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Was the evolution of humans inevitable?
Suppose we wind time back to the instance when life emerged on Earth and let evolution start over again, will human beings or any other kind of self-conscious animals evolve ultimately, inevitably?
Or do these sorts of animals just evolve as a result of some randomness processes in evolution, if so, what's the probability? Is it great or small?
If randomness does exist, then to what degree will it affect our ability to depict evolution? Will we still be able to describe the general trends of evolution, for example, the trend of more and more complicated animals evolving?

there is no way to answer this question, because we don't have other systems to observe.

@MattDMo But observing our own system is enough. I mean if we repeat our own system again and again, will there be human beings or similar creatures eventually?

@Peterchar I hope my answer will help you understanding why your question is not answerable.

@Peter It is obvious that some of us (well, me) interpret your question differently. Are you primarily interested in evolutionary processes 1) in general, 2) from Earth (4bn years ago)-like circumstances, or 3) from the exact "state of the universe" when life took off on Earth?

For the second one, yes. For the first one, I'm just asking if we could predict the general trend or even particular spices under the effect of randomness(if exist). For the third one, what does 'state of the universe' mean? Thank you!

While the present answers discuss a teleological understanding of evolution, which is rightfully refuted, OP's question is broader: Given that niches affect selection and specialization, would there be a chance for convergent evolution to create human-like animals multiple times (perhaps assuming that the first human-like species did not develop technology to spread globally)?

Evolution is largely random, because most of the processes that drive evolution are random. A few ideas you should understand to realize why it is so random.
Most people are only aware of natural selection when it comes to evolution, and think that natural selection has a goal of creating new, increasingly sophisticated forms of life. None of this, of course, is true. Evolution is not only natural selection, there's also genetic drift, gene flow, and mutation, which are random. Natural selection is not technically random, but it's not the biggest player. Secondly, natural selection does not have any goals and does not move forward, create more complex life, invent adaptations, or does anything of this sort. Natural selection is not designed to produce perfection, it just acts upon whatever variation is present in population, and favours individuals that are more successful in reproduction. Case study: 98% of our DNA doesn't code for any proteins, and presumably most of this DNA is junk. Does it sound like perfection to you, like we are the ultimate species?
The reason I tell you all this is because, in my opinion, when asking this question of "inevitability", you assume that there's some guiding hand that leads evolution towards some end-point, a climax. But there is no such guiding hand, and it takes a number of incredibly unlikely events to occur in a specific order for: Earth to be created with such conditions, life to start on Earth, collective learning to evolve in some form of live, agricultural revolution to occur so this form of life can thrive, etc. If at any stage something went different, everything would be different.
Final thoughts, why are you so sure that humans won't go extinct just like 99.9% of all the species that ever existed on Earth? A typical species goes extinct in about 10 million years, and we've been around for only 200,000 years. If you accept this possibility (which is real, in my opinion), suddenly, it doesn't seem that intelligent life, and we as its representatives, is some inevitable end-point in evolution, does it?
Edited: As to your last (new) question, "if randomness in evolution exists, are we still able to describe the general trends in evolution?". Firstly, of course randomness exists in evolution! Mutations are caused by errors in the process of DNA replication, genetic drift is caused by random sampling by definition. Secondly, there is no universal trend to more complicated organisms being evolved, as I mentioned above. Some organisms do get more complex, but some organisms haven't changed much over very long time, some are "living-fossils". Once again, evolution has no goal to create more complex life -- if, say, nautiluses or horseshoe crabs are capable of surviving and reproducing in the niches they occupy -- there's nothing else needed for their existence. Furthermore, fitness is linked to the environment, which is dynamic -- many complex species went extinct during global changes in the environment, whereas what you might call as "primitive" species of unicellular bacteria survived.

Philosophers and physicists argue among themselves whether nature is random or not and even whether this is a proper question. But, assuming for the moment, that nature is not random (a minority position), then "most of the processes that drive evolution are random" would be false.

@GlenTheUdderboat, my problem with this debate would be: "what evidence do you have to suggest that seemingly random events in evolution are not based on chance but rather follow some predetermined path?", and to my knowledge no one can give me such evidence. Thus, I prefer utilizing the principle of Occam's razor and stick to the simplest hypothesis.

Including gene flow along mutation, natural selection and drift seems a bit weird to me. Things that are random are subject to probability and you do not adress this part of the question of the OP. There are some stuff that tend to increase through evolution, why would intelligence not be one of them. YOu should argue also according these lines.

Of course I have no such evidence. But I can now see that for a biologist by far the most practical way to deal with his or her subject would be to assume a probabilistic world. (But perhaps keep in mind that this isn't a fact like other biological facts.)

@Remi.b, why is it weird for you to see gene flow, drift, mutation, and selection together? These all are the mechanisms of evolution, and my point was that only the natural selection seems to have no chance involved. Other factors contribute more to the evolution and are random. As to your other point, I addressed his question "what's the probability? Is it great or small?" by saying that it seems "incredibly unlikely", and giving example of the chain of incredibly unlikely events that should happen for modern human to appear.

@Remi.b, as to "why intelligence doesn't increase through evolution", the answer is the same as "why the body size doesn't increase through evolution". Apparently, there's no selective pressure, and all species but us do not benefit from being intelligent much, as you noted yourself, and I agree with it.

Problems of epistemology in your question
Two problems of epistemology (which discussion is a matter of philosophy rather than science)

The whole question depends on what you consider being random and what you consider being determinist. The number that come out from a dice is random unless you know exactly how the dice was thrown (and make some calculation about the cinematic of the dice).
Consciousness is in itself rather hard to define as well. Several definitions has been suggested in science and philosophy.

Anyway even with these philosophical issues behind the question, one can assume some common although improperly defined used you may have of these terms and safely answer that no, self-counsciousness is not a necessary consequence of evolution.
Evolution of cognition
The condition under which greater cognitive abilities is beneficial are quite restrictive and even today the way that human cognition evolved is under debate. This wiki article will give you an introduction into this field. The immense majority of all lineage did not evolve great cognitive abilities (Have a look to different tree of life and to the diversity of life).
In humans, a fourth of the total amount of ATP (molecule that is the equivalent of a battery of living organism) is dedicated to the brain. This is a huge cost! It seems quite extraordinary that something so costly can evolve because the benefit are quite hard to grasp. For example. A bird with a heavy brain won't fly well, therefore it is counter-selected. What would a beetle do with a big brain? Well not many things. It would only be a cost with no benefit. Natural selection does not favor cognitive abilities for most of the lineages and as already said, great cognition is favored only under some restrictive conditions. Intelligence is by no-mean the end-point, the goal or the consequence of evolution.
How to answer to "What is the probability"?
In order to calculate the probability of something to happen you need some a priori knowledge.  For example, the probability of drawing the king of heart in a deck of card obviously depends on wether you consider that you know how many cards there are in the deck. You might say that you don't know how many cards are in the deck but you know that 10% of all deck in the world have 36 cards and the rest 90% of the decks have 52 cards (it would be much more complex in reality). The probability would be different. What are your a priori knowledge? What is the probability given the that X species exist at a given time, given how the environment changed over time, given that life is made of DNA, given the size of the earth, …? But then even if you give tons of information about your a priori knowledge (which include defining life and intelligence), then it seems to me terribly complicated to determine this probability with theoretical work. Doing so with empirical work is obviously impossible. We would need many earth-like planets and 4000 million years.

