i.e. fertilisation) in higher animals like mammals requires that the genomes of the organisms be reasonably similar (or homologous; see for instance human fertilisation). This is because successful development of the fetus appears to require that a very specific combination of genes and proteins be present and in the right relative ratios (it's helpful to remember that the genome is a highly analogue computer (see here also), not just a set of instructions to build an organism) - think of the significant effects of simply having an extra copy of one chromosome in Down syndrome, or the fact that triploidy or quadruploidy are often tickets to the death of the human embryo (and so having half of your genome from two different animals could lead to an imbalance in the proteins required to develop normally). I'll be addressing mainly the feasibility of obtaining a hybrid at all; of course in order to become widespread a hybrid would need to be fertile (although see the sterile mule) which would require even more genetic similarity, specifically in order that the chromosomes from each parent can interact, they have to be similar enough that the proteins regulating this process will recognize them as homologous, and enable a process like chromosomal crossover to take place during the meiosis occurring in gametogenesis.
To answer your question about felinae and panthera first, several panthera genomes have been sequenced, and (see here) the tiger for instance has only 95.6% similarity with the domestic cat and diverged 10.8 MYA. For comparison, human and gorilla have 94.8% similarity and diverged 8.8 MYA, so that puts into perspective why you wouldn't expect a tiger-cat hybrid, or for that matter any felinae-panthera hybrids. Those dates are from the linked paper. (Edit: It appears from wikipedia as referred to by the OP above that there actually is a puma-leopard, i.e. felinae-panthera, hybrid which I wasn't aware of (although all of the reports are old, so there is no genetic evidence to prove that it was in fact a hybrid). I assume this may be an exception to the rule; what I was trying to show is why such hybrids are not necessarily to be expected, and as I said below, I'm more surprised about how many hybrids are possible. It does appear though that this particular hybrid is prone to dwarfism, which indicates that it probably does not have a particularly viable genetic makeup, and I think it was sterile).
With regards to your question about felinae hybrids, if you go to Timetree, then it will tell you that Panthera tigris and Felis catus (domestic cat) diverged 14.4 MYA, and by comparison Aciconyx jubatus (cheetah) and Felis catus diverged 9.4 MYA, so it seems reasonable to suppose that they can't hybridise. (But note that P. tigris and P. leo still diverged 6.4 MYA and they can hybridise: the relatedness of two organisms isn't the only thing at work, and a better measure is the genetic similarity; this paper mentions that hybridisation ability correlates both with genetic similarity and time since divergence). Interestingly, this paper actually indicates that the percentage alignment of the cheetah genome to the domestic cat genome is only 91.1% with 93.6% similarity to the tiger, indicating that the cheetah may be a specialised outgroup.
For a more familiar comparison to all of these, Canis lupus which is the ancestor of the domestic dog, dingo, and the gray wolf only arose around 700,000 YA according to wikipedia, although I do not know the exact sequence similarity. Domestic dogs (everything from chihuahuas to great Danes) only diverged 40,000 YA, so the different cats are only superficially similar by this comparison.
There's a diagram on wikipedia shown below which nicely illustrates the different hybrids within felinae (although some seem dubious), so you can see there are actually quite a lot, and although most of the cats involved haven't been fully sequenced, presumably some of these hybrids cross some of the boundaries which I've mentioned above. They do actually include a successful hybrid between a domestic cat and an ocelot (although I can't find another source for this, so it might not be possible), and a hybrid with a jaguarundi (which appears to be closely related to the cheetah) is described as dubious here. Unfortunately, I don't know if either of those cats has been completely sequenced. Ultimately predicting hybridization is a complicated field.

This image below shows a more detailed phylogeny of the cats to illustrate the evolutionary timescale:

And for a comparison to all of that, this image below (from here) shows the phylogeny of the dog (which you might be more familiar with in terms of hybridisation), and if you realise that the whole part of the tree in B from the bush dog down diverged 9-10 MYA (see here - comparable to the whole cat family) and that the bush dog despite its name is extremely dissimilar to modern dogs (for instance it only has 74 chromosomes compared to the domestic dog's 78), then this will illustrate that the evolution of the modern hybridisable dog family (in C in the image) is tightly packed into a much much shorter time than the entire cat branch. All of the names like D1 on the right are modern dogs.

With regards to your question about artificial creation, I think a point to remember is that a lot of these cats are rare/endangered and although such hybrids are still done, there is also criticism of such proceedings. Anyway, I think a good take-home point is that the cat family is actually very genetically old and diverse. I think it's more surprising how many cats can actually be hybridised.

Terrific answer, +1 seems too little. Welcome to the site!

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Have creatures ever evolved to become less intelligent?
Inspired by https://worldbuilding.stackexchange.com/questions/58533/is-intelligence-the-natural-product-of-evolution , I'm wondering if creatures have ever become less intelligent as a result of natural selection and evolution.
It seems plausible, because the brain can use a lot of energy, and I've heard of other aspects of an animal atrophying because they're not useful any more, such as vision in the Mexican blind cavefish.
One possible candidate I can think of is the koala: it's described as having a low brain to body mass ratio, doesn't have a great need for intelligence, and may have a need to minimise energy usage.
I'm mainly interested in cases of natural selection, as opposed to artificial breeding - I wouldn't be surprised if we selected animals to be less intelligent.

Unfortunately, measuring intelligence (assuming we would have a strict definition) is not a thing that can be done from fossil record or genetic data. The only thing one can do is to compare brain mass (or at least size of the cranial cavity) from fossil record. In this regard, no need to go very far for an example, humans are an example. From wikipedia

The evolutionary history of the human brain shows primarily a gradually bigger brain relative to body size during the evolutionary path from early primates to hominids and finally to Homo sapiens. Human brain size has been trending upwards since 2 million years ago, with a 3 factor increase. Early australopithecine brains were little larger than chimpanzee brains. The increase has been seen as larger human brain volume as we progressed along the human timeline of evolution (see Homininae), starting from about 600 cm3 in Homo habilis up to 1500 cm3 in Homo sapiens neanderthalensis which is the hominid with the biggest brain size. The increase in brain size topped with neanderthals; since then the average brain size has been shrinking over the past 28,000 years. The male brain has decreased from 1,500 cm3 to 1,350 cm3 while the female brain has shrunk by the same relative proportion.

Note however, that wikipedia does not cite any reference and I failed to find one!
Note, also that one should not confound cranial cavity (the thing that is actually measured) with brain size and more importantly no confound brain size with intelligence. Wikipedia goes on saying

However it is argued that another essential element of brain evolution in humans is rearrangement (Hoffman et al. 2004). Larger brains require more wiring, but more wiring can become inefficient (Hofman 2001). The brain has therefore become reorganized for efficiency. Furthermore, the average body size of nethanderthals was larger which led to bigger brain size (see Brain-to-body mass ratio).

I could not find the Hofman papers but I probably just did not look hard enough (and am a bit tired right now)! One might want to read Healy and Rowe 2007 for a criticism of the inference that can be done from measures of cranial cavity.

Domestication is often given as an example, though it seems to be debated.
I'm guessing almost all parasites have become less intelligent in their evolution to parasitism, you could probably find some slam-dunk examples there.
More specific but anecdotal and possibly opinion-based, I recall in the book "Adventure among the Ants" the author draws a line between the size of an ant society and how competent and intelligent its individual members are. He specifically talks about how ants evolved, how the species with the biggest colonies are comparatively recent, and how there is an inverse correlation between an individual ants' size, brain size, complexity of behavior etc and the size of the colony it's a part of.
In other words, the evolutionary history of ants involved the evolution of larger and larger colonies, and in the lineages where this happened, as the species evolved to exist in larger colonies, the individuals in that species evolved to become simpler and less intelligent.
You could plausibly find examples if you look for examples of organisms that evolved to be smaller - if only because that can involve smaller brain size.

Yes, there is one great example just off the top of my head,Tunicates which have evolved to lose their brain as they mature. The simple reason this happens is brains are expensive they cost calories and material that could be spent elsewhere so just like anything else under the right conditions (when they are not helpful (such as in sessile filter feeding sea squirts) a reduction and/or lose will be favored.

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Is Cas9 unique in it's ability to act in response to a specific DNA sequence?
As a computer scientist, I'm interested in the ability of the Cas9 protein to function as an if-gate for DNA. It opens up so many questions for me. Right now the protein works as "if the sequence matches, cleave", but perhaps you could customize it to do "if the sequence matches, [do arbitrary action]". However, I'd feel very dumb if I got all excited about this and it tuned out "no... there are plenty of things that function as [if sequence matches], the real revolution of CRISPR/Cas9 is... [something else]". Is my fear qualified?

