text:
Why are there species instead of a continuum of various animals?
As I understand it, various animal traits have to evolve gradually, but what happens to the species that are "neither here nor there"?
To put it differently, if a species evolved from another, it did so because it's somehow better, right? So why are there examples of the original species not being extinct?
What factors determine weather some species "stick"?

"if a species evolved from another, it did so because it's somehow better, right?" Evolution doesn't make species better. Evolution makes species.

There is a continuum occasionally, e.g. so called 'ring species'.

It's a fallacy to say evolution happens gradually.  Many forms of evolution involve the combining of two or more species together, which transforms their abilities.

http://en.wikipedia.org/wiki/Species_complex

Actually, the tree of life is a continuum of animals. Species is just a convenience for us to name and group those animals by their shared traits and whether they can or cannot interbreed.

Here is another post that may be of interest. Among other things, it talks about ring species

@BrianS I don't think that is quite true. If there is any selective pressure at all (and rarely there isn't) then the species will evolve to become better at proliferating in that environment. (of course, the environment may suddenly change and render all that specialization in vain)

Short answer

Why are there species rather than a long continuum?

Three important reasons I could think of are sex, non-uniform adaptive landscape and ancestry.
Long answer
I am not sure I'll answer your question so let me know if I miss your point or if I help!
To start with, you might want to read this answer on the semantic difficulties behind the concept of species

What factors determine whether some species "stick"?

Natural selection is nothing but differential fitness (fitness is a measure of both reproductive success and survival) among genotypes within a population. Individuals having greater fitness will leave more offsprings and therefore the genes of these individuals increase in frequency in the population. There are few generalities to be made about what phenotypic traits are beneficial in a given population. For example, "white fur" is a very good trait for a polar bear but would highly deleterious for a mealworm.
However, there is a thing called species selection wherein a given lineage at least, it is possible to identify specific traits that seem to either reduce the extinction rate or increase the speciation rate. This is, for example, the case for polyploidy in angiosperms (Whitton and Otto, 2000)

if a species evolved from another, it did so because it's somehow better, right?

If you observe different extant species you cannot say that any of these species evolve from any other one you can today observe. The correct way of looking at two species is that they share a common ancestor in a given past. Therefore, looking at a cat and a blue tit you cannot say that one species evolved from the other one but you can only say that these two species share a common ancestor (just like any other pair of species) that was neither a cat nor a blue tit. The example is obvious because cats and blue tits are "not so closely related" (everything is relative) but the same logic holds for any pair of species.

Why are there species rather than a long continuum?

Sex
The simplest and most obvious reason why there are species within which individuals are more similar compared to each than to individuals from other species is due to the definition (the most common definition because different definitions exist!) itself of a species. A species is a group of individuals that can interbreed. See this for more info on the concept of species.
Take two originally different groups of individuals and allow them to interbreed. Their traits will mix up and you won't be able to tell two different groups apart. All individuals within the new mixed group are a mixture of the individuals from the two previous groups (under some circumstances this process has been sometimes called "reverse speciation"). If now you take one single group of individuals. You split them into two groups in the sense that you don't allow individuals from group 1 to mate with individuals from group 2. You will see that after some evolutionary time, the individuals of group 1 will tend to resemble much more to individuals of group 1 (its own group) than to individuals of group 2. If you wait long enough so that these two groups of individuals become different enough so that they can't interbreed any more because they diverged too much, then you have what is called a reproductive isolation and under the common definition of species, you can say that a speciation (You may want to have a look to the wiki article for "speciation") occurred and therefore you have two new species instead of one ancestral species.
why the two groups tend to diverge through times?
You may wonder "But why the two groups tend to diverge through times?". There are several processes that explain that divergence:

Mutations

Different mutations occur in the different groups (just by chance)

Natural selection

The environment differs and the selection pressures differ selecting for different traits in the two species. Also, the accumulation of different mutations affects the selection pressure at other loci.

Genetic drift

Shortly speaking genetic drift is due to random events. Different random events occur between the two populations. For more info about genetic drift, see this post

If you are not very familiar with these concepts I recommend that you have a look at Understanding Evolution (UC Berkeley).
Adaptive landscape
Note also that there are other reasons for explaining this pattern. One other reason is "Because the adaptive landscape is not a flat function". What this means to the layman is that there are some combinations of traits that cannot really be beneficial.
Ancestry
Also, individual phenotypes are not independent of each other and not only for ecological reasons but also because of shared ancestry. If you consider two families, you will easily accept no to see a continuum of phenotypes but two distinct groups (maybe in one family curly hair is common while in the other they all have straight hair).

Mathematician/computer programmer's answer here:
There is a continuum of different animals — in fact it's pretty fair to say that every animal occupies a different place on this continuum. They're just not uniformly distributed over the continuum; they're clustered around forms that are most likely to survive and reproduce, and the lowest-energy paths between them.
This is because evolution is basically a stochastic optimization algorithm, one that finds the "best" set of parameters for maximizing some function by randomly perturbing an initial set of input values. In fact, some of the best optimization algorithms today are based on ideas drawn directly from evolution and called "evolutionary algorithms".
In mathematics, given enough time, these algorithms will all converge on one optimum solution and nothing else. Why isn't it like that in nature? Because in mathematics, the "fitness function" that we're optimizing for stays the same for a given problem for as long as the algorithm runs. It represents the specific problem we're trying to solve. In nature, there's no outside force imposing a fitness function; an organism's survival depends on millions of factors in its environment which change over time, many of which depend on the survival and properties of the other organisms in its environment (competition, symbiosis, predator/prey relationships, etc.) This is a chaotic system so complex that it could easily go for billions of years without reaching a steady state, and even if it did, external changes (like the odd asteroid impact, to use an extreme example) would still come around to shake things up.
Another reason for the clustering is because a lot of the "intermediate states" in the genetic space have a fitness of zero — these are the states between species that can't interbreed, or that have sterile offspring. The categorization of "species" is based on this, and although it's not exact, it's still generally true that the more different two creatures are, the less likely they can have viable offspring. This makes evolution more likely to explore the spaces near already-successful organisms, and less likely to produce radical new things by hybridization.

Genetic circuit design is a similar idea. The power of the nested loop gives a lot of insight into long processes. + 1

I like your last (5th) paragraph. I would however think that this very "selectionist" argument is weak compared to the consideration of random processes and spatial isolation.

I am not sure I totally get how your 4th paragraph really addresses the question "Why aren't individuals distributed uniformly along the axes?". Seems to me that you mostly answer why not all populations may not reach an optimum. And I am not sure whether it is really wise to say "there's no outside force imposing a fitness function". Sounds a bit wrong to me (although I agree that we should include the social environment in the fitness function).

hobbs's answer I think best answers the question of discontinuity. The species landscape is directly shaped by the environmental landscape (natural selection). And the niches comprising an environmental landscape are discrete. The shape of the interface between these two landscapes is always changing. Biology would rarely (if ever) speciate in an unchanging and uniform environment. Species diversity increases with the number of features in the environmental landscape. However, some species (e.g. people) can adapt to dominate multiple niches, reducing diversity.

I disagree that "given enough time, these algorithms will all converge on one optimum solution". It's easy to imagine that there is an evolutionary algorithm that never converges to the optimum solution.

Could you support the statement "some of the best optimization algorithms today are based on ideas drawn directly from evolution" with an example of a problem where an evolutionary algorithm is better than any other currently known algorithm? (I think it's hard to find one.)

Re "these algorithms will all converge on one optimum solution and nothing else", that's not exactly the case.  Rather, they will tend to converge on various local optima, so you try (with e.g. simulated annealing) to inject a degree of randomness that can kick the convergence out of those minima.  Which is really like evolution: a group of species converges around some optimum, and can persist for a long while before some random event - say an asteroid impact in the Gulf of Mexico - jolts the system out of that optimum and eventually into a new solution.

@jamesqf I agree entirely. Better to say that we hope to find a global optimum in the mathematical setting. There are other bits of this answer that I'm not entirely happy about either. But I'm not sure how to make it more accurate without making it distractingly wordy :)

Nothing happens to them. Organisms exist.  They breed with other organisms who are genetically compatible.  We humans might try to categorize them according to certain traits, but our labels are just labels, biology isn't governed by them.
Over time, we might see that a population used to have one trait, and its descendants no longer have it, they look different. Nothing earth shattering happened, no bright line was crossed, there was just a change in allele frequencies.

if a species evolved from another, it did so because it's somehow
  better, right?

No.  This is just plain wrong on your part.
It's just different.  Maybe it changed so that its traits better match the current environment, or maybe the change was random drift.  You can't easily categorize one species as "better" than another.

I like "better" put in context to "different". It may occur that "better" is in the inside of anything different. If a one species not different to the other specializes on worms only in their barn yard, it's "no better", but it will. It shall be forced with it, with how to fork that worms.

Typically when both new and old species still exist it is because evolution pushed the new one into a different habitat or role.
As a hypothetical example reef fish vs. deep water fish and their relative size.  Let's say deep water fish evolved into reef fish, but we still have deep water fish.  So there were deep water fish that were a little smaller than the rest of the deep water fish, and this gave them access to a new place to hide from sharks, shallow waters near reefs.  As time goes on this puts evolutionary pressure on the fish to shrink so as to better hide in the reef, those "neither here nor there" fish may have gotten some benefit from being near the reef but the smaller fish got even more benefit and eventually outcompeted the middle species.  Vice versa for the deep water fish vs this middle species. It was not as good in deep water so it was outcompeted there as well.  This continues until evolution has separated them into two new species.
edit:

What factors determine whether some species "stick"?

Evolution optimizes for the current environment, as long as that environment is stable and the species is a good fit for it then there is little pressure to change. If the environment changes then a species will adapt to it. Here environment is everything relevant to the species: predators, food availability, weather, everything that impacts their life.