"Once energy and matter after big bang has been created everything was planned and nothing random ever occurred." Are you actually claiming that? 1) It undermines the remainder of your answer. 2) Most physicists would raise their eyebrows upon hearing such a bold statement. And most (but not all) of those who actually have a belief with regards to it, would say it is false. (See here for a brief discussion.)

Yes, indeed. I did know about that, thank you. But for the point of my question, quite far from the fundamental laws of physics, I think that the all-determinist point of view of energy transfer and matter interactions on earth - processes governing life - would be fine. I'll update my answer to make sure not to include more than what I should in this all-determinist point of view.

That's interesting. It would be very nice if you could firm up the idea that quantum mechanical effects (under a probabilistic interpretation) are negligible (they are never zero) when it comes to the (full) evolutionary run. (Is this perhaps even a well-established and well-reasoned viewpoint?)

I dunno enough about this field of philosophy in order to argue further in any direction. You might throw some question of this kind on phylosophy.SE and add the link here.

Your answer still puzzles me. You start out by assuming determinism and then go on to conclude that the probability computation is very complex. But under determinism (of this kind) the probability of a repeat scenario simply equals 1. By definition.

Yes, I actually meant that if we assume what I'd expect the OP to assume, something like: We consider life made of DNA that appeared on earth (given the water) 4,000 million years ago. We assume al mutations to be random, we assume that genetid drift occur according to the model of Wirght-Fisher (although this model will not fit to all kind of population) and some other stuff! Then, we can calculate a probability that will be very low as argued by GriffinEvo.

The complex forms of life we see at this moment are the result of billions of years of random mutations. To have the same outcome (or moment - we are not an ultimate outcome) would require the same mutations (or mutations to the same effect) to occur in a similar enough sequence, we also would require the same (or similar) selection being applied and effects of drift (another random process in evolution).
Given the extreme number of mutation events that would be involved in reaching humans (and other complex life) it becomes very clear that it is highly unlikely. Further, because mutation is random, nothing is inevitable. However, the repeated evolution of humans in not impossible (given a parallel system to evolve them within). Evolve and resequence experiments offer some support of this. In these experiments strong selection is applied over a relatively small number of generations with replicate populations and the number of common changes within the replicate populations can be very small. Even over time scales which are several orders of magnitude smaller than the 3½ billion years life has been on earth we see results which vary within a selection regime - i.e. with identical selection and standing variation the populations have little concordance in their response at the genetic level but there are certainly similarities to be found when comparing to other treatments.
The amount of replication needed to evolve something similar to humans starting with the most basic building blocks of life would be unfathomable. The probability of such a sequence of mutations (and patterns in drift & selection) occurring again which are identical to the ones that have lead to humans is so extremely low (beyond calculable) because of the sheer number of possible routes along the evolutionary trajectory that could have occurred.
To clearly answer your question, no we are not an inevitable result of evolution, it is (strictly speaking) possible that we could repeat our evolution but the probability of doing so is minuscule and too small and complex to calculate.

In my experience, often times after the phrase "imagine a simplified scenario" something simple can suddenly get quite confusing. This seems to be one of such cases. How is it possible for two individuals to go through 100 generations? Your experiment would give us a nice Gaussian distribution, because it's just the classic Galton's board, but does evolution follow this distribution? How can you possibly estimate how many "forks" there are, do you know any evolutionary pathways apart from those that have occurred? I agree with your conclusion, but those "simplifications" of yours...

Philosophers and physicists argue among themselves whether nature is random or not and even whether this is a proper question. But, assuming for the moment, that nature is not random (a minority position), then "mutation is random"  would be - strictly speaking - false. (Perhaps it would only be "random" from an epistemic viewpoint.)

@herman It is just an illustration of how a path (such as an evolutionary trajectory) with even small numbers of possible deviations and opportunities for divergence (directions and generations respectively) it rapidly becomes unlikely that the same two paths can be repeated

@herman I do point out that trying to apply such a probability calculation to repeated convergent human evolution would be too complex to calculate

@glentheudderboat it is widely accepted that genetic mutation is random - I don't see what point you are raising here

@GriffinEvo I'm not used to biologists. (It actually took me a while to see that I was not on Philosophy SE. Same colours. :)) And I can (now) see why it may be common practice and useful to treat their subject as if "randomness" is, in fact, the case.

@GriffinEvo, I was just pointing out that sometimes it's better to avoid analogies at all. What you wanted to say is that the probability is very small, but instead you created an entire model, which doesn't describe evolution very well, because of the points I mentioned before. I would just say: "the probability is very small" instead, people understand what is probability, no need for analogies. Just trying to improve your answer a little, but it's your call, of course :-)

@herman I'll resimplify - you're probably right, no point in overstating probability.

@GriffinEvo You said "it is widely accepted that genetic mutation is random". That might very well be, but I'm saying that genetic mutation is merely (mostly practically and only slightly theoretically) unpredictable.

@GlenTheUdderboat, why would we make an issue of distinguishing randomness from unpredictability in this context? It is true that, in statistics, randomness can be predicted (e.g., when flipping a coin), but evolution is so much more complex than a coin, that we simply haven't learn to predict anything that complex yet. It doesn't mean it's impossible, so it can still be random. That's what I think, at least :-)

@GlenTheUdderboat can you offer any evidence that mutation is unpredictable but non-random? until you support these claims then for the purposes of this question I'm sticking with what I, and many other biologists, believe to be true - that genetic mutation is random.

@GriffinEvo It is precisely for the purpose of this question (with its "inevitable"), where the distinction between random and not-random matters. Your belief is very well suited to answering biological questions, but this question explicitly (and apparently inadvertently) wanders into another domain of inquiry: philosophy. You can't blame me for the question. It isn't mine.