There are two classes of proteins that I can think of off the bat that are DNA sequence-specific. First are restriction enzymes, which recognize a specific (usually short) sequence of DNA and cleave it, sometimes through both strands at the same spot (blunt ends) and sometimes leaving an overhang or "sticky end".
The other class is transcription factors. Instead of altering the DNA, these proteins bind to a consensus sequence and act as a gathering point for the transcription machinery to bind and begin transcribing the following gene into RNA.
What makes the CRISPR/Cas discovery unique is that the binding sequence can essentially be an arbitrary sequence, defined by the scientist, allowing for cuts just about anywhere. Transcription factors and restriction enzymes depend on the local sequence of the DNA itself, so they only bind in certain spots.
There are other sequence-specific technologies available, such as TALEN, but they are basically a combination of a site-specific transcription factor and a fairly non-specific restriction enzyme or nuclease fragment engineered into it that cuts at a specific, user-defined site, depending on which subunits are used. CRISPR is a much more powerful (and easier to implement in vivo) technology, though, so while TALEN still has a place in the molecular biology toolbox, CRISPR is rapidly eclipsing it.

Just a minor thing but the TALEN class of nucleases are actually transcription factors with a FokI nuclease domain attached to it. They resemble the old zinc finger nucleases in that they are DNA recognition proteins with a nuclease attached to it. CRISPR is unique in that it is a nuclease in its original form.

@mimat yes, you're right. I wrote that last section quickly, based off my reading on TALENs a little while back. I didn't remember that they actually have TF activities as well. I reworded that section a bit.

OK, if you want analogy, you can think of Cas9 as comparing device: if sgRNA (guide RNA) matches DNA, then cleave. You can pick this up from Wiki article or publications on CRISPR/Cas9
Read about DNA restriction enzymes. If in case of Cas9 template is provided by sgRNA (guide RNA), in case of restriction enzymes template is built-in this enzyme.
Cool thing about Cas9/CRISPR is that you can engineer guide RNA to match 20 bases of DNA for high specificity.


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Type I and Type II Topoisomerases
Type I topoisomerase changes the linking number by ±1 by changing the number of twist present in a DNA, breaking only one strand.
Type II topoisomerase changes the linking number by ±2 by changing the configuration of the writhe,breaking both the strands.
Am I right?

Sannukta. You should know better than to give a question a meaningless title like this. It shouldn't be hard to think of something involving topoisomerases and linking number.

I hope this might help. http://www.pnas.org/content/99/19/12126/F1.expansion.html and http://www.pnas.org/content/99/19/12126/F1.large.jpg. (However I confess me too feel these mathematical topics extremely tricky.

The speculations are right.
Topoisomerase I changes the linking number by changing the number of twists and Topoisomerase II changes the linking the number by changing the writhe of DNA.
Confirmed by a college professor.


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From where did the selfish gene get its selfishness?
This is in reference to the book The Selfish Gene by Richard Dawkins. Further,

Because there is a law such as gravity, the universe can and will
create itself from nothing. Spontaneous creation is the reason there
is something rather than nothing, why the universe exists, why we
exist. It is not necessary to invoke God to light the blue touch paper
and set the universe going.
— Stephen Hawking and Leonard Mlodinow, The Grand Design, 2010

What was the spontaneous creation that led to this selfish gene?

This is a very introductory question to evolutionary biology. While the book "The selfish gene" is very pleasant to read and directly offers some key notions of modern evolutionary biology, it offers little to no introduction to the basics of evolutionary biology (which is not its goal). I highly recommend that you have a look at a short intro to evolution such as Understanding  Evolution by UC Berkeley for example.
Below, I give a very brief answer to your question but taking an intro course to evolutionary biology would probably be more helpful.
What is evolution?
Evolution is a change in allele frequency in a population through time.
An allele is a variant of a gene (or any other sequence at any locus). A locus is a position in the genome.
How do alleles come to existence?
Alleles are created from previous alleles, through mutations. The process of mutation is random in the sense that the effect of the new allele is "unknown to the organism" which creates this allele. The mutation just occurs and it just has some effect on the phenotype and the fitness.
What are the forces of evolution?
There are a number of forces that affect evolutionary processes such as genetic drift, migration and natural selection for example.
What is natural selection?
Natural selection is the change of frequency of of the alleles at a given locus caused by differential fitness among the individuals carrying the different alleles.
Why one ought to expect that altruism should not exist in nature?
Here the term selfish and altruism are defined in terms of fitness effects. An altruistic individual is one that is performing a behaviour (or having some other phenotypic trait) that is positively affecting the fitness of an individual of the same species while decreasing its own fitness.
Imagine an individual (let's call him the "actor") that has a mutation causing him to be altruistic (in opposition to being selfish). Such "actors" will have a low fitness while its neighbours will take advantage of the altruism of the "actor". There is therefore a differential in fitness between those that are selfish (higher fitness) and those that are altruistic (lower fitness) which ultimately yields a decrease in the frequency of the alleles causing the altruistic behaviour until it completely disappears from the population.
The above paragraph explains why one would expect that altruism should be absent from nature. However, the story is definitely not that simple. But this extension is a story for another time. You will have to understand the difference between "true (lifetime) altruism" and "false altruism", you will have to learn some game theory and finally Hamilton's extension of game theory.
What Dawkins means by selfish gene
In his books, Dawkins uses "selfish gene" often to refer only to genes that are causing meiotic drive (which might be confusing) and to talk about the existence of intra-genomic conflict. There are various mechanisms that can cause meiotic drive. You can learn more about that in Haid and Berstrom 1995, Jeanike 2001 or Jeffrey and Neuman 2002 for examples.

The existing answer provides a very thorough discussion of evolution, which is actually the biological part of the question. I will address  more literally the spontaneous creation part ("What was the spontaneous creation that led to this selfish gene?" - OP) and touch a bit on how the first self-replicating molecules came into existence.
Remark: Note that the authors of the quote in the OP are both theoretical physicists - indeed, the question here is more about "how life emerged" rather than "how it evolved".
Symmetry
Spontaneous creation is a reference to a concept known as spontaneous symmetry breaking in physics, as emergence in philosophy, and as self-organisation in chemistry. One could think of a symmetric universe as a place where chemical elements (or elementary particles) are distributed uniformly over the space, regardless of where we are or which direction we look at. (This is a simplified vision of what is understood by symmetry in physics, but it suffices for the purposes of this discussion.) Obviously, this is not what our universe looks like: patches of very dense matter, such as stars, alternate with vacuum, some parts are extremely hot and others are extremely cold, etc. Things get even more complicated when we look at highly organized dynamic matter, such as the living organisms.
Symmetry breaking
All this complexity is a result of a chain of symmetry breaking events. The interactions between the particles, chemical elements, etc. make the symmetric states unstable, and so they disintegrate into the less symmetric ones. Exactly which less symmetric state is chosen is a matter of accident - e.g., a mutation defining a new direction of evolution an emergence of a new trait is accidental.
Example: particles and anti-particles
As an example: every particle has an anti-particle, so one could have expected that the world contains equal number of protons and anti-protons, as well as of electrons and positrons (anti-electrons). Yet, in practice the atoms are made of protons and electrons, and there are very few anti-atoms made of anti-protons and positrons in the universe. This is the result of a symmetry breaking event that happened some time shortly after the Big Bang, when the symmetry between the particles and the anti-particles was broken.
Example: chirality of organic molecules
As a similar but more biologically minded example, one can think of the chirality of organic molecules. When these are artificially synthesized, one usually ends up with an equal proportion of the molecules of both chiralities. Yet, only one chirality is encountered in the living organisms. This is a result of another symmetry breaking event, somewhere at the time when the first self-replicating molecules had emerged and those of one chirality, by pure chance, gave rise to living organisms, while the others were less lucky.
Emergence and evolution of micromolecules has been also analyzed as a symmetry breaking event, notably by Manfred Eigen, although this requires more abstract notion of symmetry.
Order from disorder
While it is fair to say that we understand well how symmetry breaking comes about in non-living matter (in physics and chemistry), and how evolution happens (in biology), it is not immediately obvious that the scientists agree on how the non-living matter becomes a living one. The interdisciplinary nature of the question certainly complicates it. Prigogine and co-workers believed that the dissipative structures were the answer, but Phil Anderson disagreed. Perhaps one could reproach Dawkins and his brand of militant atheism for hiding under the carpet the unanswered scientific questions, for the sake of fighting creationists (who are arguably a minority even among the religious folks.)
References

Erwin Schrödinger, What is life?
Manfred Eigen, Self-organization of matter and the evolution of biological macromolecules
Phil Anderson, More is different; More is different - One more time
I. Prigogine and I.Stengers, Order out of chaos: Man's new dialogue with nature, Nicolis and Prigogine Self-organization in nonequilibrium systems: From dissipative structures to order through fluctuations.
P. Anderson and D. Stein, Broken symmetry, emergent properties, dissipative structures, life: are they related?
Kauffman, The Origins of Order: Self-Organization and Selection in Evolution

there is no difference between living and non-living matter, it is all just chemistry.