Organisms on Earth did not evolve in a homogenous environment. A critical part of speciation (when you go from a single species into two or more) is a reproductive barrier.
This can be a literal, physical barrier - mountain range appears between two populations, valley in the middle of habitat floods and isolates the two halves of the population, a small group is thrown by some catastrophe on a remote island and cannot escape, etc.
It can also be a genetic barrier: Imagine a bird species where males compete for mates with their bright blue crests, and rare mutations occasionally lead to red-crested males which cannot mate at all. If some female birds happen to mate with undesirable red-crested males for a few generations, two parallel sub-populations may develop: Birds which prefer red crests and bird which prefer blue crests. These populations may be very unlikely to interbreed.
There may be more complicated ways of erecting a barrier. For instance, a population of flowering plants that could previously interbreed arbitrarily may find that the ecosystem has experienced some crisis, and now the pollinating insects have become fastidious and only visit certain flowers and not others. Another example: While humans are currently a single species, because of culture (eg. language) certain human subpopulations (such as European nations) are much more likely to breed within themselves than between themselves.
Regardless of how the barrier comes to be, once a barrier can separate a species into sub-populations, the machinery of speciation is set in motion. All species evolve over time in different ways, especially if their environment does not have a very long history of unusual stability. As populations evolve, they try to stay somewhat coherent - the changes tend to be such that they still permit everyone in the population to mate with each other; otherwise they would impose a fitness cost.
However, if two subpopulations are not in contact, there is nothing enforcing compatibility between them. Therefore, as evolution does its work, these are free to wildly diverge from each other. Recall the example of the bird species in which males with blue crests enjoy reproductive success. The color itself is not particularly important, but it is important that the males all have the same color crest and the females prefer the same color. So as these birds evolve, the crest color can slowly drift in hue.
Now let's say you took these birds, and set a few of them free in one continent, and another group free on another continent. Again, over time, the crest color will shift. However, there is nothing stopping from the color in continent A from shifting to red while the color in continent B shifts to green. There is, after all, no advantage to being compatible with a population you are not in contact with.
The example above is largely behavioral, but non-behavioral examples are also possible. A very fundamental process is fertilization: Eggs have an ECM made up of proteins unique to that species, while sperm have enzymes to digest the coat of their own species. Because of this, cross-species fertilization is very difficult. Again, once you erect some kind of barrier between two populations, the systems of coat proteins and enzymes in the gametes of either population may evolve in divergent ways - they evolve in small steps, so that the interaction partner protein can always keep up, but compatibility with the isolated population is not selected for, and if the isolated groups are reunited after a very long time their gametes may end up becoming unable to fertilize each other.

Yeah, to me it's diploidity that saveguards that what is good becomes only better, not different.

I shall introduce you to the phenomena called ring species
Examples include gulls, Ensatina salamanders, house mouse, etc
A ring species is a series of adjacent populations that can interbreed with each other.
Say population A, B, C, D, E.
A can interbreed with B
B can interbreed with A and C
C can interbreed with B an D
D can interbreed with E

All very good. Sounds like a regular species. But here is the weird part. The populations furthest from each other cannot interbreed. ie Population A cannot interbreed with Population E.
A and E are by definition different species.
And yet, population A and E are linked, genes can flow between A and E via adjacent populations.
What is most likely happening is that there is a gradual change in gene variation between populations, so that there is gradually increasing barrier between successful hybridization. This barrier increases until the terminal ends of the ring cannot hybridize.
Furthermore, if any intermediate population within the ring were to go extinct, and break the ring, the two ends of the ring would become two separate species.
A ring species is a snapshot of one species that is one local extinction event away from becoming two species.

An even better example is where A and E CAN interbreed, thus closing the ring.

But that this not the definition of a ring species.


text:
How many abdominal sclerites would be there in a cockroach?
Every tegmina of a cockroach has sclerites which are analogous to the bones of humans.
Every abdominal segment of cockroach consists of two lateral sclerite plates called pleura along with a dorsal terga and a ventral sterna. But what will be the case with the last body segment where 10th sternum is absent?
I mean will, there be any pleuron in the tenth segment because, following our textbook, pleura serve for articulation among sterna and terga and also spiracles are present in the first eight abdominal segments but the 10th sternum is absent in Periplaneta americana.
Actually there is no evidence of the presence of any pleurons in the last segment in our text book.
Moreover, there are no abdominal spiracles in the 9th and 10th segments so there is no particular reason to say that pleura are present in the 9th and 10th segments as well.

Tergal plates:
There are ten tergal plates. The $8^{th}$ tergum in the male and both $8^{th}$ and $9^{th}$ terga in the female are not visible  as they are overlapped by the $7^{th}$ tergum.
The $10^{th}$ tergum extends beyond the posterior end of the body and has a deep groove in the middle of its free end.

Sternal plates:
Only nine sterna are present as the $10^{th}$ sternum is absent.
In the male, nine sterna are visible whereas in the female, only seven sterna are visible.
In females, the $7^{th}$, $8^{th}$ and $9^{th}$ sterna together forma brood pouch. The brood pouch has two parts: the anterior – genital chamber or gynatrium  and the posterior – gothecal chamber.
[![][1]][1]
(source: lander.edu)
[![][2]][2]
(source: lander.edu)
[![][3]][3]
(source: biologydiscussion.com)
![][4]
Sources:

http://www.slideshare.net/prof_aarif/animal-types-cockroach
https://learnzoology.wordpress.com/category/periplaneta-americana/page/15/
http://zoologybaburao.in/pdfs/7.%20Unit%20VII.pdf (Best)
http://www.eskool.com/files/subject/ppt/103_11_07_04_01.pdf
http://www.sakshieducation.com/(S(clpea355rwddux55iuci1cer))/Inter(New)/Material/IstYearEM/Zoology/07_01_ARTHROPODA_COCKROACH_UPTO_LOCOMOTION.pdf

Update:
Youtube links for Cockroach dissection:

https://youtube.com/watch?v=ZwvG69ICnps
https://youtube.com/watch?v=wF7ew2w24as
[1]: https://i.stack.imgur.com/RvH9a.gif
[2]: https://i.stack.imgur.com/uJLDh.gif
[3]: https://i.stack.imgur.com/lyOQK.jpg
[4]: https://bugguide.net/images/cache/LKP/K0K/LKPK0K2KGKA01QT0PQB0GQC0EQZSVQRSXKHSWQZSGKDK4KUK4K1KLK10KKUKHKBKAQAKMKLSMK307K6K4QD0BQLSEQ.jpg

my question was about the presence or absence or lateral pleurites in the 8th and 9th body segments of a cockroach and your answers does'nt says anything about those and more over the cockroach species which i am studying about is periplaneta americana

i am asking about the pleurites not about tergites and sternites. i too know about the sternal plates and tergal plates in abdomen but the description of pleurites or pleura is not so elaborate in our textbook

No, The $10^{th}$ tergum extends beyond the posterior end of the body and has a deep groove in the middle of its free end.. because of this they lack the pleura as the upper structure directly comes down. You can check if you cut a cockroach.

you seem to be right in this context but the ting is that we do not have dissection of a cockroach in our syllabus this year while it was included untill the last 32 years

what would be the case of 9th abdominal segment??

Check out these youtube links: 1.) https://www.youtube.com/watch?v=ZwvG69ICnps 2.)
https://www.youtube.com/watch?v=wF7ew2w24as

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sort: votes


text:
Supercomputer Vs Human Brain
With supercomputers doing calculation in petaflops ($10^{15}$ Calculations per Second), have we crossed the speed of Human Brain?

Related question on Cognitive Sciences: Why do scientists say brains are faster than computers?

Did you ask this question and then immediately answer it yourself... and then accept your own answer? This doesn't suit a biology forum either, it's information theory really.

@Louis: Will it be down voted if I say, yes? :)

There's a very big difference between doing the calculations needed to simulate the human brain (or any animal brain - we can do a fairly decent job on C. elegans), and doing computations.  While a basic leaky integrate & fire model is fairly simple, to accurately simulate a single neuron in real time takes a pretty fast computer.  See e.g. these links for more, http://www.neuron.yale.edu/neuron/,  http://bluebrain.epfl.ch/ http://www.artificialbrains.com/darpa-synapse-program.
Brains do well what computers do poorly, and vice versa.  The HP12C calculator on my desk, made in the early '80s, can do many sorts of mathematical calculations faster than I can, because brains aren't really optimized for doing, for example, compound interest calculations.  But my brain, or my dog's brain for that matter, can do all the 'calculations' needed to process a stream of images, recognize that they show a ball, predict its path, and catch it - while simultaneously processing visual, auditory, olfactory, and kinesthetic inputs for obstacle avoidance and threat recognition, and (in my case, anyway) perhaps thinking about how to solve complex programming problems.
Maybe I should add that there are basically three different things that a computer can do in this context:

Complex calculations, whether compound interest, weather modeling, seismic tomography or whatever.
Simulating the actual behavior of a brain, or some subset of one, starting from a single neuron.
Trying to replicate what a brain does through algorithms, or Artificial Intelligence.

(1) is what we mostly use computers for, and they're way better at it than human brains.  (2) is a special case of (1), which we do because we don't have much of an idea how to do (3), and having a simulated brain we can alter at will might help in learning how real brains do what they do.

In my opinion this is a much better answer than Devashish Das (OP)'s answer which got 15 up votes and is chosen as an answer at the moment.

Yes, I like this one too.

It is kind of meaningless to compare an analog device with a digital one to begin with.