I'll have a go at this, from a perspective devoid of any biology (which I know nothing about). You want to wind the time back to some earlier "instant" (when life emerges on Earth) and then run the world from that "instant" on a second time around. I'm taking all that quite literally.
First remark. I put "instant" between thingies because it may be troubling from a general-relativistic perspective. Never mind that.
Second remark. You can't do that. You cannot wind the time back (and start over). Therefore, this is not a question of the normal scientific variety. Never mind that.
According to the laws of physics (as they are currently thought of; and those are freakishly accurate on our scales), if there is (objective/real/fundamental) "randomness" in the world then it can only be of the quantum-mechanical kind. Quantum mechanics typically deals with the very small stuff. (Ignoring Big Bangs and black holes.) Typically no-larger-than-atom stuff. Unless there is some kind of "natural" amplification mechanism at hand,* I don't see how quantum-mechanical randomness (if it indeed exists; there are other hypotheses and interpretations of QM around) with any significant probability can reroute a relatively macroscopic phenomenon such as evolution.
However, if quantum-mechanical randomness exists (e.g., no hidden variables, no superdeterminism, etc.), then (in my tentative** opinion) the probability that it will reroute evolution is not zero. Just very small.
I guess*** that at least 99.99% of all reruns yield exactly the same biological diversity that we have today. (And this will not change unless perhaps we start using quantum-mechanical amplifiers such as Geiger counters for our decisions regarding species demolition.) And if evolution was to be rerouted during the second run, it would most likely be immediately after the start of the second run, when life was barely existing and thus most vulnerable to quantum-mechanical mishap.

*I can only think of some intermediate chaotic process, but even that doesn't do it for me. (It might change the weather a bit, but evolutionary history? Nah, very unlikely.)
**The tentativeness is due to personal uncertainty regarding the causes of DNA errors. However, I now believe them to be (by far) mostly chemically describable in nature (especially those that produce offspring), not only quantum-mechanically describable.
***An actual computation of a good lower bound is impossible. I think I'm on the safe side.

NB: To those who "know" evolution to be inherently random, I would ask: Could you distinguish between evolution based on "true" randomness and evolution based on pseudorandomness? I would suggest that for all biological-theoretical purposes they would be equivalent.
Evolution (assumed true) doesn't come close to proving (or even suggesting) that the world/universe has inherent "true" randomness. Evolution doesn't require "true" randomness. It is perfectly fine (from a consistency-perspective) to accept evolution and be agnostic about "true" randomness.

It is precisely for the purpose of this question (with its "inevitable"), where the distinction between random and not-random matters. The “normal” assumption of randomness is very well suited to answering biological questions, but this question explicitly (and apparently inadvertently) wanders into another domain of inquiry: philosophy.
The OP's question asks about "inevitable". It is precisely in that word only, where the distinction between randomness and, say, pseudorandomness is crucial. If reality is pseudorandom then things are inevitable. If reality is random then things might be less inevitable. So, for the purpose of this question, we need to acknowledge that we really don't know about this aspect of reality (and usually we wouldn't care, because for normal questions it doesn't matter one iota).

Don't think that I have any kind of educated opinion in this area, but how would you explain pseudorandomness in the Universe? Is someone just running a random number generator, which happens to be our Universe? :-) Even if it is true and everything is pseudorandom in the Universe, it's of no help to us, because we don't know the underlying deterministic process. If this knowledge is useless, we could as well consider everything to be random, because randomness would be our best theory of how pseudorandomness really works, if this makes any sense :-)

Yes but nature does have amplification on the impact of randomness created by quantum mechanics. You know that the evolution is a huge process, and every tiny step in it can be affected by this randomness. As the errors accumulate, the outcome may be totally different every time. We can certainly call that 'inherent randomness'.

@Herman Excellent! That is very good. And now have a look at the OP's question, if you don't mind. It asks about "inevitable". It is precisely in that word only, where the distinction between randomness and, say, pseudorandomness is crucial. If reality is pseudorandom then things are inevitable. If reality is random then things might be less inevitable. So, for the purpose of this question, we need to acknowledge that we really don't know about this aspect of reality (and usually we wouldn't care, because for normal questions it doesn't matter one iota).

@Peter No, I don't think that there is much quantum-mechanical instability in DNA beyond chemistry. I therefore assume that there is no significant accumulation or amplification of quantum-mechanical randomness, if any.

@Peter Although I would certainly like that particular claim evaluated by a chemical-biologist.

Assuming randomness is certainly a proper model for scientific researches. You say that in this question, the distinction between randomness and pseudorandomness is crucial, and because there is still argument about which one of them is true, it is currently impossible to answer this question, right?

@Peter The majority viewpoint is that nature is random, but there are those who argue for other positions. It's a muddled debate. However, there is no debate about the "size" of the randomness, only about whether it is real. The question whether nature's inherent QM-randomness (if any) significantly impacts ongoing evolution should be answerable given some assumptions, I think. (In fact I answered that, but without a good argument.)


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Will neurons live after the death of a human? If so, how long?
I don't know if this is correct or not, but I have heard this from a friend and I want to get a clear explanation about this.I hope there is some one who can help me.

This is called "necrobiosis".

isn't brain death the definition of death in many medical cases?

Yes, brain death is what medical professionals [generally] use to define death, as modern medicine is often able to keep a human body physiologically functioning for an extended period of time through technology and medication - and it is often possible to do this well past where the body would have originally died on its alone.  This is done when there remains hope that the body will recover and consciousness will return.  However, if additionally cerebral function is also convincingly lost (discussion of how we test for that is another topic), the concept of medical futility comes into play.

I think that depends somewhat on how the human dies - in particular on the conditions. If they die in a very cold environment (say at the top of some icy mountain range), they'll freeze and metabolic processes will slow down considerably, and so will cell death. But such hypothermia-based slowing down is a special case. Normally, if your heart stops or you are not getting oxygen to your brain (perhaps due to a stroke), your neurons will start dying pretty quickly. Within many minutes there will certainly be considerable permanent cell loss - certainly within hours. If oxygen is significantly depleted, ATP production will also significantly drop. If this happens, the various ATP-dependent processes will slow to a crawl (including the Na/K ATPase and other ion pumps and channels that are needed for maintaining and changing the voltage difference between the inside and outside of the cell). This in itself is bad enough as a lot of the enzymes and mechanisms that are dependent on the voltage difference will fail (and probably enough of a reason for many cells to start dying), but one of the effects of this is apparently an increase in the extracellular glutamate, which ultimately leads to (via NMDA receptors for example) an influx of calcium ions into the neurons. Too much of the calcium ions is once again toxic for a variety of the processes inside the cell and is an additional and big reason for neuronal cell death.
In short, as far as I know, neurons don't have a good time living without sufficient oxygen and therefore after a typical human death.