@John the degree of organization and complexity. I know that appeal to authority is a logical fallacy, but note that all the people that I named are Nobel prize winners (Schrodinger, Phil Anderson, Prigogine, Eigen).

@John why do you think biology texts refer to a cell as the elementary unit of life? Are viruses alive?

crystals are far more ordered  than living tissue and a rock is just as complex, they are all part of the same spectrum of chemical interactions. living and nonliving matter are both results of the exact same laws of chemistry interacting in the same ways. None of the papers you link claim otherwise. the rest are books by people with no expertise in the subject. a nuclear physicists opinion on the fundamentals of biochemistry is as bad as a biochemists opinion on the fundamentals of  nuclear physics.

Is ice a rock? Is pluto a planet? Is cereal a soup? Is a taco a sandwich? is self replicating RNA alive? Is a single member of a sexual species alive? human subjective categories have no impact on the function of matter. This is the reason there is no universal definition of "alive" or "life" because there is a continuous spectrum of matter that both living and nonliving matter fall on. cells are the elementary unit of life as defined as things made of cells.

@John crystals have very simple symmetries. The fact that chemical reactions are the same says nothing about complexity Anderson's More is different discusses why everything is not reducible just to fundamental interactions. Importantly, live systems take energy and use it to decrease disorder = to construct themselves, contrary to normal direction of entropy; this is something that non-living matter cannot do (unless artificially designed for this purpose).

nonliving matter decreases disorder all the time, every endothermic reaction decreases disorder, it does so at the expense of creating more disorder somewhere else, just like living things. the formation of solid salt due to evaporating water is a decrease in disorder for the salt.

@John very good, we found some common ground. Do you know what is a heat engine?

Yes they exist naturally too, the Hadley cell is an example of a self organizing naturally occurring heat engine. technically the mechanical energy exerted by freezing ice is also a heat engine. self replicating molecules are also technically heat engines.

@John indeed, but these are very simple examples of ordered behavior. Living things have many more levels of complexity. In a way, one can say that there is a continuous increase of complexity from non-living to living matter, and one cannot draw a sharp distinction somewhere.  This is explained in my answer  and the references.

It is not even mentioned in your answer, in fact your answer says the opposite.

@John "All this complexity is a result of a chain of symmetry breaking events." I suggest that you read my answer more carefully and look up the references before further discussion. Less aggressive attitude is also welcome.

@John note also the question that I am answering: "What was the spontaneous creation that led to this selfish gene?"

@John I have added Kauffman's book to the list fo references - this is probably more accessible to people with biological background.


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Is it possible to perfuse chemicals into brain after removal from body?
I've read studies where fixatives (eg glutaraldehyde) have been perfused into the brain while it is still inside the skull. I would have thought that this could also be done after the brain is removed, provided all the veins/arteries are connected to a perfusion machine. Is this possible, and are there any major obstacles?

Of course it is possible to perfuse an organ once it has been removed from the body. It is probably unwise to do so with the brain as the delicacy of the structures and high levels of lipids make rapid fixation necessary and difficult. I think the major obstacle is the speed at which the brain could be removed with arteries intact and then perfused as ultrastructural changes occur rapidly once ischemia (oxygen deprivation) begins.

The main obstacle would be connecting all of the arteries to a perfusion machine.
 The neurovasculature is complex, and begins branching prior to entering the brain, therefore it is easier to do in situ. With a larger brain, the meninges and skull are also important for supporting the brain stucture. If unfixed brain is removed from the skull, it will begin to deform and collapse under its own weight. For fixation, especially, it is much safer to fix in situ and remove post-fixation.


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What is the name of this black-ochre striped snake?
I've seen the following snake (?) near Calvi (on Corsica):

I guess it was about 50cm long.
What is the name of this type of snake?

Great find!  Based on the picture and location, I believe this is the Corsican grass snake (Natrix natrix corsa).  It is a pretty rare subspecies, and is listed on Annex IV of the European Union Habitat and Species Directive.  Worth mentioning that it's nonvenomous.

Photo cred to Frank Deschandol/Philippe Sabine
Unfortunately, I was not able to find too much more info on this subspecies.  I know Natrix natrix are pretty widespread throughout Eurasia, but this subspecies is much more restricted.


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User friendly phylogenetic tree editing software
Background: I have Hackett 2009 (from birdtree.org) phylogenetic tree and I need to reorder it according to Prum 2015. I also work only with some species relevant to my project, not the entire tree.

I currently use Mesquite, and it is absolute purgatory. Doing any reordering in Mesquite takes insane amount of time. I'd also like to add higher taxon information to each species (like order) to help my my orientation in the data.
I understand some of Mesquite's shortcomings might be shortcomings of Nexus format. As I don't need to analyse the data myself, I can work in some better format like PhyloXML as long as it's possible to export back to Nexus format in the end.
Is there any way to do this? Some software with better visual editor (and overall better UX) or other method to do this in effective manner? I find it hard to believe that much bigger data is handled in such clumsy way.

Can you just start with the Prum tree and cut it down to your taxa?

If one of the answers is helpful for you, it would be a nice gesture towards the author to accept it. Additionally the system will not bump the question anymore.

Yes, I think that you should consider using MultiSeq which is a package of Visual Molecular Dynamics (VMD). You can use visual molecular dynamics to make phylogenetic trees based on sequence/structural/other statistical means.
If you want to check it out and see if it works for you, then install visual molecular dynamics: http://www.ks.uiuc.edu/Development/Download/download.cgi?PackageName=VMD
and try out these tutorials under Bioinformatics from the distributors:
http://www.ks.uiuc.edu/Training/Tutorials/
Note: VMD doesn't work very well in 64-bit Windows operating systems if that's what you use. To get it to work well, I suggest you install virtualbox from Oracle, and install your favorite free open-source Linux operating system into virtualbox or into your guest linux machine on your host machine.
I suggest installing your guest Linux OS on virtualbox with 1/2 the ram of your host physical computer allocated, and like 100 GB of space for when you discover that you love LINUX so much and have lots of information on there.
To full-screen your guest Linux OS, you need to install guest additions.
My favorite Linux OS is Kali Linux.
To install guest additions on Kali Linux and most linux guests on VirtualBox,
you have to do this:
But as I've discovered you have to upgrade Kali Linux to Kali Linux Rolling to get Kali Linux to fullscreen. How you do that is via this:
And you probably shouldn't do your work as user "root" the default user. You have too much power so to increase security create a new user on Kali-Linux:
If you are already using linux, then you won't have any problem with getting VMD to work. But by the way, you have to install VMD from the command terminal in linux and this is how you do it.
The instructions as for how this guy does it (and sorry he doesn't speak English) are in the README file when you download VMD.
Sorry, apparently, I don't have a high enough reputation to cite you all the links. I'm sorry that I had to remove them.

To install Guest Additions: https://www.youtube.com/watch?v=kmnyJ9x0szM

As I said, you have to upgrade Kali Linux to Kali Linux Rolling:
https://www.kali.org/news/kali-linux-rolling-edition-2016-1/
And you also have to install VMD:
https://www.youtube.com/watch?v=5TN_DV3F198
Also, you shouldn't run Kali Linux as "root" user so to create a new user:
https://www.linkedin.com/pulse/20140502074357-79939846-adding-a-new-user-in-kali-linux

If virtualbox still doesn't work for installing a linux distribution, you will have to "enable virtualization technology" in your system BIOS.

I had good experiences with Archaeopteryx. This is a java package so it should be easy to run but I recommend the BioLinux if you don't want to spend too much time installing and get straight to the biology. You can run it as a virtual machine or install it side by side. It is getting a bit older but everything works just out of the box and there is a wide array of tree editing tools installed. Just look through the package list.