I will just show the statistics of last attempt to mimic the brain process.
In 2011 fastest computer in Japan was launched:
K computer OR SPARC64 VIIIfx 2.0GHz
Features:

Manufacturer:    Fujitsu
Cores:   705,024
Linpack Performance (Rmax)   10,510 TFlop/s
Theoretical Peak (Rpeak) 11,280.4 TFlop/s
Power:   12,659.89 kW
Memory:  1,410,048 GB (16GB RAM per CPU)
Processor:   SPARC64 VIIIfx 8C 2GHz (88,128 CPUs, 8-core each)
Operating System:    Linux

It's currently world's 4th fastest supercomputer.
Source: Top 500 Supercoputers

Image Source: http://wondergressive.com/wp-content/uploads/2014/01/WG-k-computer.jpg
Now,

An 83,000-Processor Supercomputer Can Only Match 1% of Your Brain
...The most accurate simulation of the human brain to date has been
  carried out in a Japanese supercomputer, with a single second’s worth
  of activity from just one per cent of the complex organ taking one of
  the world’s most powerful supercomputers 40 minutes to calculate.
  Researchers used the K computer in Japan, currently the fourth most
  powerful in the world, to simulate human brain activity. The computer
  has 705,024 processor cores and 1.4 million GB of RAM, but still took
  40 minutes to crunch the data for just one second of brain activity...
Source: http://gizmodo.com/an-83-000-processor-supercomputer-only-matched-one-perc-1045026757

Human Brain:

Do we have brain to spare?
by David A. Drachman, MD
Within the liter and a half of human brain, stereologic studies
  estimate that there are approximately 20 billion neocortical neurons,
  with an average of 7,000 synaptic connections each.1 The cerebral
  cortex has about 0.15 quadrillion synapses—or about a trillion
  synapses per cubic centimeter of cortex. The white matter of the brain
  contains approximately 150,000 to 180,000 km of myelinated nerve
  fibers at age 20, connecting all these neuronal elements. Despite the
  monumental number of components in the brain, Szentagothai estimated
  that each neuron is able to contact any other neuron with no more than
  six interneuronal connections—“six degrees of separation.”

Image Source: http://www.nature.com/polopoly_fs/7.2933.1329907514!/image/far-to-go.jpg_gen/derivatives/fullsize/far-to-go.jpg
Why Brain beats Supercomputer?

Why is it so hard for computers to reproduce what your grey matter
  does as a matter of course? Volume. The human brain consists of about
  200 billion nerve cells (neurons) that are linked together by
  trillions of connections called synapses. As the tiny electrical
  impulses shoot across each neuron, they have to travel through these
  synapses, each of which contains about 1000 different switches that
  route that electrical impulse. In total, one human brain could contain
  hundreds of trillions of these neural pathways. It's like a Choose
  Your Own Adventure book that stretches from here to Jupiter.

This is a great answer!

It is not just processing speed that affects the speed of calculation. Algorithms also play a great role. I am very sure that electrical circuits have a much much faster response than the ion-current based neuronal circuits. Speed of information flow is not the sole criteria.

@WYSIWYG: They have used open-source Neural Simulation Technology (NEST) = http://www.nest-initiative.org/

Fuzzy mathematics and neural networks can play vital role in up bringing  computer science to higher grounds of Artificial Intelligence. But only considering the computational and memory speed couldn't be a right criteria in the development. While we increase the computational power and memory of a computer finally it is the quality of the software that decides what we achieved.

I don't think that difficulty of simulation is good measure for such comparison.

What this simulation is doing is basically hardware emulation, which is always slow (try compared the speed of a video game on native hardware with an emulator, even on a faster computer).  By this logic, weather has much greater processing power than a supercomputer, because a supercomputer cannot accurately simulate weather.

Computers work very different from brains.  Douglas Hofstaedter wrote an excellent essay to explain this:  http://themindi.blogspot.dk/2007/02/chapter-11-prelude-ant-fugue.html

A simple calculator (which is a computer) calculates 298465+46547 much faster than us. a PC forecast possible events faster than us. But even the fastest computer can't recognize a new pattern faster than us (the computer may never do that). So each one has its relative advantages.

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text:
More entropy: Atom or Macromolecule?
A question that appeared on my last exam was :

Which of the following has greater entropy A) An atom B) A
  macromolecule

The question doesn't specify anything else(i.e. type/size of atom or macromolecule). The macromolecules we learned class were proteins, sugars, nucleic acids(DNA/RNA) or lipids. What is the correct answer and why(hypothetical calculation, if possible) ?

I see the close vote is for off-topic.  I think this question is safely in the intersection of chemistry/physics and biology. Entropy is very important in biology and I think this standard question is not off-topic.

This is an exact duplicate of a recent question on chemistry SE, though by different users. Don't know if that's allowed or not. http://chemistry.stackexchange.com/questions/14438/greater-entropy-an-atom-or-macromolecule

The OP should have indicated the question was cross-posted. Otherwise it is allowed. The answer at the other SE points out a weakness of the question but  cross-pollination is good. It looks like I will be making my case on Meta again.

Link to Meta question: (http://meta.biology.stackexchange.com/questions/640/is-a-basic-question-about-entropy-off-topic-here)

@daniel.. i dont think this is on-topic even if it was not cross posted.. this is a very general question and general principles of physical chemistry are applicable everywhere.. this doesn't make it a biological question.. it is not that we cannot answer it.. it is better suited in chemistry se.

@WYSIWYG: While I think "better suited in ___" is not a basis for closing the question is just not very good so I think it should be closed anyway. Thanks.

@daniel.. i see your concern.. But don't you think OP will benefit more from asking this question in a forum that is more dedicated for this kind of questions. I agree that this question is fine. In fact there are posts which I have voted to close after giving an answer; just to avoid further discussions.. Defining the scope of a forum is important. If we wish to participate in this discussion then we can join the more suitable forum and then post our opinions. I would have totally agreed with you a year back :)

To whoever moderators concerned, I see this question is causing question of relevance. You are free to delete it if you wish-the wonderful users on this site has already given me the answer to the question...

Ahh entropy. The bane of many undergraduates. You won't need a lot of mathematical rigor needed to solve for absolute entropies in most biological fields so it's best to think of it abstractly.
Consider the atom. What can it do? Well if you remember from chemistry class, it can bounce around a process we call translate, and the electrons can basically switch spins. For the most part, if you had a single atom alone in the universe, that's all it could do. Move around and have its electrons switch states. It's best to think of these as "states" of the atom.
Let's see, the atom can move in the X direction and be in spin up. It can move in the x and y direction and be spin down...etc. But the point is, there is not a whole lot the single atom all by it's lonesome can do.
On the other hand, if we start adding other atoms to the mix, say across chemical bonds, then they can start to do more. If two atoms are bonded, they can stretch and contract (vibrational states), they can rotate around each other, and they can do everything the atom can do as well.
As you can see, there a lot more "things" or "states" that the two atoms can be defined in at any one time. They can be rotating one direction, vibrating in one way, moving in another... etc etc...even this sentence seems to be getting more chaotic! And that is really all entropy is. Adding up more and more ways for matter to get into all these possible configurations.
So the answer to your question is the macromolecule. It has tons of atoms and bonds. An uncountable number of ways to rotate, translate and vibrate, and be struck with photons, and emit light, and do all kinds of chaotic "stuff" (you can count it actually, it's just really hard).

Being struck by photons and emitting light have nothing to do with entropy in this setting.

sure it does. if you have a bond in molecular orbital theory that has a ton of states that can an excited electron can sit in, they are microstates

Number of microstates, yes. Being struck (or not) by photons, no. Incoming photons may affect the entropy of a system but the entropy is defined in terms of  possible microstates (restrictions on freedom of rotation, etc.). I think the language is confusing.

Ok first off, this is a biology forum and I said to think in abstract. Second off yes it does, because the same photon can be strike an N number of microstates. Oh my god!!! what is with trolls on SE.

Entropy is a measure for the number of states accessible to a system. The more states available, the higher the entropy.  If you think of an atom confined in a volume V, then, without further restrictions, the atom can be anywhere inside that volume, i.e. the number of states will be a function of the volume V. The bigger the volume, the bigger the entropy. Now, if you add another atom to that volume so that the two atoms form a gas, i.e. they do not bind, then these atoms can access states individually. The number of states for the system will be the number of states of atom1 times the number of states of atom2. Thus, in a gas, the number of states, and therefore the entropy, increases with the number of atoms. What happens now, if the two atoms bind together. They now can't access states individually, so the total number of states, and thus the entropy, will be smaller than that for a gas of the same atoms. But the two atoms can still access states similar to the one atom gas, plus they can do new things like rotating around each other. So the number of states of a molecule of two atoms will be bigger than the number of states of just one atom.Thus, if you compare the entropy of a single atom to the entropy of a molecule of N atoms, the entropy of the molecule will be larger.  If you compare the entropy of a gas of N atoms to the entropy of a molecule build from these N atoms, the entropy of the gas will be larger.

As this table shows, the more complex a molecule is (in general) the more entropy it has.
Entropy is an absolute quantity which is zero at $0^o K.$ When an atom or molecule has no way to rotate (is 'frozen') there is only one state in which it can exist. An atom of a gas or a molecule of a diatomic gas at $25^oC$ is also somewhat constrained compared to a complex molecule like sugar at the same temperature and pressure. The carbons and hydrogens in sugar have more possible states in which to exist. So, for example, chlorine gas, $Cl_2 (g),$ has lower entropy than propane, $C_3H_8.$
Trends for $S$ for various atoms and molecules generally reflect the idea that S is determined by molecular mass and restriction of motion.
A typical calculation.
If you want to measure the entropy of a simple molecule you assume the entropy is 0 at $0^o K$ and measure changes in entropy as the molecule is heated. In practice this might mean measuring the decrease in entropy of the surroundings as a substance heats up. By measuring the changes carefully up to a standard temperature (25$^oC)$ you get a number that is characteristic for each substance.
The equation used in chemistry courses is usually given as
$$\Delta S  = \frac{\Delta H}{T}$$
In English, the change in entropy equals the change in heat (per mass or per mole), usually at some phase change, divided by the temperature in degrees Kelvin.
As a simple example, if liquid benzene is converted to vapor at its boiling point $80.1^o C$ and the heat of vaporization for benzene is 394 J/g then for 50 g of liquid benzene ($C_6H_6$) the entropy change is
$$\Delta S = \frac{(50 g)\cdot(394 J/g)}{(80.1+273.15)^oK} = 55.7 J/^oK$$
Chemists have created tables that measure entropy changes for states of various molecules. With the exception of very simple molecules predictions of entropy based on structure are difficult and the tables are empirically derived.