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Breathing in and out
I was reading my textbook and it says that breathing involves inhaling and exhaling but it doesn't say whether they happen simultaneously or sequentially.
Also is my overall understanding of breathing competent?  When you breathe in air, air ends up in the lungs passing through the nasal passages (heated, moistened, cleaned) through the pharynx, through the glottis through the larynx, through the trachea and into the bronchi and then into the bronchioles. Once air gets to the lungs, Is their already carbon dioxide in the lungs waiting to be expelled or will carbon dioxide diffuse into the alveoli and into the lungs when oxygen diffuses into the blood. And after this the carbon dioxide will be expelled?

My understanding is that gas exchange is a simple diffusion process in the alveoli level. When there's a concentration difference, it happens. It happens for every molecule simultaneously.

I think you should: 1) change the title to reflect your question and 2) edit the body and decide whether you are asking about inhaling & exhaling (which are sequential) or gas exchange in alveoli (which is simultaneous).

Inhalation and exhalation happen sequentially as Herman stated in the comments.
Yes, your general understanding of inhalation is correct. After the air gets into the lungs, the oxygen is diffused into the capillaries covering the alveoli. The now oxygenated blood travels back to the heart to be circulated throughout the body. As this blood enters capillaries in other regions in the body, the oxygen diffuses out of them and into the surrounding cells. Carbon dioxide (CO2) produced by the cells as a waste product then diffuses into the blood vessels. The CO2-rich blood is then circulated back to the heart to be pumped back to the lungs. This blood flows into the capillaries surrounding the alveoli, and diffuses out. The exchange of carbon dioxide and oxygen occurs simultaneously. So, as oxygen is diffused from the lungs into the bloodstream, CO2 in the bloodstream is diffused out into the lungs.
Here are diagrams to depict what is described above.

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How does the body repair extracellular damage caused by glucose?
So we know that glucose is an aldehyde that can cause cell damage to the lysine and arginine residues on proteins through the Maillard Reaction (among other damaging reactions that glucose participates in). Since everyone needs glucose to survive, though - I'm wondering - how does the body repair damage to its proteins+blood vessels that are caused by all this glucose? I'm especially interested in the blood vessels, as the damage to blood vessels is common in diabetics.

Is the fructose-glucose mixture found in most beverages and many processed food even more damaging than just glucose?

The Wikipedia article on "Advanced Glycation Endproducts" (or AGE) is quite nice and in this case especially the section on "Clearance", which also contains a few references.
In short the AGE which are inside of cells are taken up by the lysosome and then broken down until AGE-amino acids are left. These are secreted into the blood stream and excreted with the urine. Bigger extracellular AGE which cannot pass through the cell membrane are taken up by special receptors first and then processed, here macrophages and Kupffer cells are included. An involvement of the liver is also discussed.
The following articles are also interesting:

Advanced glycation end-products: a review
The biology of the receptor for advanced glycation end products and
its ligands
Pathogenic effects of advanced glycosylation: biochemical, biologic,
and clinical implications for diabetes and aging.


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Calcium levels and nerve hyperexcitation
Why does lower blood calcium levels (or lower calcium levels in ECF) cause nervous hyperexcitaton? Why does it cause over stimulation of nerves and muscles and spasmic contractions of muscles?
This is why undersecretion of parathormone causes parathyroid tetany.
I am aware of the role of calcium in opening the synaptic vesicles for transmission of impulses and the role of calcium in muscle contraction but fail to understand how that might hep me understand the overexcitation of nerves and spasmic contraction of muscles. It actually seems that higher calcium in ECF might cause over stimulation and spasms of muscles due to sustained contraction.

I read up on the said article, and yes, it does make sense.
I however don't understand how a low ECF value of calcium would cause hyperpolarisation. Technically, for that diffusion to happen, the ECF Ca has to drop below the ICF Ca, which is extremely low.
Is there a disproptionate decrease in Ca levels, causing the ECF to drop way below the ICF level?
Also let's assume that it's not the membrane permeability to Ca that's causing the stimuli. Would a reduced ECF Ca level cause a decreased threshold level of AP in case of application of an external stimulus?
In which case, for tetanus to occur,

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From Uptodate on Clinical Manifestations of Hypocalcemia:

Acute hypocalcemia directly increases peripheral neuromuscular irritability [ 1 ]. As measured electromyographically, tetany consists of repetitive high-frequency discharges after a single stimulus. Hyperexcitability of peripheral neurons is probably the most important pathophysiologic effect of hypocalcemia, but hyperexcitability occurs at all levels of the nervous system, including motor end-plates, the spinal reflexes, and the central nervous system.

Guyton and Hall Textbook of Physiology:

The concentration of
  calcium ions in the extracellular fluid also has a profound
  effect on the voltage level at which the sodium
  channels become activated. When there is a deficit of
  calcium ions, the sodium channels become activated
  (opened) by very little increase of the membrane potential
  from its normal, very negative level. Therefore, the
  nerve fiber becomes highly excitable, sometimes discharging
  repetitively without provocation rather than
  remaining in the resting state. In fact, the calcium ion
  concentration needs to fall only 50 per cent below
  normal before spontaneous discharge occurs in some
  peripheral nerves, often causing muscle “tetany.”This is
  sometimes lethal because of tetanic contraction of the
  respiratory muscles.
The probable way in which calcium ions affect the
  sodium channels is as follows:These ions appear to bind
  to the exterior surfaces of the sodium channel protein
  molecule. The positive charges of these calcium ions
  in turn alter the electrical state of the channel protein
  itself, in this way altering the voltage level required to
  open the sodium gate.

It is a question of transmembrane potential. Ca++ being a cation, means that if you decrease the amount of ionized calcium in the extra cellular fluid, it conceptually is nearly equivalent to having a more positively charged intracellular fluid. This in turn means that the cell will be closer to its threshold potential for depolarization, therefore accounting for its hyper excitability.
What you should keep in mind, is that when we say something as: "this cell has a transmembrane potential of -70 mV", we always define it relatively to the extra cellular fluid.
edit: I am leaving this incorrect answer because of the interesting comments below.

Just read this answer because the question got bumped...this answer is very wrong, and exhibits a common misconception about what sets the membrane potential. Reducing extracellular calcium concentrations, if this had no influences on other channels, would have essentially no change on resting potential, because resting permeability to calcium is very low. Even if there was some permeability to calcium, reducing extracellular calcium concentrations would hyperpolarize, rather than depolarize, because calcium is low in cells.