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Cell nanoparticle dynamics within blood
I am trying to mathematically model the dynamics of a particular cell in circulation and its binding to another nanoparticle that is intravenously injected. The concentration of this cell is very low (about 5 cells per mL of blood). I want to see how many nanoparticles are needed to bind to as many of these rare cells as possible.
So first, I am trying to model the cell dynamics in the blood flow. I am not sure how to start. I wanted to model the cell movement through the entire cardiovascular system, but I would have to simplify it. I am thinking of modeling the blood flow through some of the major organ systems, and estimating the absorption through the capillaries. I am thinking something like the physiologically-based pharmacokinetic model (PBPK). However, there would be some parameters that I wouldn't know about that I would need for the model (at least that is what I think, I am new to pharmacokinetics) Also for the actual fluid dynamics, I'm not sure how to model this, because the blood isn't just a fluid, and has many other cells, so I don't know if there are some other effects.
So, my question is, in what direction should I go to model the dynamics of this cell in circulation? I want to model the circulation in the entire cardiovascular system, because I need to also model the other nanoparticle dynamics, and how likely it is to find and bind to some of the receptors on the cell. Is there an example of a similar model that has been done?

I'm not terribly knowledgeable in this field, but I've come across it once or twice in my work doing pharmacokinetics/pharmacodynamics (PK/PD) studies on both large and small molecules. To my knowledge, there should be existing published studies on modeling the circulation of cells in blood. While you are correct that blood itself is a complex non-Newtonian fluid, its physics are pretty well established by now. Nanoparticles are also becoming more and more common, so hopefully you should be able to find multiple published reports on modeling them as well, then put the two together.

So, you should be fairly accurately able to determine the dispersion of your cell type of interest as well as the nanoparticles, then it's just a matter of calculating the probability of their meeting and the avidity needed for them to bind - say, for example, that the nanoparticle has a receptor-specific scFv coated on its surface, and the correlating receptor density on your target cell is such-and-such, and the Pk of binding is so many nM or pM or whatever. Good luck, I'm not a math guy (I just take care of the biology)!

This question is a bit opinion-based and would most likely be put on hold for that. However, this is my suggestion. Start with the simplest model and add complexities if the model is insufficient. Don't start with modelling the blood flow: you'll get into PDEs which are more complicated than ODEs. Start with an assumption that the blood stream is a well mixed vessel. You can consider different organs as compartments with different volumes (based on how much vascularised they are).

@WYSIWYG in what sense is it opinion-based? There are only 2-3 possible models that have been previously done. So, it might be a little opinion-based, but is it really bad that it would be put on hold?

I am not saying that it will definitely be put on hold. But different people would have different suggestions on how to model a certain system. Technically, there are infinite ways to model something. If your question is explicitly about reference request (previous models etc) then it is fine; you can add the relevant tag and clearly mention that you are looking for references.

To go the PBPK route:
I would recommend using the organism parameters and structure from the whole body platform model by Shah and Betts.

Shah, D.K. & Betts, A.M. J Pharmacokinet Pharmacodyn (2012) 39: 67. doi:10.1007/s10928-011-9232-2

They have assigned a plasma space volume, plasma flow, blood cell space volume and blood cell flow for each organ and the total body.  The base model structure for circulation is complete if you use the equations for the blood cell space in this paper as the foundation (Eq 2 and Eq 5).
Once the model structure is complete, step 2 is to model all processes that can affect the cell in each compartment.  If the cell is adhering to a nanoparticle, a compartment equation could then be:
d[cell]/dt = (flow in - flow out)/volume + Kon x [nano] x [cell] - Koff x [cell-nano complex]
To model the interaction of the cell with the nanoparticle you will need to model both within the same structure.  A review of PBPK modelling for nanoparticles can be found here:

Physiologically Based Pharmacokinetic Modeling of Nanoparticles
Mingguang Li, Khuloud T. Al-Jamal, Kostas Kostarelos, and Joshua Reineke
ACS Nano 2010 4 (11), 6303-6317 doi: 10.1021/nn1018818

A pharmacokinetic (top-down, classical) model for nanoparticles in the circulatory system may also give insight to how to model the processes that affect nanoparticles in vivo.  This model accounts for fluid dynamics, pore size and specific nanoparticle properties.

Kirtane, A. R., Siegel, R. A. and Panyam, J. (2015), A Pharmacokinetic Model for Quantifying the Effect of Vascular Permeability on the Choice of Drug Carrier: A Framework for Personalized Nanomedicine. J. Pharm. Sci., 104: 1174–1186. doi:10.1002/jps.24302

I am not understanding the compartment equation. Wouldn't it be one for each organ, modeling the concentration and flux of the cell into and out of the organ? I plan to keep the model simple and assume there are no major effects on the cell, in terms of growth, and elimination. However, maybe the elimination of the nanoparticle by immune response might be important.

You're right.  The words "compartment" and "organ" are interchangeable.  Every organ is modeled as a compartment.

Can you fully explain the differential equation you wrote down? Also what parameters do I need to know about the nanoparticle and the cell? Where can I find a good introduction to PBPK modelling?

What does the Kon and Koff model?

Kon is the rate constant used for calculating the rate that the nanoparticle and the cell adhere together, proportional to the concentration of each.  The term [Kon x nano x cell] gives you a rate in mol/time of nano-cell complexes that are formed.   Koff is the reverse rate constant.  https://en.wikipedia.org/wiki/Binding_constant


text:
Why do cockroaches and flying beetles survive high levels of radiation?
Apparently it's a fact that cockroaches survive nuclear radiations.
How can they survive this?

I'm puzzled by your comment that humans are invulnerable to insecticides. Dosage is key; organophosphate poisoning is pretty common (and it is a pretty common insecticide.)

They survive radiations because of their slow cell replication, Humans are NOT invulnerable to pesticides at all. Most pesticides will have really negative effects on humans, and can cause deaths in certain concentrations.

Cockroaches have slow cellular replication rates and radiation is known to be the most dangerous to replicating cells, thus making cockroaches (and several other insects) more resistant to radiation than us, but not immune.
This was the subject on a Discovery episode of MythBuster


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Why is there debate about thymus being an endocrine gland?
I read on my textbook that there is debate about whether thymus is an endocrine gland. But they do have glandular cells no? Is producing T Cells the only point for thinking it not as a part of endocrine system?
So, Q: What's the reason behind this debate and has it reached any conclusion?

In my mind as an immunologist, there is no debate. In order to be part of the endocrine system, a body structure needs to be a gland that secretes one or more hormones to induce signaling at distal targets. These hormones can have multiple chemical forms. However, the thymus does not do that. It was proposed beginning back in the 1960s that the thymus contained and produced something called thymosin, which was eventually separated in 40 separate substances, none of which acts as a hormone, and most of which are now known to be present in many other tissues. T cell production and maturation occur as a result of signaling induced by cell-cell interactions (ligands and cognate receptors on the cell surface) as well as the action of many cytokines and chemokines. These compounds are not classified as hormones, though.
It is possible that some hormones might be expressed in the thymus in very small quantities; however they are not secreted. This is due to a part of T cell development and maturation known as negative selection, where the thymus can ectopically express proteins typically only found in other tissues, such as the nervous system, pancreas, or lung, for example. This process allows for the removal of potentially auto-reactive T cells, which recognize self antigen.
Basically, knowing what we do about the function of the thymus in human and mouse, and how it does what it does, I honestly don't see how someone today could classify it as part of the endocrine system, even though histologically it may appear similar to glandular structures, and small traces of one hormone or another may be found in thymic extracts.

In short, yes the debate has reached a conclusion (years ago), and no the thymus is not an endocrine organ as it does not produce any real hormone.

@Armatus you are absolutely correct. Now, we just need to find an image to replace the one in the Endocrine system article on Wikipedia...

Well, I went and did it myself. Hooray for Photoshop!


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Why does decreasing intake of protein prolongs the lifespan of a fly?
A book I read about aging suggests that it is established that a fly lives much longer when it is fed less protein. What does protein intake has to do with the lifespan of an organism? Why not carbohydrates?

In which book did you read this?

It is a Korean book of which author is a professor at New York University. I can search for the exact title, but I doubt it will help you.

Hmm. Do they have references to scientific articles in that? Korean would indeed not help me :-)


text:
What is the surface area of the cardiovascular system?
In this question says:

An adult human has been estimated to have some 60,000 miles (96,560
  km) of capillaries with a total surface area of some 800–1000 m2 (an
  area greater than three tennis courts).

But the question is about the length and only mentions area in the body not the title, and the answers don't cite the area.

Does the Coastline paradox affect this?

Friction? Drag in blood vessels is much more complex than friction...

@Aron Ok, but maybe I can calculate a lower bound.

@Andrey Very interesting point. To that I can answer this: imagine a blood vessel section of 0.1 meter long, and 0.01 meter in "average diameter" (that needs to be estimated. Then you say the surface area corresponding of that section of the circulatory system is the area of the abstract cilinder we use to represent it. Also, if we specify the ruler size, the area becomes more well defined (althought still subjective a little).

Friction is a very bad word to describe it. But the simplest way to estimate the drag is to use Newton's 3rd. The drag is equal to the force on the blood, assuming the blood is at a steady speed. Figure out how hard the heart pushes.