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How does the frequency of a visual stimulus affect the steady-state visually evoked potential?
I want to design a project for EEG signal processing. In my research I found the concept of SSVEP. SSVEPs represent the electrical activity of the brain as measured via EEG, and are evoked by visual stimuli with low frequency applied to the eye.
My question is whether it is known how the electric activity of brain will change? And a second thing, does it mean that each frequency applied to the eye has a fixed reaction for the brain?

Explained perfectly in http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1880883

I corrected your title since the SSVEP is the pattern in the EEG activity and is not the stimulus for it.

I slightly modified question wording. Feel free to roll back.

Short answer
SSVEP frequency corresponds to stimulus frequency and SSVEP amplitude decreases with stimulus frequency.
Background
The simplest form of steady state visual-evoked potentials (SSVEPs) are those to flash stimuli. Herrmann (2001) studied the SSVEP by recording the EEG from the visual cortex at various flash frequencies. He found that SSVEPs occurred at a frequency corresponding to the flicker stimulus. Amplitudes decreased steadily with frequency and SSVEPs could be recorded up to ~90 Hz flicker frequencies. The shape and frequency following of SSVEPs are shown in Fig. 1.

Fig. 1. SSVEPs and FFT spectra at various frequencies. Source: Herrmann (2001)
Interestingly, SSVEPs in response to some frequencies showed resonance phenomena, indicating a selective frequency preference of the neural oscillators. Specifically, SSVEPs at around 10, 20, 40 and 80 Hz resulted in higher amplitudes than stimuli flickering at adjacent frequencies (Fig. 2).

Fig. 2. SSVEPs showing resonance at 80 Hz. Source: Herrmann (2001)
Reference
Herrmann, Exp Brain Res (2001); 137: 346–353


text:
Question about the DNA glycosylase enzyme assay/formamide gel loading buffer
Often for the DNA glycosylase enzyme assay we can see that the DNA glycosylase is incubated with oligonucleotide in 37C and then reaction is stopped by addition of formamide gel loading buffer (80% formamide/1 mM EDTA, pH 8.0y0.1% bromophenol blue/0.1% xylene cyanol). How the reaction is stopped by this buffer?

Do you have a reference for that?

Cloning and Characterization of a Functional Human Homolog of Escherichia coli Endonuclease III
Aspinwall, Richard ; Rothwell, Dominic G. ; Roldan-Arjona, Teresa ; Anselmino, Catherine ; Ward, Christopher J. ; Cheadle, Jeremy P. ; Sampson, Julian R. ; Lindahl, Tomas ; Harris, Peter C. ; Hickson, Ian D.
Proceedings of the National Academy of Sciences of the United States of America, 1997, Vol.94(1), pp.109-114 [Peer Reviewed Journal]

Formamide is a common loading buffer for denaturing gel electrophoresis of nucleic acids. I'd assume that it also denatures most enzymes and stops the reaction that way.

Escherichia coli endonuclease III (which I will now refer to as Nth), and the human homolog hNTH1, has both glycosylase and AP lyase activity. The section of the article you're referring is describing an assay of lyase activity. The assay tested both Nth and hNTH1 as well as HAP1, a human AP hydrolase that cleaves 5' to the AP site. Nth and hNTH1 were found by this assay to cleave 3' to the AP site. HAP1 is dependent on $Mg^{2+}$ for catalytic activity. hNTH1 (and likely Nth, given the high conservation) are dependent on $Mg^{2+}$ for substrate specificity (Eide et al., 2001). hNTH1 and Nth contain an $Fe-S$ cluster that is involved in DNA binding (Thayer et al., 1995).
Originally I thought that the reaction is stopped with EDTA. EDTA is a chelating agent; it binds and sequesters metal ions and prevents their use by enzymes. EDTA would prevent catalysis by HAP1 and DNA binding by Nth/hTNH1.
However, Chris pointed out that the loading buffer contains 1 mM EDTA while the reaction buffer contains 5 mM $MgCl_2$. While the paper doesn't give the volumes of reaction and loading buffer mixed together, it is perhaps unlikely that EDTA chelation of $Mg^{2+}$ is the sole mechanism for stopping the reaction. The high concentration of formamide (80%) in the loading buffer could then be responsible. Formamide is commonly used to denature nucleic acids and, at high concentrations, would likely have an effect on enzyme function.
References

Eide L, Luna L, Gustad EC, Henderson PT, Essigmann JM, Demple B, Seeberg E. 2001. Human Endonuclease III Acts Preferentially on DNA Damage Opposite Guanine Residues in DNA. Biochemistry-US. 40(22):6653–6659
Thayer MM, Ahern H, Xing D, Cunningham RP, Tainer JA. 1995. Novel DNA binding motifs in the DNA repair enzyme endonuclease III crystal structure. EMBO J. 14(16):4108–4120.

How much magnesium is present in the buffer? The EDTA in the buffer is only 1mM, so only 1mM of magnesium is complexed. I doubt that this is enough. Additionally, this buffer is not only TE but contains 80% Formamide.

@Chris: Thanks, that's a good point. The reaction buffer contains 5 mM &Mg^{2+}$. However, they don't give the volumes of reaction and loading buffer that are added to each other and electrophoresed. Do you think that formamide is the major factor stopping the reaction? I assumed it was there to denature the DNA. Does it also denature enzymes? Or perhaps the enzymes don't function on ssDNA.

I think so. I haven't checked if formamide reacts with proteins. That would be one possibily.

I've edited my answer, though I don't feel it answers the question anymore. I wish I could find some literature about it.

Thank you very much for your help. As you mentioned in your response, AP andonucleases may  incise 3’ and 5’ to the AP site. I read more about it and I am confused at some point. I have found:
There are four possible incision sites for AP endonucleases, and the enzymes have been classified according to their sites of incision:
class I and class II AP endonucleases incise 3’ and 5’, respectively, to the AP site, both leaving 3’-OH and 5’-P termini.
If for class II AP endonucleases incision is at 5' to the AP site, how it is that there is generated 3'-OH and 5'P?

Gary M. Myles and Aziz Sancar (1989). "DNA Repair". Chemical Research in Toxicology 2 (4): 197–226

@Piesel Perhaps you should ask that in a new question. Basically the phosphate will be on the 5'C of the AP ribose.


text:
What is this black insect (wasp-like?) South America?
I live in the Pacific coast of South America. Seems to have two wings, like a wasp's. The "tail" is a bit bulky but is only connected to the rest of the body by a thin part. It's black overall. The antennae in the photo are downwards but they just spring normally to the front...

The Evaniidae, also known as the ensign wasps or hatchet wasps

Actually I took photoshop to help me find this little guy, Ensign Wasp(Evaniidae)
Google Images:

My Photoshop research:

How did you do that? Photoshop search?

Np, I actually used Photoshop to identify the color of it's eyes and Antenna. It was quite clear it was wasp after that.

@jleeothon: Welcome to Biology SE, Can you mark as answer if this is what you were looking for?


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Schedules of mating for men

It’s simple deductive logic to follow that for a species to survive it must provide it’s offspring with the best possible conditions to ensure it’s survival – either that or to reproduce in such quantity that it ensures survival. The obvious application of this for women is sharing parental investment with the best possible mate her own genetics allow her to attract and who can provide long term security for her and any potential offspring.
Thus women are biologically, psychologically and sociologically the filters of their own reproduction, where as men’s reproductive methodology is to scatter as much of his genetic material as humanly possible to the widest available quantity of sexually available females. He of course has his own criteria for mating selection and determining the best genetic pairing for his reproduction. This is evidenced in our own hormonal biology; men possess between 12 and 17 times the amount of testosterone (the primary hormone in sexual arousal) women do and women produce substantially more estrogen (instrumental in sexual caution) and oxytocin (fostering feelings of security and nurturing) than men.

From a biological point of view, is the bold sentence correct? And is the quantity of hormonal differences the only explanation of this?
Link to article: http://therationalmale.com/2011/08/23/schedules-of-mating/

Edit question and add a link to the cited paragraph!

Females are defined as the sex that produces that bigger gamete (ovule) while the males are those from the gender that produce the smaller gametes (spermatozoid). Because producing big gametes is costly, the number of females fix the reproductive limit in the population and in other words the variance in reproductive success in males is higher than in females. In the same logic, because females fix the reproductive limit in the population, males have to compete to access the females while the females are choosy. You may want to have a look at the wikipedia articles for Bateman's principle and Parental Investment.
The conclusions of Bateman's principle holds in general but not systematically. In some species males produce huge amount of parental care and therefore, the females become choosy for example.

[..] men’s reproductive methodology is to scatter as much of his genetic material as humanly possible to the widest available quantity of sexually available females.

Yes, in many cases but not everytime. Human are an example of the cases where this statement is wrong.

[..] for a species to survive it must provide it’s offspring with the best possible conditions to ensure it’s survival – either that or to reproduce in such quantity that it ensures survival.

It sounds a bit weird! The reason is that the sentence almost implies that individual's strategy evolved in order to increase the probability of survival of the species which is totally wrong. By the mechanisms of natural selection a population evolve in the direction so that each individual favors its number of offsprings which can be in some cases very detrimental to the species as a whole.
Reading some bits of what I found no the webpage you linked i your question, it doesn't seem to me that the author is a good evolutionary biologist…but I haven't read much.