@BryanKrause I do not understand why would hyperpolarization occur rather than depolarization. Could you please explain? I understand the membrane permeability problem, but then what is your answer to the original question about hypocalcemia?

I'd say the mechanisms are still under study, though there is good experimental evidence for a couple mechanisms: OneFace's answer suggests one of these, particularly the effects on voltage gated sodium channels. Here is one recent paper that seems to identify one mechanism, and their introduction has several other useful citations. When I have time I will write up a full answer.

As far as your answer, the Goldman equation is crucial. Permeability to calcium is effectively zero at rest, so we normally ignore calcium, but say for a moment it isn't. Opening a calcium conductance shifts the membrane reversal potential towards the calcium reversal potential, which is typically very depolarized, maybe +100mV. If we reduce extracellular calcium, the calcium reversal potential drops, though you have to reduce it a LOT to see a big effect, since the intracellular concentration is so low.

Also, no charges have to move to change the equilibrium potential: you could run the sodium/potassium pump all day long and if there is no permeability to sodium or potassium, there is no change in the membrane potential. It isn't meaningful ever to just "add positive charges" - they will always come with some other negative species, it's just that that other negative ion might not matter if there is no permeability.

You can also play around with this GHK calculator - although only Na+, K+, and Cl- ions are available, changes in external sodium concentration will give you at least the same direction of effect as changes in external calcium concentration, because both are positive ions.


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Enlargement of thyroid gland
Why does thyroid gland enlarge both in hypothyroidism and hyperthyroidism?
Hypothyroid goitre is due to lack of iodine in diet and hyperthyroid goitre (Exopthalmic goitre, Grave's disease) is due to oversecretion of thyroxine, or Thyroid stimulating Hormone. How does these two apparently opposite effects produce similar physical manifestation of the disorder (symptom) i.e is the enlargement of the thyroid gland?

I would bet it has to do with retaining water and/or minerals.

Check  this out. It is a very similar question.

The primary activity of the thyroid gland is to concentrate iodine from the blood to make thyroid hormone. The gland cannot make enough thyroid hormone if it does not have enough iodine. Therefore, with iodine deficiency the individual will become hypothyroid. Consequently, the pituitary gland in the brain senses the thyroid hormone level is too low and sends a signal to the thyroid. This signal is called thyroid stimulating hormone (TSH). As the name implies, this hormone stimulates the thyroid to produce thyroid hormone and to grow in size.
In Graves' disease one’s immune system produces a protein, called thyroid stimulating immunoglobulin (TSI). As with TSH, TSI stimulates the thyroid gland to enlarge producing a goiter. However, TSI also stimulates the thyroid to make too much thyroid hormone (causes hyperthyroidism). Since the pituitary senses too much thyroid hormone, it stops secreting TSH. In spite of this the thyroid gland continues to grow and make thyroid hormone. Therefore, Graves’ disease produces a goiter and hyperthyroidism.

Source: American Thyroid Association. What is a Goiter - Causes


text:
Does our brain really "flip" images perceived by our eyes?
I know a similar question has been asked and this is closely related to cognitive science. However, I want to know whether is there any mechanism or structure in the visual cortex which is proved to be flipping the images upside down.

I recommend you go over to cogsci.se and have a look at this thread. Its basically the same question and the answers are pretty nice including some references.

@Chris.. i wonder why cognitive sciences is a separate SE. It is a part of biology.

@WYSIWYG It is true that many questions asked here on Biology could equally be asked on cognitive science. However, there are many questions in cognitive science that are part of psychology and therefore has nothing to do with biology. How are we supposed to treat a question that is a duplicate on another SE website? Should we close it as off-topic even if it is not really off-topic? The comments are not the right place for having this discussion. Sorry :)


text:
Question regarding Rate of Photosynthesis AP Biology Lab
We are doing a lab on the effects of light intensity/wavelength on the rate of photosynthesis in AP bio and we were asked to visit this website here: http://mhhe.com/biosci/genbio/biolink/j_explorations/ch09expl.htm
The link takes you to a shockwave applet in which you can change the wavelength/intensity and record the ATP production (%). We were supposed to try out as many different combinations of intensity/wavelength and record the respective intensity, wavelength and ATP production (%) in a chart. Now the problem I'm having is that we are to graph this data. How should I go about graphing this? One problem is that for some values in the data, the intensity might be the same with different wavelengths or the wavelength maybe the same with different intensities. Can I do two graphs? One graph? Which one would be best and how should I go about doing so? And here is the chart just in case you want to see the data:
https://drive.google.com/file/d/0B4A27kix-0naMk4wNmNQejd3cGc/edit?usp=sharing

Why ecology tag? Come to think about it, why energy tag? To be completely honest with you, it is not strictly a photosynthesis question either, and I think you could have asked this question on stats SE or math SE too, because the question is "how to plot?" rather than about photosynthesis. Personally, I still think it's an okay question to ask on biology SE, but maybe we should edit the tags a little. Anyway, I'm happy to help you to the best of my ability, welcome to biology SE :-)

Ty for the welcome and I have not posted this question on any other stackexchange sites. And yes I agree that the question really is about graphing but still the graphing is directly related to biology and so I thought it would be reasonable to post this here. Also I couldn't find any other related tags; these were the ones that came closest to the question =S.

Your task is to determine how light intensity and wavelength affect ATP production. Therefore, we know for sure that your dependent variable (or response variable) should be ATP production. It is customary to depict the response variable on the vertical axis (Y-axis), so let's trying doing this.
Now we need to sort the other two variables. I suggest that you make one variable a control variable -- a variable that you don't change and keep constant, and the other then will be an independent variable (or explanatory variable). Then you swap them around, producing at least two plots.
In a nutshell:

You pick one value of wavelength and don't change it. Then you change the light intensity and record ATP with constant wavelength. You plot ATP (vertical axis) vs the light intensity (horizontal axis).
You pick one value of light intensity and don't change it. Then you change the wavelength and record ATP with constant light intensity. You plot ATP (vertical axis) vs the wavelength (horizontal axis).

Make sure to generate enough data points in order to be able to fit a smooth curve.

Another option would be to make a 3-D graph, with 3 axes: Y for ATP, X for wavelength and Z for light intensity. Initially, this might seem like a better approach, however 3-D graphs are not very common in science, and maybe there is a reason for it. Your goal is to make your data intuitive, easy to read and straight to the point. Science can be rather complex even without additional effort to complicate it with confusing graphs.
I would try it out as well, and see which one of two approaches shows you the trend more clearly. If I had to pick one straightaway -- I would probably go with the previous option that included a control variable.