@Aron I edited out the friction part, it wasn't part of the "question part" of the question. Indeed, it was why the doubt arised but not the doubt itself. Now the question is simpler. Thanks for your help.

@Santropedro so what is your question? Are you asking if the area estimation is correct?

@MattDMo Now the title make it obvious, the question is how much meters squared of surface does the circulatory system posses.

Even that is a difficult question to answer. It really can only be answered with "it depends on what you are asking".

@Aron To wich comment are you answering? I don't understand why it depends on what I'm asking, I'm clearly asking one specific thing. There is no variables that can't be handled in the answer that I see, if there are tell me what they are. I don't understand where the ambiguity is for you, explain please. The cardiovascualr system is a well defined closed system, and a vein for example in wich blood circulates, has a certain shape wich can be asbtractly treated as a tube cilindrically shaped that is curved, with a certain diameter.

See the first comment...the coast line paradox.


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8 abdominal muscles but 10 pack

Simple question, how is it possible that there are people who appear to have 10 pack abdominal muscles while the human body has only eight?

I've seen use of word 6 (six) packs in advertisements. Never heard about 10 packs.

While each muscle has a single "belly", many have multiple "heads". That is, portions of the muscle attach at different locations. These attachments follow, as separate bundles, down into the belly of the muscle. Biceps, for example, have two heads. I suspect it's possible these may appear as different bulges in a well developed gym rat.

The only "way" someone can have a 8-pack or 10-pack is due to genetics. Across the rectus abdominis muscle you have either 3 or 4 tendinous bands going over it, consequently resulting in either a 8 or 10 pack.


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How does boiling water release dyes from vegetables?
Why does boiling water always seem to release and become the colors of whatever vegetables I am boiling?
For example, beet root and red cabbage both vividly color hot water.
I'd assume it's something to do with collisions with water particles breaking down cell walls and releasing anthocyanin, but how would this work on a cellular level? I.e., how does boiling water succeed in breaking through (correct assumption?) cell walls?

Cell walls are permeable to small molecules.

I'd like to add that it depens on the solvebt too. anthocyanins are water soluble and hence beetroot gives the purple color when boiled in water. Similarly, boiling a carrot in water wont gove orange. Boiling a carrot in oil would. Carotenes are fat soluble.

take a look at this answer: http://chemistry.stackexchange.com/questions/61138/how-does-boiling-water-extract-dyes-from-vegetables your question is exactly the same

@RickBeeloo Really? I don't believe you

You posted it yourself @theonlygusti

@RickBeeloo I know. Why are you telling me about my own questions?

https://books.google.nl/books?id=o-0XDAAAQBAJ&pg=PA246&lpg=PA246&dq=how+boiling+breaks+cell+wand+in+plant+cells&source=bl&ots=5T4siBQPEH&sig=h1PvS0FrmH41rl_VEE6ABBuTpeA&hl=nl&sa=X&ved=0ahUKEwi9rYTNluXPAhUF1xQKHUWNC5UQ6AEIHjAA#v=onepage&q=how%20boiling%20breaks%20cell%20wand%20in%20plant%20cells&f=false maybe this book will help you

@RickBeeloo Wow, that is awesome! Than you so much, that is a perfect answer :D

Nice I'm glad I could Help!

Why boiling water releases dyes from vegetables:

In general, one would need a solvent to extract compounds from the vegetables. Water is a solvent for the coloured pigments. In air or oil, the same pigments are less or even not at all soluble.
Hot water can damage cells. Proteins, which give structure to cells and membranes, denature at hot temperatures. Cell walls, by the way, are much more robust than membranes.
But even in cold water, some pigments can pass through membranes or membrane channels by diffusion. This will only take more time.

There are possibly other factors that are more case (vegetable) specific.

Would the cell walls break down in boiling water? I.e., which of your listed factors contributes most significantly towards the final dye extraction?

Not the cell wall (fibrous structure), but cell membranes (oil bi-layer). With boiling water I assume it to be the most significant factor.


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How does glutaraldehyde kill bacteria?
How does glutaraldehyde kill bacteria?
After disinfecting, does it leave the corpses of the bacteria to count?
Does it leave bio-film in tact?

Modifies proteins by reacting at the amino group. Same what formalin does

Gluteraldehyde interacts with amino groups to block the dynamic movements that biology requires.
Yes the corpses of the fixed bacteria can be counted and bio-films will be intact but the bacteria will be fixed in place.
Biofilms that are fixed with gluteraldehyde may shrink when prepared for imaging due to the effects of dehydration.


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Flight trajectory of domestic pigeons on sudden noise
In places where people feed pigeons, its a common sight to see them fly off suddenly when there is a sudden disturbance.
When they do, there is an interesting pattern that these birds follow.
Say there is a huge noise in the surrounding, all the pigeons fly off together, and return to the very same place, traversing a semicircular path of some fixed radius. The flight of each bird relative to another is also interesting, looks like some sort of a wave. It seems more like a formality rather than of some utility (since they return to the same place).
I assume this has been studied and has some significance. Does it happen in other birds too? What is this phenomenon called?


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Why are there 2 copies of RNA in the HIV virion?
There are two copies of the RNA in the HIV virion. These are retroviruses. So, they can make cDNA from even just one copy using reverse transcriptase.
What is the use of the other? Are both integrated into host chromosomes?
My guesses are:

To ensure increased chance of getting integrated. But, if one gets in, the other also should be able to.
To increase the amount of protein translated (if both get integrated).
Two for two sets of chromosomes. (Seems juvenile but still a possibility. although, I do not think there are specific sites of preference for the viral DNA. Are there?)

You've probably worked it out by now, but I've added an answer to your cardiology question on Physics SE.

You are not totally correct because these two strands don't have to be the same, they can be genotypically different, which occurs when a cell is infected by two distinct HIV strains. Also HIV uses reverse transcriptase which can "jump" from one strand to the other so sometimes pieces get repeated, skipped etc. So you will get a recombinant --> more genetic diversity(see this article) I won't go into to much detail but if you want to know more I would highly recommend to read the article I linked after genetic diversity. So to summarize:

genetic diversity, because of switching between the two strands (this makes it so hard to cure AIDS e.g.)
If one RNA strand gets damaged it can use parts of the other RNA strand as template, so to synthesize DNA
apparently the dimeric form of RNA in HIV is essential for successive replication of the virus

Source: previous mentioned article(HIV-1 RNA dimerization: It takes two to tango.)

This indeed is the best article on the matter and is worth the time to read.


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How many neurons are stimulated by electrodes in memory engram experiments?
Researchers have recently identified "engrams" in the mouse hippocampus, "sparse populations of neurons" or "small clusters of cells", stimulation of which elicits a specifically trained fear memory association. For example...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4874022/
http://www.nature.com/nature/journal/v484/n7394/full/nature11028.html
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3331914/
http://www.smithsonianmag.com/innovation/meet-two-scientists-who-implanted-false-memory-mouse-180953045/
My question: Roughly how big -- how many neurons -- are the regions stimulated in these experiments? I looked through a number of papers and was unable to find this information.
10/18 -- Changing the title and wording to clarify that I am asking just about experimental procedures with electrode implants, not fMRI studies, and not about how engrams might actually work.

It's possible no one has measured accurately yet, but a more likely explanation is that it varies. I would assume that different memories take up a different amount of space - I have many detailed memories of my wedding day, for example, but not so many of the soccer game my child played in a month ago - it was very wet, that's all I remember :). So, it would make sense that, since the wedding memories are much more detailed, and there are many more of them, more neurons would be assigned to hold them.