Good post remi, Bateman's principle and parental care was worth looking into. I think the article present the theories in a very simplified "layman" terms. Some malformulated statements(like your last comment observed) but overall I see no fallacies.


text:
How much energy is required to blind someone?
As I understand the ravages of sunlight upon the (human) eye; the cause of ocular damage and blindness is too much energy delivered to the cones and rods that ultimately make up our eyes; so the questions arise:
How much light can a (human) rod take?
How much light can a (human) cone take?

there are different kinds of damage.. high energy/high intensity

Light can affect retina in many ways [1]:

photothermal mechanisms - exposure to intense flashes of less than 20 microseconds that cause a rise in temperature of at least 10 degrees Celsius [5];
photomechanical mechanisms - exposure to flashes shorter than 5 nanoseconds [5];
photochemical mechanisms - light is absorbed by a chromophore and leads to the formation of an electronically excited state of it, resulting in chemical transformations [5].

The retina is more susceptible to light induced degeneration at lower wavelengths [2, 8]. The damage degree also depends on intensity and exposure duration. 12 hours a day of more than 500 lux light, more than three consecutive days can affect rat retina [3]. 2 hours  exposure to white light of 3000 lux has lead to apoptosis in rats retina [4].
Sunlight irradiance is about 11 W/cm2 (ranges between 1.5 and 122 W/cm2) and causes damage when exposure time is tens of minutes or even less [5].
Light induces apoptosis by different mechanisms:

Intense light triggers cell death in cones and rods by two distinct mechanisms: rapid, necrosis-like cell death occurs in cones; prolonged, apoptotic death is displayed by rods. However, the areas of cone and rod loss coincide, suggesting some interrelationship [6].

Cones and rods have different vulnerability [7].

References:

Youssef PN, Sheibani N, Albert DM. Retinal light toxicity. Eye (Lond). 2011 Jan;25(1):1-14. doi: 10.1038/eye.2010.149. PubMed PMID: 21178995.
Rozanowska, M. B. (2012), Light-Induced Damage to the Retina: Current Understanding of the Mechanisms and Unresolved Questions: A Symposium-in-Print. Photochemistry and Photobiology, 88: 1303–1308. doi: 10.1111/j.1751-1097.2012.01240.x
Jin X, Wu L, Zheng H, Mishima S. [Retinal light damage: I. The influences of light intensity and exposure duration at moderate and low intensities of cyclic light]. Yan Ke Xue Bao. 1998 Dec;14(4):215-9. PubMed PMID: 12579740.
Remé CE, Weller M, Szczyesny P, Munz K, Hafezi F, et al. Light-induced apoptosis in the rat retina in-vivo. In: Anderson RE, LaVail MM, Hollyfield JG, editors. Degenerative Diseases of the Retina. Plenum Press; New York: 1995. Via http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831109/
Malgorzata Rozanowska, Bartosz Rozanowski, Michael Boulton. LIGHT-INDUCED DAMAGE to the RETINA (2009). Available from http://www.photobiology.info/Rozanowska.html (accessed 20.07.2014).
Cortina MS, Gordon WC, Lukiw WJ, Bazan NG. Light-induced photoreceptor damage triggers DNA repair: differential fate of rods and cones. Adv. Exp. Med. Biol. 2004;533:229-40. PubMed PMID: 15180269.
Okano K, Maeda A, Chen Y, Chauhan V, Tang J, Palczewska G, Sakai T, Tsuneoka H, Palczewski K, Maeda T. Retinal cone and rod photoreceptor cells exhibit differential susceptibility to light-induced damage. J. Neurochem. 2012 Apr;121(1):146-56. doi: 10.1111/j.1471-4159.2012.07647.x. PubMed PMID: 22220722.
Kuse Y, Ogawa K, Tsuruma K, Shimazawa M, Hara H. Damage of photoreceptor-derived cells in culture induced by light emitting diode-derived blue light. Sci Rep. 2014 Jun 9;4:5223. doi: 10.1038/srep05223. PubMed PMID: 24909301.


text:
Are there any air-plants with parts that are edible for humans?
Are any air plants (Tillansia sp.) safe for humans to eat? I haven't been able to find whether or not there are. Pineapple is in the same family (Bromeliaceae), but isn't an air plant.

Many species of the genus Bromelia produce edible fruits altho they also are terrestrial bromeliads.

Monstera deliciosa seems to fit the bill. From Wikipedia:

This member of the arum family Araceae is an epiphyte with aerial roots...
Wild seedlings grow towards the darkest area they can find until they find a tree trunk, then start to grow up towards the light, creeping up the tree.[6][dead reference link]
Fruit

The fruit of Monstera deliciosa is up to 25 cm long and 3–4 cm diameter, looking like a green ear of maize covered with hexagonal scales.
Fruits of plants of the Araceae (Arum family) often contain Raphides and Trichosclereids – needle-like structures of calcium oxalate.
The fruit may be ripened by cutting it when the first scales begin to lift up and it begins to exude a pungent odor. It is wrapped in a paper bag and set aside until the scales begin popping off. The scales are then brushed off or fall away to reveal the edible flesh underneath. The flesh, which is similar to pineapple in texture, can be cut away from the core and eaten. It has a fruity taste similar to jackfruit and pineapple. The unripe green fruits can irritate the throat and the latex of the leaves and vines can create rashes in the skin, because both contain potassium oxalate: that is the reason why the fruits have to be consumed when the scales lift up.[9]
Plants grown indoors in temperate regions occasionally produce flowers and fruit.
In Mexico, a leaf or root infusion is drunk daily to relieve arthritis.[6][dead reference link]
In Martinique the root is used to make a remedy for snakebite.[6][dead reference link]

Here's a picture of the fruit by Bruno Navez:

Dragonfruit (Hylocereus undatus) is also hemiepiphytic. You may also be interested in this page about epiphytic cactus fruits and this post on Yahoo! Groups where I found M. deliciosa. The author claims:

I have eaten the fruits off my Acanthostachys strobilacea, an epiphytic bromeliad, and they are reminiscent of the related terrestrial pineapple just slightly more acidic but still very palatable (to me at least). [Hyperlink added.]

Self refilling fruit bowl?

I can't find anything on anyone growing these without an environment like soil to surround them, not just by just placing them down indoors and spraying them once or twice a week with water for example. Everything says or shows planting, sowing, plants in soil, plants in plant pots full of soil, etc…


text:
How did the horned lizard evolve?
It's a lizard that has the ability to burst blood vessels in it's eyes and shoot blood as self defense.
How can this behavior be explained evolutionary? Wouldn't it mean that there had to be some intermediate evolutionary step where the lizard could bleed from it's eyes only slightly? How did that not cause it's extinction?
To generalize more, how does a specific trait evolve when it seems the intermediate traits are detrimental to survival?

I like this question. Hope someone has a good, scientific answer.

each specific case is a separate question.

@user813801 I'm asking this about this specific case then.

The behavior can be explained evolutionarily just like any other trait. It came about either through adaptation, neutral evolution, or as a by-product of another adaptation.
An intermediate step, like the one you suggested, is not required. But if it did occur, there's no reason to believe that such a trait would cause extinction. Bloody eyes, whether they squirt or not, could be beneficial in some species. We know that blood-squirting eyes appears to be a defensive trait. Take away the ability to squirt and the blood could provide defense in some other unexpected way, or it may have had nothing to do with defense at all. Maybe the blood was just a lubricant before, or maybe the blood somehow enhanced vision during a stressful event. Or maybe it was just there and didn't do anything; nothing good, but nothing bad.
There's nothing special about this lizard. It does have a unique trait, but there's something novel in every species.

I'm speculating here, but it's likely that the taste of the blood has something to do with this. The blood of the horned lizard tastes foul to feline and canine predators. Therefore, a small amount of blood leaking out of the eye might put predators off immediately after the first attack, if that attack was aimed at the head.
Obviously, this is an advantage for the lizard, but since a large percentage of attacks to the head would result in debilitating injuries, there is a selective pressure to take this further so that the taste of the blood is "communicated" to the predator before the initial attack.

There isn't always an intermediate step like "oozing blood eyes", I suspect that this particular trait is pretty easily explained by having an area of weakness in a blood vessel that made the lizard bleed under high stress situations.
maybe in early version the lizard had to get some trauma or could intentionally hit its head on a rock or something... I don't know, but it doesn't really require any novel structure.


text:
To what extent do domestic animals understand language?
Note: Please tell me to re-post this in Cogsci or pets if this doesn't belong here.
Hello All,
I want to know how dogs or other domesticated animals differentiate between normal chat and a command. Do they understand their master's language or body language?
If they understand the body language of the master alone, then how come they can do the same trick (in most of the cases) if some other person gives the same command?
And to what extent do they have this understanding, meaning how many words does a domesticated animal understand?

Yes, they can understand some words and even simple sentences.
Here is what Animal Planet says:

Studies show that the average dog can understand about 165 different words, in some cases more if you make a point of training them. This includes the basic commands such as "sit," "stay," and "go," as well as a range of other terms, assuming they're tangible words and not abstract ideas.

Here are some supporting studies:

Some domestic dogs learn to comprehend human words, although the nature and basis of this learning is unknown [1].
A female mongrel dog, Sofia, was initially trained to respond to action (point and fetch) and object (ball, key, stick, bottle and bear) terms which were then presented as simultaneous, combinatorial requests (e.g. ball fetch, stick point). Sofia successfully responded to object-action requests presented as single sentences, and was able to flexibly generalize her performance across different contexts [2].

References:

Tempelmann S, Kaminski J, Tomasello M (2014) Do Domestic Dogs Learn Words Based on Humans’ Referential Behaviour? PLoS ONE 9(3): e91014. doi:10.1371/journal.pone.0091014
Ramos D, Ades C (2012) Two-Item Sentence Comprehension by a Dog (Canis familiaris). PLoS ONE 7(2): e29689. doi:10.1371/journal.pone.0029689


text:
How to make sure a stem cell culture is cancer free?
Say I take a blood sample from an adult, extract the white cells and apply to them the process described in <this article>. Assuming this actually turns the adult white cells into stem cells, which I then transfer to a culture in order to grow an arbitrary quantity, how can I make sure in the end this culture is free of cancer stem cells? Is there a last step that can be applied which would eliminate any potential CSCs leaving only healthy cells in the culture?
Thank you.