This is a great idea and this is how I initially thought I should do it but I actually ended up doing it differently and handed the lab in today =]

@genius12, did I overlook a better solution? Do you mind sharing it? Good luck with you report.


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How many species have existed on earth?
I found a paper estimating the number of species currently living on earth. Now I'm wondering If anybody tried to estimate the number of species that have lived on earth. I'm familiar with problems of "species concepts". But I'm sure, there is at least a number of all known fossils.
EDIT: In contrast to the question How many organisms have ever lived on Earth?
I'm asking for species and not for individuals. The answer to my question can be used to ansewer the queston for the number of organisms. But still, The questions is different.

Did you read the answer to the linked question? I believe it adequately describes the problems with estimating the number of species (along with the number of individuals) that have ever existed on Earth, and gives some links for further reading.

See the answer to the linked question

In my opinion, as it is, it is not fair to mark this question as a duplicate, because it doesn't duplicate any other question (even though there is an answer to this question in another question). My more practical suggestion is to 1) reword the linked question just like this question or 2) transfer shigeta's answer here. I like the wording of this question better, because I don't see how would the number of individuals that have lived on Earth be of any use to someone, it would be impossible to comprehend such a number. Species is a more interesting wording.

It's patently incorrect to mark this as a duplicate. The distinction is huge--species number versus individual number (which is 1 and 8 billion, respectively, for humans). Someone so empowered should remove that designation, because it discourages answers.

A quote from a Discovery movie:

Scientists have estimated that over the course of Earth's history, anywhere between 1 and 4 billion species have existed on this planet.

I know, I know... sorry. I hope someone has the original research, but in case no one does, or if you are just curious, and Discovery is fine for you, I decided to share what I know for the time being.


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Is there a hypothesis that attempts to explain patterns of species richness along all three energy-related environmental gradients?
My question is related to one of the oldest question in ecology: "What determines global patterns of species richness?". However, I want to focus on one particular part of this question, which has been bothering me for a long time.
Background information
One of the most widely recognized ecological patters on Earth, which is found at most scales and in most biological taxa, is the latitudinal diversity gradient (LDG) -- there are more species in the tropics than in the temperate regions, and the further away you move from the tropics, the fewer species you encounter. Furthermore, such pattern exists not only along the latitudinal gradient, but species richness also covaries with altitude in terrestrial environments and depth in marine environments, showing the same diversity gradient!
It seems to be fair to suggest that energy should somehow underline all these diversity gradients and create some sort of universal mechanism that would ultimately affect all species richness patterns on Earth. Unfortunately, there is no consensus on questions as grand as this one, but I'm looking for hypothesis that would specifically attempt to explain all three gradients together.
Question
Is there a hypothesis that attempts to explain patterns of species richness along all three energy-related environmental gradients together: latitude, altitude and depth? If there is, what it's weakness? If there's no such hypothesis, do we have reasons to believe that such a broad link across the three gradients can exist?
Please note how I'm trying to emphasize that I don't want you to list all the hypotheses that describe LDG only, but rather the three gradients together.

Neat question! I imagine any responsible theory would have to take into account the associated gradients of total area (that is, there are few square meters of space to inhabit as you go higher in elevation and as you go up in latitude). I haven't thought about depth, but I guess it might be a skewed hump– there is some area at low depths, much more at mid-depths, and then declining area at lower and lower depths.

Are you only concerned with richness, or with biomass too?

What did you mean "energy related gradient"? Can you give more words about that? Are you talking about temperature? If so, can your question be reduced to "How does temperature influence species diversity"?

@Remi.b, not exactly temperature, however the guy who first discovered LDG (von Humboldt) related it to mean annual temperature. Energy is different from temperature, not only from a purely physical point of view, but also biologically available energy explains why there is not many species in deserts, where temperature can be very high.

Well, I think for a start, except for thermal vents, energy comes from the sun.  So more sun = more energy captured by plants, which can support more non-plant life.  At higher altitudes, the limiting factor is the thin air, which limits plant life, which limits everything else.

@Oreotrephes, good point, I corrected species diversity to species richness in the title and the question. I.e., richness only.

@Oreotrephes, I don't think area can explain the three gradients. Some issues: it relies on area-species positive correlation in the first place, there are places beyond tropics with very high species richness that cannot be explained by area, the deep ocean provides huge volume for life, yet there's not much life there. Clearly, energy must have something to do with it.

@swbarnes2, right, but how does it create more species :-)

@Herman I think the first issue of the question has to do with the concept of energy that you use. You said biologically available energy. So you mean solar radiation + geothermy + warm winds(?) + input of sugar (through a river for example)? You are not talking about photosynthesis over respiration ratio?

Could we replace you question by: "If I take two huge boxes and add many different species from all lineage to make a somehow functioning basic ecosystem. In one box I set the temperature at 11°C and in the other box the temperature is set to 19°C. In which box will I have the greatest species richness if I wait 10,000 years?"

@Remi.b I meant energy + water availability in my desert example. Ok, it's getting a bit confusing. Let's go back to where it all started: "[C]an your question be reduced to 'How does temperature influence species diversity'"? No, I don't think so, because: 1) not species diversity but rather patterns of species richness (gradients) 2) temperature could be one hypothesis, but I believe that there is such a hypothesis and it's flawed. However, I cannot tell you right now with high confidence how exactly it is flawed, I wouldn't ask if I knew everything. I still haven't read the answers though.

@Herman - I agree with you that area alone can't explain the gradients we see; I just think it needs to be included in the null model.

This is a big question and a very active field of research. I'm not deeply into this litterature, but you should look into the the different scaling relationships (often power laws) that have been described on metabolism vs body size, species-area relationships and species richness vs biomass. Also consider that energy-use by species in a community is considered a zero-sum game both in the neutral model (Hubbell, 2001) and in Red Queen models of evolution. You will probably not find a definite answer to your question though, but there are some interesting intersections of ideas out there. As others have suggested you also need to consider and take into account differential historical extinction rates, and how this will influence current patterns (Mittelbach et al. 2007).
Points of entry could be:

Gaston. 2000. Global patterns in biodiversity (essential reading!)
Chave. 2013. The problem of pattern and scale in ecology: what have we
learned in 20 years?
Venevsky & Veneskaia. 2003. Large-scale energetic and landscape factors of vegetation diversity
Mittelbach et al. 2007. Evolution and the latitudinal diversity gradient: speciation, extinction and biogeography
Marquet et al. 2005. Scaling and power-laws in ecological systems

A couple of caveats/ideas though; first of all, it has been argued that the latitudinal gradient of species richness is likely to be due to many different mechanisms in different taxa (see Gaston, 2000). Here you are looking for a hypothesis to explain not only this single pattern, but all three of them, which makes a single explanation even less likely. Second, many non-exclusive explanations have been put forward for the latitudinal gradient. Even if we don't know which ones of these that are the true mechanisms, some are clearly incompatible with being explanations for all the three patterns you mention, while others might be applicable to all of them. For instance, environmental stability in the tropics is one suggested mechanism for the latitudinal gradient, but this doesn't make much sense for a gradient along ocean depth (deep sea has arguably been a more stable environment both over shorter and longer time-frames). It might be relevant for an altitude gradient though. Going through different hypothesised explanations for the latitudinal gradient in this way (from what I know, the best studied of these gradients) could give you a list of ideas that are most interesting to target (maybe somebody has already done this though).
I hope this helps.