I understand that there probably isn't a standard fixed size, though there probably are specific figures for the studies in question, but for some reason that is not published. I'm just looking for an order of magnitude to go with "sparse populations" and "small clusters". Is it 10, 100, 1000, whole fMRI voxels (100K-1M, which I doubt), etc.? IOW, how finely can implanted electrodes read and stimulate neurons?

edit: More directly answering the initial question, thank you, I misread what you wondered and was mislead a bit by a previous comment and your response to that comment.
In these experiments, they are using optical, not electrical techniques. Therefore it is a bit difficult to estimate exactly the number of cells activated directly, because light will scatter in the tissue but also fall off with distance. Based on the density of labeled and affected cells (to be stimulated, the cell has to be both a) labeled by a virus injection, and b) active in the engram) pictured in the second link you included, it seems like no more than a few to a couple dozen cells would have been activated directly.
In your comment, you said "IOW, how finely can implanted electrodes read and stimulate neurons?" - this is a different question. Implanted electrodes can read from and stimulate single neurons, or populations, depending on the electrode and experiment. It is difficult to target particular neurons with electrodes without an additional optical technique.
In the experiments you reference, optogenetic tools are used to selectively label cells that were active earlier in an experiment, and then reactivate those same cells with light. These sorts of experiments have only become possible recently with the development of those tools.
(original answer below)
Standard answer of biology applies here: "it varies", probably by species, type of memory, brain structure, etc.
But, to give you some ideas, one area that has been studied a lot in this field is the dentate gyrus of the hippocampus (the second and third links you sent, for example). One paper showed that a given memory activated something like 2-4% of the cells in that structure in a mouse http://www.sciencedirect.com/science/article/pii/S0166432811006462 with something like 1,000,000 dentate gyrus cells total in a mouse. So, that's a lot of cells, but those cells might be doing something special (pattern separation), so maybe it isn't right to think of them as the "engram" itself, or maybe we should be counting them PLUS all the cells activated in CA1, PLUS all the cells activated in cortex, etc. Whatever the case, one thing that is clear is that cells are involved in many many different engrams - if you are familiar with pop neuroscience you might recall the excitement about "grandmother cells" and "Jennifer Aniston" cells from a few years back. That's almost certainly not how engrams work, but that out of the subset of neurons and stimuli they examined, there was only limited overlap in those cases.
For fMRI studies, it's pretty hard to get a handle on the number of cells involved, but it isn't really possible to measure from "small clusters of cells" in fMRI on the same scale as in other measurement techniques. What is going to be more important for the fMRI decoding studies is "variation within a brain region" where the total number of neurons is many many millions, but the exact number involved in any one engram can't be measured with current technology.

Thanks @Bryan, but this does not address my question. I am not asking about fMRI images -- voxel cell counts vary but are well-known (for example -- link). I am asking about the reverse problem, stimulating cells directly and observing behavioral results. How many cells are stimulated in such experiments -- just roughly? So it's just about the experimental procedures, not about how big engrams are or how they are structured (which I agree is a tough question).

BTW, I am also interested in how many neurons are typically observed in experiments with implanted receptors. Again, this is just a question about experimental procedures, and not abut fMRI, but electrode implants in animals (and occasionally in humans as adjunct to medical procedures).

Hi David, hope the edits help a bit. To add more to your comment here, with a single electrode, one can either record action potentials/spikes from a single neuron, or a population of dozens (but not easily discriminate them from each other), or record "field potentials" which correspond to membrane currents in hundreds to thousands of cells (this would be like a "very local EEG").Electrodes with multiple recording sites (often "tetrodes") can record from a few cells at once. Many implants especially in larger animals may have dozens of electrodes.

yes that helps a lot -- thanks, and sorry for my sloppy wording and my neglect/ignorance of the role of optogenetics. And that's my clue -- searching it turns up this SciAm article by Diessseroth -- link which gives me the impression that it can stimulate a single neuron under some circumstances. But the figure you give -- up to a couple dozen -- is what I need. So you get the bonus.

Yep; if you either a) Shine light on only a single cell (most likely using 2-photon techniques or some other new tricks people are starting to use), or b) Express the gene in only a single cell in the light path, only that one cell would be affected. In the experiments you referenced, they shine light out of a 200um fiber optic cable placed into the brain area of interest. link has some information on how you can expect the light to travel out of the fiber and into brain tissue.


text:
Is there a gold standard for syphilis?
When you say the Venereal Disease Research Laboratory test (VDRL) has a specificity of x% and sensitivity of y%, what are you comparing to? What is considered as the truth?
Because, Wikipedia says, even a gold standard needn't be perfect. It is just the best test available(?). It too has its specificity and sensitivity (<100%)
So, my question is, when we say that the VDRL has a 75% sensitivity, what are we comparing it to? Is it the clinical diagnosis of syphilis according it the case definition? Wouldn't it be much less accurate?

This is usually meant in a clinical setting: So I think this is about detecting 75% of the infections.

@Chris essentially. See my answer for a bit more (I tried to keep it short). Specificity is also related to how specific the reagents are for their intended targets, vs. binding to related proteins/hormones/chemicals/whatever the test is measuring. Some tests are yes/no readouts, but I focused more on quantitative tests, which tell you how many virus particles per ml, for example.

Specificity and sensitivity are terms used in the pharmaceutical and in vitro diagnostics (IVD) industries that have specific meanings relating to how the particular assay in question was validated. Generally the values are being compared to spiked standards in matrix using recombinant protein or purified virus or whatever the antigen is (depending on how the test operates) where the analyte concentrations are known. With a certain number of titrations and assay repeats, along with a bunch of statistical calculations, you can then compute your expected and actual recovery, as well as values like the LLOQ (lower limit of quantitation) which gives you your sensitivity (we can reliably detect 1e4 viral particles per ml, for example).
Specificity is calculated using related antigens, such as proteins from other types of bacteria that are of varying degrees of relation to syphilis, or perhaps of different serotypes that aren't claimed to be detected by the test, or whatever. Again, you spike known amounts of these materials into your testing matrix (blood, sputum, urine, semen, whatever) and see what your test returns. So, say I have a virus with 2 serotypes (A and B) that I claim recognizes A specifically. I spike in perhaps equal amounts (for example, 100 units) of A and B, then run the A-specific quantitation assay. The readout might then say the sample only had 75 units of A, meaning 75% specificity of the reagents.
For more reading, search for "clinical assay validation" or something similar. There are a ton of papers out there giving guidance for particular types of assays, as well as regulatory agencies' interpretations of the relevant laws covering the tests. There are also many books, reviews, etc. if you're just looking for an overview. It's a huge field, and I've just given a very basic description to avoid writing pages and pages.

Thanks! How would these then account for the biological variation in the population? The same amount of bacterial load in one person may test positive but not in another. Do these terms not talk of that? Because, in syphilis there is a special term called biologically false positives (BFP) for VDRL, are they just a subset of normal FPs or excluded from it?

@Polisetty I don't know the specifics of this test, other than what is on Wikipedia, so I can't answer directly. I do know that the VDRL does not test the levels of the spirochete directly, rather it looks for levels of anti-cardiolipin antibody that increase after syphilis infection, and apparently have been shown to have a good correlation with viral load in the absence of confounding conditions like lupus. There are other direct tests that identify the bacterium specifically - they are used for diagnosis. I'm not sure how the BFPs (such as lupus cases) are differentiated from other FPs.


text:
Mixed-mating plants: is the number of mixed mating plants supposed to be trivial?
I am referring to Winn et al. 2011
Last sentence of the first paragraph is

Although sampling bias against both selfing and highly outcrossing species may inflate the frequency of mixed-mating populations, the number of species reported to show mixed mating is not trivial, and calls into question the status of mixed-mating populations as transitional, and therefore the sufficiency of the theory to explain the observed distribution of mating systems in hermaphroditic species.

I do not really understand what is the logic behind the highlighted part and what is its purpose.

Is the number of mixed mating species supposed to be trivial in a case where the number is inflated (So there is a need to clarify it is non trivial)?
How does the fact that it is not trivial bring up the question below the highlighted part?

I edited your post. Feel free to roll back if you don't like the edit

I think the main message of the quote is
"Many would have expected that mixed mating can only exist as a transitional state and thought that stable equilibriums are either pure selfing or pure mixing (or both). The observation of a non-trivial number of mixed mating populations suggest that our expectations were wrong."
The first sentence of the quote is a statistical detail of their paper and not a premise for the conclusion that there is a non-trivial number of populations that show mixed mating.
The evolution of selfing is a large topic in evolutionary biology and cannot really be summarized in a single post (even more so that many question are still open to debate). Goodwillie et al. 2005 is a review on the subject that will help you understand the work that has been done on the evolution of selfing. Very related is the evolution of hermaphrodism, dioecy and other mating systems in plants. Pannell 2002 is a very good paper on the evolution of androdioecy and the maintenance of these unexpected mating systems.

If the first sentence is only a detail, then why does it use "although" to begin the sentence? I would assume the first sentence is somehow supportive of the opinion that the number of mixed mating species should be trivial. That is exactly where I do not understand why (the relationship that "inflation" implies "trivial").

As I understand the section, it could be rephrased as:

Even though the frequency of mixed-mating populations might be artificially inflated due to sampling bias against both selfing and highly outcrossing species, this is only a partial explanation. Also when taking the sampling induced bias into account (i.e. controlling for sampling bias), the number of mixed-mating species is still not insignificantly small. This observation challenges the notion that mixed-mating populations are supposed to be transitional, and therefore also the current theory used to explain the observed distribution of mating systems in hermaphroditic species.