I doubt that this differentiation between these cells is possible. Stem cells are not expressing very much surface markers and are relative inconspicuous. So you can only cultivate them and look for the outcome.

HAT media additives?

The moethod described in this paper has never been reproduced outside the Riken Institute (which claimed to have to developed the method). The papers describing it have since then been retracted due to scientific misconduct (falsified figures, which of course only have been wrongly put in there and so on) which caused a major scandal.

It would not be possible to differentiate CSC from normal population non-invasively and select them out. You may do a single cell expression analysis to say if a CSC is present in a population or not but there is no magic bullet method for eliminating them. Also there are several oncogenes and some of them are also required for usual stem cell function. HAT kind of methods will not be able to eliminate potential cancer cells. Also, usual cancer chemotherapeutic drugs also affect other actively growing cell.
Bottomline: Not possible with the current level of knowledge and technology.


text:
Why are mammals unable to produce Essential Fatty Acids?
Why do we have to get them from our diet, and if they aren't taken in our diet we will face disease? Then why we don't have the enzymes which are require for EFA synthesis?

It's not really like your body can decide like 'hey, lets synthesize the enzyme required to catalyze the reaction for the creation of this EFA'. Apparently, we're just fine without them due to ample EFAs in our diet.

Have a look at this topic: http://biology.stackexchange.com/questions/16962/can-animals-make-their-own-unsaturated-fatty-acids

i don't understand will u plzz elaborate it more

I would speculate that since essential fatty acids are so abundant in our diet, there was no selective pressure for the maintenance in our genome of the enzymes that produce them.

@canadianer can you add more details if you can and post your comment as answer

@WYSIWYG I would if I could find any literature about it.

I agree with @canadianer - from an evolutionary standpoint it takes a lot of energy to maintain genes required for enzymatic synthesis of essential nutrients. If there's no selective pressure then the body has no reason to "waste energy and resources" on unnecessary enzymes.

Well, the essential fatty acids that humans fail to produce are not the same ones that other species fail to produce. For example, while cats produce their own Vitamin C and will therefore never develop scurvy, they can't produce their own taurine and will become sick if they don't consume enough of it.
To answer why a species might lose the ability to produce an essential amino acid, you have to consider what that species is eating most of the time. If its diet is rich in the amino acid anyway, individuals who lose the ability to synthesize it either feel no cost or--possibly more likely--even benefit by not wasting resources synthesizing compounds that may be abundant already in the diet and must be excreted if unused.
Turns out that this loss of ability to synthesize your own fatty acids is a particularly common consequence of evolving parasitic lifestyles, which makes sense: if you're just stealing someone else's acids, why bother to produce your own? Even outside of parasites, there's some interesting discussion on why the nine amino acids essential to all animals might have evolved from a genomics paper here, discussing which amino acids you really do have to make on your own and which you can get away with consuming depending on your species' lifestyle and dietary habits.

Are you confusing essential fatty acids with essential amino acids? I'm sure the general principles apply, but still…


text:
Why does ant queen keep the eggs out of her hive?
I have captured an ant queen and now I'm trying to create an artificial ant nest.
I have noticed that though she has dug a hole to hide in, she keeps the eggs out of it unless she feels that they are in danger.

I have two theories explaining why she does that:

Ants naturally put eggs in sunlight to keep them warm. In her situation, they are not gonna be any warmer of course - the jar is whole about the same temperature.
She is digging a nest and she needs some space. If this is true, where is all the dirt?

Theory number 3 suggests, that she is proud of them and she knows how curious am I to see them...

Can you post a complete picture of the ant (Please don't pull her out)?

She is very shy, and ever since she dug the hole, I can usually just see them for a moment (much like the alien in the first Alien movie). But I have one photo of the queen.

Theory number 4 could be it is maybe too warm in your jar and she is trying to keep them from heating up in the warm dark earth.

Is this the same queen as in the question, "Can I identify this black ant queen?" There is a picture on that question @skymninge.

According to various websites and literature I found,
Starting a new colony
During the mating season, Queen Ant grows wings and mate with male (flying) ant. In most of the species the queen will fly away to a new place where, she will loose her wings and dig a tunnel. She may lay eggs inside or outside because of the humidity and temperature, mostly they wait till spring, so that the humidity is high as well as warm temperature.
For laying eggs she will dig a tunnel inside and close the gates. She won't eat or move and completely avoid light, if the eggs are unhatched or some other problem occurs she will eats her own eggs. After around 8-10 weeks eggs will pop and you will get new worker ant babies. They will form the hive and feed the queen ant.

More info: http://antnest.co.uk/colony.html

My queen already ate lot of sugar. Are you really sure? I have noticed you post tons of content on this board without putting much effort in all the posts (I've been watching you). Remember that all this is not just about earning reputation.

Follow the link... http://antnest.co.uk/colony.html

I can see the link. The fact that something is written there doesn't necessarily mean it's 100% right. You've also said various websites. But in fact, it's according to Myrm's ant Nest website.
But most importantly you didn't answer my question. Neither you answered my comment.

@TomášZato No need to be rude. Devashish is a great user, and has started an unanswered questions event, to take care of some of the unanswered questions. Note that he's put more info into your question than anyone else has. Again, you were wrong to be rude, don't do it again.


text:
What are some atypical examples of positive transcriptional cooperativity?
Cooperativity in gene expression is an important feature of many regulatory networks. Described using the Hill function, the most common example is a transcription factor (TF) that when bound to its target regulatory site, increases the rate of binding of other transcription factors (usually through TF-TF dimerization).
There are numerous example of TF dimerization-based cooperativity in the literature. However, I am trying to find examples of positive transcriptional cooperativity that involve mechanisms other than TF dimerization. In the dimer model, an unbound TF binds to its cognate promoter (containing multiple enhancers) with a certain affinity. With the first TF bound, another identical TF now has increased affinity for its target - binding to the enhancer and binding (dimerization) to the first TF. The expression profile is sigmoidal (near binary) and represents sharp on/off switching in activity.
Although peer-reviewed articles experimentally or theoretically characterizing alternative mechanisms are preferred, I'm also interested in user hypotheses and discussions that are more speculative. Specifically, I'm interested in positive cooperativity that occurs without feedback from the regulated genes.
One potential mechanism could involve a DNA-binding TF consisting of a transcriptional activator domain and a chromatin remodeling or DNA methylation domain. When the TF binds it not only activates transcription but remodels local chromatin. If the remodeling increases affinity for the next TF, they act cooperatively (and positively). Perhaps something similar to this has already been described.

What proteins do you think about? Transcription enhancers which are not involved directly in transcription but enhance it?

Yes, transcription enhancers, not the core machinery.

A similar mechanism to the one I proposed in the last paragraph above, but without the chromatin remodeling domain, does appear to result in cooperativity. http://www.pnas.org/content/107/52/22534.full

Positive co-operativity without feedback from the downstream genes:
I guess Polycomb/Trithorax complexes will fit this criterion nicely.
Polycomb group (PcG) represses Hox and other differentiation related genes (such as neurogenin) while Trithorax (TrxG) group promotes their expression. They are not like usual transcription factors that bind to promoters and recruit/exclude RNA-polymerase; they bind at regions called Polycomb Response Elements/Trithorax Response Elements and mediate epigenetic regulation of nearby genes by histone modifications (primarily methylation).
PcG froms two main complexes PRC1 (Polycomb Repressive Complex-1) and PRC2. Different components of the complex have different molecular functions. For e.g SuZ has a Zinc finger domain and can bind to DNA/RNA, Ezh has histone methyltransferase activity etc.
This is an old review but is still quite informative.

Can you explain or propose (or reference to) the underlying mechanism for polycomb/trithorax cooperativity? Thanks.

@nbogard Edited the answer..

The Polycomb/Trithorax system looks like it does exhibit cooperative activity. Thanks for the reference. I found this one also: http://www.nature.com/nrm/journal/v15/n5/full/nrm3789.html
Specifically, the last section and fig. 7 where the authors propose that Polycomb/Trithorax Response Elements, found in target enhancers, promote bistability in target expression. Thanks!

Interesting question. I think I have two examples for you which might be interesting.
The first is the co-regulation of the microphthalmia-associated transcription factor (MITF) in pigmentation by SOX10 and PGC1a/b. See this paper:

PGC-1 coactivators regulate MITF and the tanning response.

The second is about the regulation of brown fat tissue by PGC1a and IRF4 which seem to interact in these cells. See this paper:

IRF4 Is a Key Thermogenic Transcriptional Partner of PGC-1α.

In both cases a transcription factor (SOX10 or IRF4) interacts with the co-activator PGC1 proteins to regulate gene expression. If the co-activator is missing, the expression is at least downregulated. These activations are not so atypical or rare but are occurring quite often. If you have problems in getting these articles, let me know.

Thanks, @Chris but I could not find an example of measured cooperativity in either of the two studies. I've edited my question to better define what I mean by 'cooperativity'.

In the first paper SOX10 interacts with the PGCs. The knockdown of the PGCs leads to reduced pigmentation. The same is true for the knockdown of the PGCs in the pigment cell of the mice, which leads to much lighter pigmentation. In the second paper the interaction happens between IRF4 and PGC1a. If one of the partners is not present, the regulation in the fat tissue is not working. They also present data on from co-ips on the interaction of both proteins.

I do see that the activity described in these papers requires binding between the different factors, but I do not see where they measured cooperativity. I think there is some confusion about what cooperativity means. I'm specifically referring to cooperativity of biochemical binding that results in a non-linear response. http://en.wikipedia.org/wiki/Cooperative_binding#Examples_of_cooperative_binding


text:
High frequency human genetic oscillators?
The most well studied genetic oscillators in human genomes are involved in regulating the circadian clock (which operates on an approximately 24-hour cycle) and cell cycle activity (with single cycles usually lasting several hours to many days). Are there any known genetic oscillators in humans (or other mammals) that operate on shorter timescales?