Thanks, it does. I have a simple question that you should be able to answer without any research (maybe add it to your post?), and which I tried to include in my original question too: "What's wrong with just saying that all these gradients correlate with the amount of solar energy available for primary producers?" I can't seem to answer it myself. Is the difference in solar radiation really significant for plants in tropics and temperate regions? Is there really less available solar energy at higher altitudes? Does it fail to explain some biodiversity hot-spots outside tropics? Cheers.

I tried to squeeze everything in one comment, but what the heck. I actually remember doing a presentation for an ecology seminar at uni on this very Mittelbach paper :-) I absolutely agree that there might be no actual answer to this question (but that's why I agreed to accept even flawed hypothesis that attempt to explain the three gradients). I also agree that the best way to answer it is to read everything you cited... but to be honest, I was looking for a shortcut specifically on the  three gradients together :-D Just saying, I'm still grateful for your answer.

Well, for one, the amount of solar energy doesn't explain differences in species richness between hemispheres, and I doubt that it can explain gradients over altitude.

Nice question!
For the concern of plant diversity over altitudinal gradient it has been shown in several studies in the alps and in Andes that the greatest abundance and diversity is not found in high altitude neither in low altitude but in middle altitude. Some argue that the abundance and diversity depends on temperature and human impact that is what explain this pattern. There is a theoretical model that cut the mountains into three patches along the altitudinal gradient and assume that plants - when they reproduce - either send seeds in the same patch or in a nearby patch. Because, the patch in the middle can receive gene flow from both "sides" while the "extremities" can receive gene flow only from one "side", the diversity is greater in the middle patch.
In aquatic communities, there is very few physical barrier to gene flow and therefore, speciation often occur through sympatry (I think!). Depth has an important role in isolating population (allowing allopatric speciation) because of the sensory drive evolution. Some fishes (to talk only about fishes) have opsins (proteins involved in vision) that are adapted to deep water while other fishes have opsins adapted to shallow water. This divergence, allows to push fishes to chose a preferential habitat and prevent gene flow.
High temperatures lead to high mutation rate and high mutation rate leads to high speciation rate (I think).
Because of past glaciation, it has been found that species in southern hemisphere are younger in average than those in northern hemisphere. Therefore, past ecology has to be taken in account when talking about present diversity. Land mass of different size might also impact species diversity differently.
I don't think a theory that explain species diversity along these three gradients might be easily found. I would tend to think these three gradients are important because they are correlated with parameters that influence species diversity in several ways. Those correlated variables are temperature, humidity, light, time of daylight, land mass, connectivity (rivers that increase gene from mountain to valley or surrounding land mass for example), human impact, …
What did you mean "energy related gradient"? Are you talking about temperature? If so, can your question be reduced to "How does temperature influence species diversity"?
Sorry for the missing references!

This wiki article lists pretty well (better than what I did in my above answer!) different hypothesis for explaining latitudinal gradient in species diversity. Some of these hypotheses can be used to describe effect of depth or altitude.

Cheers, @Remi.b. As to your paragraph 1, if it's temperature, than the foot of the mountain should have the highest biodiversity, no? Next issue, due to the gravity, shouldn't the seeds move much more easily down the gradient (which, again, would contribute to the biodiversity of the lowest region). Finally, even if the middle patch receives more gene flow, it should reduce species richness, because gene flow acts against speciation, no?

Yes, even though both you and fileunderwater wrote great answers, I must admit that I did know about the Wiki article you cited, and I read some literature on LDG too... but I thought I should ask about the three gradients combined, not just LDG, partly because I have no idea where to look for an answer to this phrasing, partly because I'm curious, and partly because I didn't want to make you write me a book with all these theories listed :-) Thanks anyway. I still hope someone else might chew this up for me so I have only to swallow, but if not, I'm happy to dig deeper into this myself too.

Now let's get back to our temperature/energy thing, maybe I do need to paraphrase the question a little. I was mainly referring to the amount of solar radiation available for photosynthesis. You can't really call it temperature, can you? Does it answer your question or not really? But with this definition, I'm not too sure whether the amount of solar energy decreases with increasing altitude... If it doesn't, than maybe "energy" doesn't correlate with all three gradients either. Also see my question under the fileunderwater's post, maybe we should answer it first.

I've studied diversity of euglossine bees along altitudinal gradients in amazonian mountains. The references I've read showed no consensus regarding altitude. For some groups, diversity were higher at low altitudes; for other groups, it was in the middle. I've found the biggest diversity in the middle altitudes (the mountains were around Equator line). One hypothesis was about randomness: throw a lot of species inside any gradient, and most of them will overlap in the center by chance alone. Other hypothesis said about chance of recolonization. You can have extinctions anywhere, but close to Equator (low latitude) and close to sea level (low altitude) you can have species recolonizing faster, because there is more land around. After all, I don't think one simple rule will explain each and every case. And I have never thought about that below sea level. Aren't marine vulcanoes a rich environment?

Well, I guess they are biologically rich environments, but they would be an exception to the general rule where the deeper you go, the less sunlight penetrates the water, the less plankton to eat there are, the colder it gets, and even the pressure is higher (which is not related to energy). So I guess overall there is such a gradient.

What about the plants that your bees ate, did they exhibit the same trend? I also don't get your randomness explanation: if it is a uniform distribution, by chance alone the bees should be distributed, well, uniformly, no?

In the sea, temperature isn't linearly related with profundity. Look the second image here: http://marinebio.org/oceans/temperature.asp

I see the plants changed with altitude, but didn't measure their richness or diversity. Imagine a gradient from 100 to 3000 meters. Some bees will have a height span of 200m, others of 2000m. Imagine this is random, too. When you put them all together, most will overlap in the center, not in the borders. Look: http://www.sciencedirect.com/science/article/pii/S016953479901767X


text:
recombination frequency problem

Three loci C, D and E are located on the same chromosome in this
  order. We found that the frequency of recombinants between C and D is
  10% and that between D and E it is 20%. Assuming that crossing over
  occurs randomly on the chromosome, what is the expected frequency of
  recombinants between C and E?