So, for you questions, I would say:

The number of mixed mating species is non-trivial (i.e. not small and insignificant), even after removing the inflated numbers caused by sampling bias.
The fact that the number is non-trivial, and not only caused by a sampling artifact, fits poorly (according to the authors) with the idea that mixed-mating populations are supposed to be transitional. Therefore, by extension, the observation of a non-trivial frequency of mixed-mating populations also challenges the theory used to explain mating systems in hermaphroditic species.

As a final sidenote, this question could just as well be posed at English-SE (or SE-English language learners), since it is mostly a question about the english language.


text:
Why is it cool near the trees?
I can understand that trees produce oxygen in daylight but why is the area with vegetation much cooler than the environment's temperature?

Is there evidence that this a general phenomenon?

Near trees and weedy places... not only at evening... throughout day it feels much cooler than bare places, perhaps due to moisture content. Rather at evening to early night, sometimes I feel little-bit warmer beneath trees and weedy places which too is plausibly due to high moisture content resisting evaporation. Perhaps plants act as a buffer against extremities of environment.

Why it can feel chilly close to trees in the evening:

Water coming out of Stomata vaporises, reducing the surrounding temperature.
There is normally no direct sunlight reaching the ground beneath the tree, hence the moisture content of soil is higher, giving it the "chilly feeling"
If there is other vegetation (e.g. grass) growing beneath the tree, then point the first point is repeated for the other vegetation, consequently the combination of point 1 and 2 decreases the temperature noticeably.

An empirical study that estimates the cooling effect of trees from evapotranspiration can be found in Konarska et al (2016). Transpiration of urban trees and its cooling effect in a high latitude city.. In the study, they specifically find a cooling effect at evenings, but less so during nights and at daytime:

With an estimated night-time latent heat flux of 24 W m(-2), tree transpiration significantly increased the cooling rate around and shortly after sunset, but not later in the night. Despite a strong midday latent heat flux of 206 W m(-2), a cooling effect of tree transpiration was not observed during the day.

Why is it more noticeable during the summer?
If the temperature is warm, the atmosphere has a greater capacity to hold water in its vaporous state than if it was cold.
Relative humidity
The ratio between the actual amount of water vapor present to the capacity that the air has at a particular moment. For any given temperature, the air has a particular capacity for water vapor. If that capacity is exceeded, the excess spills out as liquid water.

When you meant "the excess spills out as liquid water", I guess you are meaning there will be a state change when water molecules get cohesive.

I added a reference to your answer that felt suitable. Hope that's ok.


text:
True definition of Biology
I just started biology and im pretty clueless on what it really means. So before you vote this question down, can you tell me what it really means.
P.S. Is plate tectonics related to biology? or Chemistry? or Physics?

Typing "biology" into google turns up an adequate definition so in its current form, your question might not receive many answers. Please
take a look at the How to Ask
page and try to improve your question according to the guidance found there. This may require you to show some effort on your part in terms of attempting a solution or showing research. If you have questions about what to do or if you don't quite understand what this means, please ask for clarification using the add comment function.

Every expert will give a different answer on this depending on their own experiences in studying a biological features. The fact you're asking about plate tectonics in the same question makes me wonder if you've even bothered googling any of these terms. Try this link.

In which class do you read? since you just started; so I guess you are in class 4, 5 or 6. Is that? Biology means study about living organisms. (( Etymology: greek Bios (= life) + logos (=discussion) )). It is also known in many other names such as Life-science, Life sciences, Biological sciences, etc.  But they are same.

@AlwaysConfused just FYI, there are different "grades" (as they're called in the US) in different parts of the world. I don't know if your "class 4" is the same as my "grade 4". Simply asking the OP's age would be a better way of going about it.

Though this question too-basic; thereis one significance; the approach we  break the world into "physics", "chemistry", "geology", "mathematics" etc. just to sort information. But in nature all they exist together and are interrelated. We can't think biology without chemistry (because we're made of atoms). Similarly we cant think biology without geology since we live on Earth and our history is mixed with origin, changes and structure of Earth. Similarly mathematics since to comprehend any process it is urgent, The approach "mad guy asking biology question to chemistry teacher hehe" is wrong

@MattDMo ok I'll keep it in mind.

Now I could understand significance of this meta post http://meta.biology.stackexchange.com/questions/3439/biology-se-and-professional-biologists/3468#3468

Here is the definition of Biology as given by Dictionary:

the study of living organisms, divided into many specialized fields that cover their morphology, physiology, anatomy, behavior, origin, and distribution.

Tectonic plates are not living, thus it isn't biology.
It would be Geology:

Geology is the study of the Earth, the materials of which it is made, the structure of those materials, and the processes acting upon them

Source: Geology.com

If you have criticisms or concerns about the question, please put them in comments, not an answer. You may use several comments if necessary. See this discussion on meta for more.

@MattDMo Thank you for your constructive comment. I have updated my answer to better serve the OP and eliminate any criticism.


text:
If you didn't have an utricule or saccule would you still know if you are accelerating and going up or down?
In the vestibular system the utricule and saccule makes you that you know whether you are going up or down (saccule) or backwards/forwards (urticule).
But imagine you don't have them anymore or they are damaged, would you still be able to know if you are accelerating or in an elevator? I thought it still would be possible because you would feel the pressure in you back when accelerating or on your feet when going up. But is it true that you still know what is going on by registrating the pressures in you body, or is it not possible any more? If it is still possible what would the surplus value of the urticule and saccule?

Your semicircular canals are concerned with balance (or spatial orientation). Proprioception, on the other hand, deals with where the body parts are with respect to each other and the physical world. (Some people lump the two; it's easier to think of them independently, because they really do quite different things.)
Proprioception (and closely associated kinesthetics) is possible because of nerve signals from skin, tendons, muscles, and joints. This gives us the senses of limb position and movement, the sense of tension or force, the sense of effort, the sense of gravity.[1] Propioception alone cannot compensate for serious balance problems.
The vestibular system exists through input from three semicircular canals located in the inner ear on each side. The canals are oriented at (basically) 90° angles to each other so that we can maintain our balance no matter which position our head is in. These are also connected to one's ocular reflexes. Together they're called the vestibolo-occular system, which functions as a reflex (VOR).

Three sensory systems, vestibular, visual, and somatosensory/proprioceptive, serve our sense of balance. Each of these systems provides unique sensory information to the brain where it is integrated (often in complex ways) to produce a final motor output to muscle groups for maintaining gaze, head and body posture, and controlling static and dynamic balance.[3]

Without these systems, we would be completely unable to get or stay in a standing position. We certainly could not walk.
An analogy would be to get strapped into one of those spinning seats, in this case, one that rapidly spins inverting you, alternating between forwards and backwards (which would kind of include up and down) but not sideways. You would be unable to focus your eyes on anything. You would see your world spinning, and you would have lost your sense of balance. You would immediately go to the ground, even though your proprioceptors were working perfectly.
However, once you did "go to ground", say, in an elevator, you probably could tell if you were accelerating upwards or downwards. Closing your eyes would help to drown out the more unpleasant 'noise' (input).
So, long story short, the answer is yes. Likewise, you would probably still be able to touch your nose, etc. But it would not be possible to do more complex things, like walk, or even sit unless your back and sides were supported.
[1] Proprioception From a Spinocerebellar Perspective
[2] mpairments of reaching movements in patients without proprioception. I. Spatial errors
[3] Anatomical and Physiological Considerations in Vestibular Dysfunction and Compensation


text:
What is the name of this bush with red fruits?
I have seen this on Corsica (Island of France):

If possible to go near that-one individual tree once again (don't take pressure; just if possible); take few fruits, photograph a TS and an LS (just in a way we cut tomato in halves) that would help understand carpels. If you find any flower in the tree it would be very helpful. Take few close-up of twigs, so that i can try to understand apical buds, axial buds  leaf-bases, stipules (if any), sheath-like structure (if any), etc. Usually high-resolution (many kb or megapixel) images do NO help than defocus; Actually just how much "fingerprints" you captured and presented, come in work.

I'm  sorry if I use much terminologies (due to brief place) about whom you are unfamiliar... I was just trying to give you a hint about what may come into work. Plants are not so-simple as may look to a beginner.

@AlwaysConfused I'm sorry, but I'm not several 100km away from it. However, in the future I will think about cutting the fruit and photographing it. Thank you for the hint.

But don't try to taste if there is any place of doubt. As well, I'm not familiar with Arbutus unedo, and there exists scope of wrong-identification (one example you have seen few days ago) even sometimes by experts; and when identification is via photos, web or such, the chances of mistake are more.

It is Arbutus unedo, called "strawberry tree" in English, "arbousier" in French and "medronheiro" in Portuguese. The fruits are ripe around October or November. They are full of little seeds, but if you bear the annoyance, they can be quite tasty. They are used to distill an alcohol in Portugal.