Many mammalian cells (or cell lines) have cell cycle period < 24hours. What timescale are you interested in. Usually it takes few hours for proteins to achieve steady states.

I'm looking for an example where oscillations occur within hours and are not coupled to the cell cycle. Thanks!

Natural or synthetic ?

Natural, and the simpler (fewer parts) the better. I'm looking for an endogenous oscillator that can be coupled to synthetic circuits.

Here are some examples:

electric oscillators:

neural activity
cardiac automatism (0.8 ... 1 Hz)

mechanical oscillators (as a result of neural activity):

heart beats
breathing (0.2 ... 0.3 Hz)
intestinal peristaltic waves
vocal chords activity (up to a few kHz)
muscular spasm (pathological)

chemical oscillators:

insulin variation in concordance with glucose intake
endocrine oscillations
menstruation
feedback enabled metabolic pathways

See this Wikipedia page too: http://en.wikipedia.org/wiki/Oscillation#Human
When it comes to genetic oscillators, some of them follow circadian rhythm.

A typical proliferating human cell divides on average every 24 h. This division timing allows cells to synchronize with other physiological processes and with the environment. The circadian clock, which orchestrates daily rhythms, directly regulates the cell division cycle and is a major synchronizing factor [5].

Immune system:

In every single cell an oscillator goes ticking through a molecular clock operated by transcriptional/translational feedback loops driven by the rhythmic expression of circadian genes. This clock gene machinery steers daily oscillations in the regulation of immune cell activity, driving the periodicity in immune system function [1].

Glucose homeostasis:

The master circadian clock, localized in suprachiasmatic nucleus (SCN), regulates multiple metabolic pathways, while feeding behavior and metabolite availability can in turn regulate the circadian clock [2].

Retina:

... the retina itself possesses intrinsic circadian oscillations, exemplified by diurnal fluctuations in visual sensitivity, neurotransmitter levels, and outer segment turnover rates. Recently, it has been noted that both central and peripheral oscillators share a molecular clock consisting of an endogenous, circadian-driven, transcription-translation feedback loop that cycles with a periodicity of approximately 24 hours [3].

But there are others which don't.

Genetic oscillators are ubiquitous regulatory motifs in the molecular control circuits of living cells. Prominent examples include the cell cycle and cellular signaling [4].

The frequency is much lower in some human cells [6]:

Cell Type      Process    Time
______________ __________ ______________________
fly embryo     mitosis    8 minutes
bacteria       mitosis    20 minutes
yeast          mitosis    2 hours
human skin     mitosis    20 - 24 hours
human sperm    meiosis    about 64 days
human liver    mitosis    1 year or more
human egg      meiosis    up to 40 years or more
human nerve    mitosis    never, once mature

References:

Vinciguerra M, Borghesan M, Pazienza V, Piepoli A, Palmieri O, Tarquini R, Tevy MF, De Cata A, Mazzoccoli G. The transcriptional regulators, the immune system and the the circadian clock. J. Biol. Regul. Homeost. Agents. 2013;27(1):9-22. PubMed PMID: 23489683.
Chrościcki P, Usarek M, Bryla J. [The role of biological clock in glucose homeostasis]. Postepy Hig Med Dosw (Online). 2013 Jun 20;67:569-83. doi: 10.5604/17322693.1053906. PubMed PMID: 23799401.
Ramsey DJ, Ramsey KM, Vavvas DG. Genetic advances in ophthalmology: the role of melanopsin-expressing, intrinsically photosensitive retinal ganglion cells in the circadian organization of the visual system. Semin Ophthalmol. 2013 Sep 6;28(5-6):406-21. doi: 10.3109/08820538.2013.825294. PubMed PMID: 24010846.
Davit A. Potoyan and Peter G. Wolynes. On the dephasing of genetic oscillators. PNAS 2014 ; published ahead of print January 27, 2014, doi:10.1073/pnas.1323433111
Samuel Bernard and Hanspeter Herzel. Why Do Cells Cycle with a 24 Hour Period? Genome Informatics 17(1): 72{79 (2006).
wiseGEEK.org. How Long Does it Take for Cells to Divide? (accessed 21.07.2014)

Great list! Thanks! Sorry, I was too vague in my question. I've edited it to refer specifically to 'genetic' oscillation. Do you have an example of a 'feedback enabled metabolic pathway' where high frequency oscillations depend on RNA/protein expression and degradation? Sorry for the confusion.

Thanks! This is a solid answer. Reference 4 is especially helpful.


text:
Can I identify this black ant queen?
I have an ant queen in a jar. This is what she looks like:

Because I'm planning to start an artificial ant nest, I'd like to learn something about that specific species of ant. This particular queen is very common in the Czech Republic, central Europe. It's also very common in cities.

Could you tell what kind of queen is that?
Is there any image reference that would help me find out? Ideally with some location search possibility.

I am not an expert of ants, but it looks very much like the common black garden ant. http://en.wikipedia.org/wiki/Black_garden_ant

For a moment, I hoped she will be some special badass ant queen. But I love her anyway.

This is not a common black garden ant "Lasius niger" because these ants do not have alternate mat and shiny bands on the gaster.

This cannot be a Lasius queen, it is a Formica queen. Although one of the main characteristic is the shape of the first segment of the funicula which cannot be seen on this picture, the general aspect of this queen (elongated, with red legs, does not have a bulky aspect) indicates this queen is from the genus Formica. It is similar in shape and coloration to many queens in the subgenus Serviformica, for example Formica cunicularia, Formica cinerea.

As @skymnige said it is definitely Black garden ant (Lasius niger)

This is wrong, the pronotum is not elevated enough, the tergites that are half mat and half shiny don't match with Lasius, same for the general aspect of the ant (more elongated than Lasius), the legs are dark red which is common in the genus Formica whereas they are more often black or yellow in Lasius.

@Nakx: I believe you are right. https://www.antsrus.com/store/p80/Formica_%28Serviformica%29_cunicularia_Queen_with_1-5_workers_%28Starter_pack%29.html

Thank you @Devashish_Das, I am an ant taxonomist and most ant identifications on stack biology are wrong.


text:
Horizontal gene transfer versus convergent evolution
There are several often noted examples of convergent evolution (eyes, bat/bird wing evolution etc.)  How do we rule out horizontal gene transfer in these cases?

You know that bat wings are modified hands, while bird wings are modified arms.  And human eyes and insect eyes are very different.

Without any molecular evidence you could infer convergent evolution if the species being compared shared a common ancestor that lacked the trait in question.
With genomic and developmental data you would measure the degree of similarity shared between the relative factors in each species. Little or no similarity indicates convergent evolution.
Horizontal gene transfer is predominantly found in bacteria. Although there are examples of limited gene transfer in eukaryotes, the donor is almost always bacteria. And there are currently no known cases of multi-gene transmission of complex networks.
It is interesting to contemplate how a full network might be transmitted horizontally. Horizontal Network Transfer would first require a mechanism for segregating the relevant genes from the rest of the genome. It would also require invasive machinery that allows the large amount of foreign genetic material to bypass the host's defense systems. Furthermore, integration of a foreign network is increasingly more difficult with the more genes you transmit due to positional and regulatory effects of the host genome. And on top of that, it is highly unlikely that a full complement of genes involved in a complex developmental process would function in any way resembling eye or wing development. These networks have been coevolving within massively complex genomic environments for hundreds of millions of years. Expressing a large network in a foreign cell would likely prove toxic.
A looser definition of HGT might include bioengineering, specifically stable transgene integration.

A small comment on the use of the term homology. Homology is an absolute state, i.e. genes (for instance) are either homologous or not homologous. Referring to degrees of homology is misusing the term. Genes can be identical to a certain degree which not necessarily means that they are homologous.

@RickardSjogren you're right. I've edited the answer to use the correct term. Thanks!


text:
Location of nucleotide synthesis and transport
I couldn't find this question directly asked so I thought I would ask it
In Fundamentals of Biochemistry 3e (Voet et al), it has a small small little comment about pyrimidine synthesis:
(In a diagram showing UMP synthesis)
"In the eukaryotic enzyme, which contains FMN and nonheme Fe, is located on the outer surface of the inner mitochondrial membrane where quinones supply its oxidizing power. The other five enzymes of pyrimidine biosynthesis are cytosolic in animal cells."
So it seems for the most part pyrimidine synthesis occurs in the cytosol??
When the book talks about purine synthesis no mention is made of where this is actually happening in the cell.
Also, if nucleotides are being made in the cytosol, I suspect there must be some kind of membrane protein that allows nucleotides to cross the nuclear and mitochondrial membranes... what are they??
I'm a visual person, and knowing where and how these things are happening in the cell helps me understand it better than just following what's happening after each synthesis step.
Thanks!

Correct, all but one step in pyrimidine synthesis occurs in the cytosol, and purine synthesis occurs in the cytosol only.
Nucleotides freely diffuse through nuclear pores but are actively transported through mitochondrial membranes via embedded membrane transport proteins (i.e. ATP-ADP translocators, GTP transporters, and pyrimidine nucleotide transporters).
http://themedicalbiochemistrypage.org/nucleotide-metabolism.php

I should add that nucleotides can also pass through nuclear and mitochondrial membranes as cofactors for some proteins.


text:
Identify this Harvestman
I spotted this guy in Switzerland. It's clearly an Opilione (Harvestman), but I really know nearly enough about this diverse group to be able to identify the species.

Sorry, I didn't think to place any reference near it for scale. Can anyone tell me the species or at least the genus? (Bonus points if anyone can guess what it's feeding on)

you smashed the poor guy?

@DevashishDas No of course not; I didn't harm either one. I saw him, took the photo, then moved on.