Arbutus unedo (member of Ericaceae according to wikipedia) is not to be confused with commonly whom we know as strawberry which is Fragaria cultivars, is a member of rosaceae.

The fruit looks like lychee (Litchi chinensis). But this was a hasty guess and now I see that there is a much better answer here!

(image from Wikipedia)

The leaves look different. Lytchee have a kind of crust that can be peeled. This is not the case with Arbutus. Besides, I'm not sure they can grow in Corsica.

You're probably right! I was misled by the fruits.
In the Wikipedia it says "They require a warm subtropical to tropical climate that is cool but also frost-free or with only slight winter frosts not below −4 °C"

OP is Litchi tree? not my forte except prickly appearance of fruits, which is too superficial.

@AlwaysConfused It looked so similar that I didn't check if it is possible to grow there. Corsica isn't frost-free, so I guess it is rather the Arbutus unedo.

@MartinThoma Still they are 'guess'. However though I've never studied with Ericaceae however it looks like ericaceae like Rhododendron and Arbutus. However if you could access near the tree, take a close-up photo of  the twig axis focusing leaf-base, nodes and internodes; and a TS and an LS of the fruit.

Please don't delete the Litchi answer, since it would help a lot the visitors.

@AlwaysConfused Do you have a justification for why this answer would be useful to people and not misleading?

@WYSIWYG The discussion below an erroneous answer might be useful. And it is useful to know that one might make this kind of confusion between lychee and Arbutus. But maybe it would be better to edit the answer to warn the reader.

@WYSIWYG Since comments can't host images, if this answer edited with mention "fruits shows similarity with litchi"; would help the visitors distinguish/ disambiguate between the 2.

Since manual-identification requires deal lot of mental-imagery; there is even role of wrong possibilities... for distinguishing purpose.

i added a note about being wrong. the downvotes should also be a good indication to not listen to me!

also, of course it would be nice to have it removed since it's embarrassing, but hey, if it's possibly useful it can stay!


text:
Do the two catalytic cores of DNA polymerase III operate in the same direction?
This diagram is from Molecular Cell Biology by Lodish, 2000 which states:

The other core-polymerase molecule, which elongates the lagging strand, moves with its β-subunit clamp in the direction opposite to that of the fork movement.

Again the images provided in Principle of genetics by Simmons, 2015 and Cell Biology by Karp, indicate that the catalytic cores are directed in the same direction. The following diagram is from former book.

Which one is correct and why(please provide citations)?

The DNA polymerase-III holoenzyme moves in one direction (along the fork). One of the DNA polymerases works on the lagging strand but the enzyme is oriented in the same direction as the one that is working on the leading strand. For details see this review (it is old but this fact is also old enough).
The second diagram shown in your question is an accurate representation of what happens. This, statement is confusing (and misleading):

The other core-polymerase molecule, which elongates the lagging
  strand, moves with its β-subunit clamp in the direction opposite to
  that of the fork movement.

Both polymerases move in the same direction but elongate DNA in opposite directions. The opposite elongation direction, as shown in the second figure, is facilitated by looping of the lagging strand.
You can simply google "DNA polymerase-III holoenzyme" and you'll get many sources that will corroborate this.


text:
Books: DNA replication
In what books can I find a detailed literature on the mechanism of function of different enzymes and proteins involved in DNA replication of E. coli ?

Please have a look at the tag-wiki for book-recommendation. You have to provide more details.

Check this online book on NCBI: An Introduction to Genetic Analysis. 7th edition

Let’s examine each of these components and see how they fit together to produce our current picture of DNA synthesis in E. coli, the best-studied cellular replication system

I used it a bunch while studying E. coli for my master degree, lots of really usefull information.

it is Griffith et al. Also available pdf in http://www.bio.bg.ac.rs/materijali_predmeta/med-eng-griffiths-an-introduction-to-genetic-analysis.pdf

Here's just the right book - Lehninger Principles of Biochemistry, 6th Ed
By David L. Nelson, Michael M. Cox.
A Google.book link to it.

Molecular Biology of the Gene
(James D. Watson
Cold Spring Harbor
Laboratory
Tania A. Baker
Massachusetts Institute
of Technology
Stephen P. Bell
Massachusetts Institute
of Technology
Alexander Gann
Cold Spring Harbor
Laboratory Press•
Michael Levine
University of California,
Berkeley
Richard Losick
Harvard University) has a detailed description of the various processes involving genetic material.
Find a pdf file here: http://tocs.ub.uni-mainz.de/pdfs/118526545.pdf

Biochemical Pathways (G. Michal, D. Schomburg) has nice old-school schematics such as this one, in addition to the text.


text:
Can some one identify this plant with really sweet smelling flowers?

Could someone help identifying this plant?
The flowers on it have a very sweet smell, similar to the night queen.

Could you add the locale?

Does it have square stems? If it does then it appears to be mint. If doesn't... I don't know :)

@ sanjukta - This was in Singapore

It's most likely a buddleia of some kind, perhaps Buddliea davidii:

You can see the flower is tubular and has four 'petals' at the end. They also have paired leaves, the underside of which is lighter than the top.

The flowers are generally rich in nectar and often strongly honey-scented.

I never thought it smelled like honey, but it does have a very pleasant and strong sweet smell.
It is present on four continents.


text:
Why is black and yellow such a nice camouflage?
Many people can`t differenciate between cheetahs, leopards and jaguars, but there are serveral other animals with a similar pigmentation (servals, ocelots...), why is it so effective? It gets exciting when you realize that cheetahs and leopards are evolutionaray relatively far away, and therefore that their resemblance exsists due to evolutionary convergence.

Nature's background contains much yellow (Hay or Straw colour) (especially if it is a grassland)...Which comes from soil and sand's colour + colour of dry plant-material. As well dark-corners and some portion of plant-matter (stems, inflorescence, fruit-grains, some dry leaves etc) looks dark, brown-to-black. So a similar pattern helps to camouflage (difficult to distinguish from background). Applicable to both predators and prey.

What makes a camouflage effective? It has to match the colors and color patterns of the habitat.
Here are two cheetahs

Here is another cheetah

Here is a leopard

Here is a jaguar

Overall, it looks like their yellow and black pattern is a pretty good camouflage.
The jaguar habitat is a mixture of open and forested habitats. One would think, the jaguar would gain by being a little greener but there is a good reason for the jaguar not being green (see Why is green fur not a thing?).
Note also that it would be a mistake to think that any species should be perfectly adapted to its environment. You might want to have a look at the paragraph Did you say Natural Selection? in this answer for a very short intro to why populations might sometimes be less adapted than a naive observer may expect. There might have an important phylogenetic signal among these felidae (you might to have a look at the paragraph Why 4 legs? in the same answer as indicated above).

wonderful answer. Seems same for tigers, lions, foxes ,wild cats etc. (predators) as well as deers, rabbits etc (prey). perhaps for same purpose army dress contains 'patches' of ochre-yellow, brown, grey, brown-green, grey-black etc.


text:
Reduce protein structure representation dimensionality.
In my lab we are trying to extract spatial features from protein structures. The software we develop makes use of CUDA for all heavy number-lifting, thus we are limited by the GPU's memory (12GB). Using standard voxel-based 3D-representations proved to be too memory hungry, hence we are trying to find a way to reduce the dimensionality to 2D, while preserving as much spatial information as possible. Our absolute goal is to preserve spatial colocalisation of different chains and secondary structures, to understand how important that is during folding. Standard techniques, such as PCA and PCoA on euclidian distances between amino acids, seem to preserve too little information on chain folds. We believe there should be a better way of doing that, but, having little experience in structural biology, we struggle to find any relevant work regarding this issue. Can you recommend any methods or relevant readings?

I'm not entirely sure I understand the question. What more spacial information do you need beyond .pdb files which hold the relative atomic co-ordinates? After this, dss can be ran to evaluate chain angles and overlay a secondary structure.

Maybe you could use a protein SSE graph? http://ptgl.uni-frankfurt.de/about.php

@James the question is how to project 3D structures from .pdb into a lower-dimensional space without losing the information on relative position of chains.

@gilleain this is actually quite interesting, though it lacks residue-level resolution.

I suppose you already solved this, but did you consider something like non-linear dimensionality reduction with a regularization energy term that penalized the sort of chain fold deformations youre trying to avoid? E.g. using diffusion mappings with a kernel that combined say geodesic distances with an extra term for handling the chain folds.

@user3658307 Unfortunately, we've only managed to optimise our 3D-representations so that they require less space. We've tried plain-old NMDS with stress optimisation to no avail, but I'll definitely look into your proposal.