Sorry, i was just kidding. Anyway, is this is the one? http://www.fcps.edu/islandcreekes/ecology/Arthropods/Harvestman/harvestman.jpg

It could be. The coloration is similar. Can you find another image that more shows back a bit more clearly and cite the species?

It is probably Daddy Longlegs (Leiobunum vittatum)

this invert color image show the resemblance.

Source:
http://www.insectidentification.org/insect-description.asp?identification=Eastern-Harvestman
http://bugguide.net/node/view/840130

Might be eating a cockroach:

UPDATE:
OR
It might be Mitopus morio(modern harvestman)

Thanks for the response. I'm a little skeptical of this identification though. First, in my image, there is a dark stripe down the back behind the eyes, but in yours, the body appears almost entirely dark with light fringes on the side and light joints. Second, several sources claim the distribution of Leiobunum vittatum is limited to North America, but my specimen was from Switzerland. I'll leave the question open for now, but I'll keep looking into it.

@p.s.w.g: I think you are right. But I am pretty sure genus is correct. Look for a species which have two parallel sets of dots on the back in that genus.

Age and sex may be a factor for body color.

Yes, I'm pretty sure it's a Mitopus morio. The coloration and patterning is correct, as well as the distribution.


text:
Can nosebleeds cause death?
Can epistaxis or nosebleeds be a cause of death?

if u have a bleeding disorder, then yes..https://www.hemophilia.org/Bleeding-Disorders/Types-of-Bleeding-Disorders

Can you explain a little bit?

Great image choice.

I have heard of it happening:  A small kid is hit in a pretty minor traffic accident.  The impact caused a nosebleed and knocked him on his back.  The impact with the ground knocked him out.  Head injury--they waited for the paramedics.  The kid drowned.

Well if you are driving at the time and have a car crush due to thinking about the nosebleed...

Yes, it can, but it is extremely rare.

... nosebleeds are rarely fatal, accounting for only 4 of the 2.4 million deaths in the U.S. in 1999 [1].

The main issue is that epistaxis can be a sign of potentially fatal diseases:

The instances in which nosebleed is potentially fatal are those in which there is a history of recent head injury, severe arteriosclerotic cardiovascular disease or an underlying vascular tumor in the nasal chambers. Fatal nasal bleeding has not been reported in children [2].

Here are some causes which can lead to fatal complications if left untreated [3]:

Leukaemia
Hypertension
Coagulation disorders
Hepatitis
Head injury
Myelodysplastic syndromes - Epistaxis

Death by massive hemorrhage can occur when epistaxis is the result of a ruptured aneurysm [4, 5, 6]:

An instance of fatal epistaxis is reported in a patient with an unsuspected aneurysm of the infraclinoid portion of the internal carotid artery. There was no known history of trauma. The aneurysm was subsequently detected on an old X-ray film. Epistaxis from an aneurysm at this site is nearly always preceded by significant head trauma and is associated with cranial nerve palsies, a syndrome with a high mortality. Epistaxis from rupture of a non-traumatic aneurysm is very rare [4].

References:

Work Table I. Deaths from each cause by 5-year age groups, race and sex: US, 1999 Page 1922. U.S. Centers for Disease Control Published 2001-05-11. Via Wikipedia contributors, "Nosebleed," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Nosebleed&oldid=617613780 (accessed July 21, 2014).
QUINN FB. Fatal epistaxis. Calif Med. 1961 Feb;94:88-92. PubMed PMID: 13738727.
Right Diagnosis (tm). Epistaxis Deaths. Available from http://www.rightdiagnosis.com/symptoms/epistaxis/deaths.htm (accessed 21.07.2014)
HORNIBROOK, J. and RHODE, J. C. (1981), FATAL EPISTAXIS FROM AN ANEURYSM OF THE INTRACRANIAL INTERNAL CAROTID ARTERY. Aust. N.Z. J. Surg., 51: 206–208. doi: 10.1111/j.1445-2197.1981.tb05942.x
P. N. Pathak (1972). Epistaxis - due to ruptured aneurysm of the internal carotid artery. The Journal of Laryngology & Otology, 86, pp 395-397. doi:10.1017/S0022215100075423.
Urso-Baiarda F, Saravanappa N, Courteney-Harris R. An unusual cause of massive fatal epistaxis. Emerg Med J. 2004 Mar;21(2):266. PubMed PMID: 14988378.

Any injury, that results in external bleeding can lead to death, since it is a breach in the body's defenses and an entry point for pathogens.
Explanation:
When you have nose bleeding the blood must be coming from somewhere. Usually from inside your body.
That means there is a hole in your body which is big enough for blood to stream out.
That in return also means that through the same hole things can get back inside your body.
For example any kind of virus or bacteria.
That does not mean every bleeding is potentially lethal. But depending on the environment the body is in the chance of infection is certainly greater with a lesion (hole in the circulatory system) than without it.

Good Answer, Can you explain a little bit?

Thanks. Was that sufficiently explained?

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


text:
Has anyone used Crispr/Cas to induce a knock-in in MEF cells?
Does anyone have experience with the CRISPR/CAS9 platform performed on MEF? Or does anyone recall any relevant articles?

Is this the paper you are looking for? http://genesdev.cshlp.org/content/27/23/2602.long

From this paper:

We chose to test for Cas9-driven targeted mutagenesis on the
  endogenous Trp53 gene in mouse embryonic fibroblasts (MEFs), a cell
  line in which the biology of p53 has been thoroughly characterized and
  where the gene is structurally intact.

Furthermore:

Seventy-two hours post-transduction, cells were cultured in the
  presence or absence of Nutlin-3a, a specific inhibitor of the MDM2–p53
  interaction (Tovar et al. 2006). Cells were scored for the fraction of
  GFP+ cells after 4 d of Nutlin-3a exposure using flow cytometry (Fig.
  2B). Nutlin-3a potently activates a p53-dependent anti-proliferative
  cellular response, which strongly and specifically selects for any
  cells with disrupted Trp53 function (Efeyan et al. 2007). Much like
  MLP-p53.1224 infected cells, the pQCiG-p53 GFP+ cells were rapidly
  enriched for in the presence of Nutlin-3a, suggesting that
  CRISPR-mediated gene disruption had initially occurred in at least a
  proportion of the initial Cas9-expressing cells.


text:
Is humans' height ideal?
More or less we humans are around 1.70 meters tall.
My question is, would it be possible to scale us? that is, is it in principle possible having humans 1 cm tall, or 10 meters tall or is there some reason that makes our height somehow ideal?

I will go with the fact that BMI may be a factor.

Imagine what would happen to your brains when you're 10 meters tall and you stumble, fall and bump your head to the ground. Natural selection at its core.

I remember there is a vsauce video about that https://www.youtube.com/watch?v=DkzQxw16G9w

There's also limits due to the structural strength of atom bonds. Larger animals needs stronger bones to support their weight. The buildings that we create are static structures, which demands less strength than a constantly moving animal requires.

Humans can, to some extent, be scaled: While most humans are two meters tall; the human body essentially works throughout the entire range from around a meter to around two and a half meters, although you tend to run into problems at the extremes.
However, outside of that range you run into the tyranny of the square-cube law:
As you scale a creature (or, in fact, anything), it's mass increases proportionally to the cube of the scale, while its surface area increases proportionally to the square of the scale.
This means that as you scale humans down, their mass, and hence their ability to generate heat would drop faster than their skin area, and hence their ability to dissipate heat; meaning that if unaltered, smaller humans would rapidly run into problems of freezing to death.
(Small animals typically solve this through a number of methods: Higher metabolic rates, rounder bodies, and more fur. Small humans, i.e. babies also suffer under this, and solve it by having what is typically referred to as "baby fat", a blubber that, among other things, aids thermoregulation.)
Similarly, as the human body is scaled up, the opposite problem arises: The body becomes unable to dissipate heat quickly enough. Larger animals solve this problems with giant organs specifically suited to radiate heat, such as elephant ears; or through submersion in water, as seen is cetaceans and hippopotamuses; or simply through living in cold climates, such as the polar bear. (All of this is typically augmented by lower metabolic rates.)
Heat economy isn't the only problem with size, however:
Especially when scaling up, the strength of various structures in the body become problematic. Unusually (yet not even freakishly) tall humans generally have some manner of bone problems, and also often have problems with too small hearts, leading to low blood pressure, or too big ones, leading to heart failure.
If the change was gradual enough, with sufficient adaptation, this wouldn't necessarily be a problem. After all, giraffes and elephants get on perfectly well; but a pump-valve heart such as we have cannot be scaled up indefinitely.
With a continuous-flow heart, this limit could probably be stretched, but how that would even begin to work biologically I have no idea.
Further problems with very large humans include getting enough air flow through the lungs, the enormous chore it would be to stand up or sit down, and of course, just getting enough food to drive the enormous body.
The long and short of it is: Anything less than about half a meter would probably leave us freezing to death; and anything more than two and a half meters is quite frankly a stretch (if you'll pardon the pun).
(There are people alive now that are more than two and a half meters tall, but they are not generally speaking in good health, although some do get on.)
Of course, all of this is predicated on the specific gravitational and atmospheric conditions on Earth.
On another planet with a greater or lesser gravity, a different proportion of oxygen in the air, or just a denser atmosphere; many of these limits and limitations would be quite different indeed. (Which is why whales, living in such an alien world as the sea, can be an order of magnitude bigger than any animal that lives on land.)

Amphicoelias fragillimus disagrees with your last paragraph

@silvrfück: Indeed; last paragraph clarified. It is, however, worth mentioning that A. fragillimus itself lived under somewhat alien atmospheric conditions. There are of course also more vegetative beings on land, such as giant fungi and clone forests; many of the outlined limitations apply specifically to animals.

"While most humans are two meters tall..." I'm deemed tall at 180CM. Most people I know are not 200CM?

@James: I'm rounding; which is why I said 2 meters, not 200 cm.

That's a pretty big round up @WillihamTotland