I know that it should be less than 30% (10%+20%) but the answer given is 26%. I don't understand how they figured that out.
Edit :
The frequency of recombination is <30% because of the chance that a crossover happens between C and D & also between D and E. The probability of that to happen is 2% (10/100 X 20/ 100)
So, why is it 26% instead of 28% ?
Another posssibility : Am I totally off the track ?

I got $26$% as the answer.
To get a recombination between C and E, there are two possible mechanisms:-

C and D produce a recombinant, but D and E remain linked, therefore the final genotype will be a recombinant considering C and E(Chiasmata between C and D). Here $P_1=P_{CD}\times P'_{DE}$ where $P$ is the probability of recombination and $P'=1-P$ is the probability of linkage.Hence $P_1=0.08$
C and D remain linked but D and E undergo recombination (Chiasmata between D and E). Here, $P_2=P'_{CD}\times P_{DE}=0.18$

If there is a chiasmata between both C and D, and D and E, the resultant will not have a recombination in C and E locus due to double crossing over. If there is no crossing over, there will be no recombination at either loci.
The net probability of recombination $P_{CE}$ will be the sum of these two, as any of these possibilities can occur to give a recombination between C and E. $P_{CE}=P_1+P_2=0.26$
And Biogirllajja, your calculation (the Edit) was almost correct, but you have to subtract $2$% from both $10$% and $20$%, because, both of them include the probability of crossover at one loci, including the case where the other loci has also crossed over. Hence, you need to subtract it from both, and then add to get $26$%. Tell me if you want me to expand on my explanation or provide some clarifications.
If we simply add the map distances, we get the actual map distance which disregards the possibility of double recombinations. All map units greater than 10cM have significant chances of double crossovers between them, and hence, the observed recombination frequency would be less than the expected 0.1. Hence, for distances greater than 10cM, the observed frequency of recombination will not be the same as (map distance/100).


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Is it possible for a human and another ape species to reproduce?
Is it possible for a human and another species to reproduce?

When you say "naturally" I guess you exclude behavior? Because behavior would obviously be one thing that would prevent such mating! Well, let's assume we can find a crazy human and a crazy monkey that would accept doing such thing. The question still holds!

you are right.I have edited  the question according your comment.thank you

With our closest relatives, the bonobos/chimpanzees at least, this isn't possible due to differing chromosome counts.

@ChinmayKanchi is it actually impossible or will it just lead to deformed offspring? Would an egg be fertilized and then die during development or is fertilization itself impossible?

@ChinmayKanchi: Horses have 64 chromosomes, and donkeys have 62.

@ChinmayKanchi do you mean that if we find an animal with same chromosome counts then we can have a hybrid of that and human?thank you


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Why do you need the intrinsic pathway when you have faster extrinsic pathway?
There are two pathways in blood clot fromation; the extrinsic pathway and the intrinsic pathway.
The extrinsic pathway is faster than intrinsic pathway because it has less number of steps. So, why do we need intrinsic pathway then?

in general there are very few functions in organisms which have a single mediation - redundancy is typical in biology at the level of gene action.  it makes the system robust

This question embodies two unjustified assumptions that keep cropping in questions. 1. How do you know that a pathway with fewer steps is faster? You don't. It depends on amounts of enzymes and their catalytic characteristics. 2. How do you know that a slightly faster faster pathway will have an advantage? Again you don't. Other factors may be limiting or more important. Moral: when you have written your question out, read it and consider the validity of your assumptions.

In short: The extrinsic cascade reacts to damages of the blood vessel, the intrinsic pathway reacts to damages of the walls. But as with all things, the long version is ways more complicated:
The extrinsic pathway is activated when you damage tissue and factor VII come in contact with tissue factor (also known as factor III). Tissue factor is located in the membrane of the cells and is only released when the cells are damaged.
Then the cascade starts and delivers a very fast large amounts of active thrombin, which then converts fibrinogen to fibrin to build a block of the damaged blood vessel. The step from the thrombin is common between both pathways.
The intric pathway is also called the "contact pathway", which starts when the factor VII comes in contact with collagen or anionic surfaces.
The main advantage of this pathway is the strong amplification of the initial signal from the intrinsic pathway by a factor of about 1000 fold. The intrinsic pathway is also co-activated by active thrombin (which stands at the end of the cascade) meaning it is also a powerfull feedback loop to make the initial reaction much stronger. This also overcomes weak activation which where the active thrombin will be inactivated by Tissue Factor Pathway Inhibitor.
The coagulation cascade has a pretty nice article in the Wikipedia.
Interestingly it is now believed, that the start of the intrinsic pathway plays no or almost no role in vivo. There are people which "suffer" from a deficiency in factor XII which is necessary to start the intrisic cascade. These people have absolutely no problems with their coagulation, so the first steps are not necessary (any more?). This article presents findings, that it stabilizes a thrombus:"The intrinsic pathway of coagulation is essential for thrombus stability in mice."
Here are some further articles about the intrinsic pathway:

In vivo roles of factor XII.
Factor XII: what does it contribute to our understanding of the
physiology and pathophysiology of hemostasis & thrombosis.

Do you mean extrinsic pathway by "initial signal"?

Nope, ny initial signal I mean the initial signal from the intrinsic pathway. Activation of Factor XII which in turn activates Factor XI and so on. Each step of the cascade magnifies the signal.

The extrinsic pathway is activated by extrinsic trauma , that makes blood escape out from the vascular system , and then after the formation of a small amount of fibrin , a substance called Tissue Factor Pathway Inhibitor ( TFPI ) is released , this inhibitor prevent more activation of factor x , it’s thought that TFPI is responsible for preventing more un-needed fibrin , but if the injury need more fibrin to cure , at this point the intrinsic pathway will be activated to form more needed fibrin

Welcome to SE Biology. On this site we're looking for answers in which explanations or assertions are supported by references, preferably with links. Without these neither the poster nor anyone else can tell whether or not you are correct, or learn any more about the topic. See the Help for "how do I write a good answer?".

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


text:
Why do farts stink, but perfume does not?
Why is it that natural things like farts, poop, halitosis etc., from which we are always surrounded smell "bad"; whereas manufactured products, such as perfume or glue smell "good" to most of us?
In my understanding, things smell "bad", because they are not good for us. But how are farts not good? And shouldn't artificial things like perfume or glue, which are relatively new to us, smell "bad"?

There are loads of "natural" things that smell good: flowers, food, your lover, your offspring, babies in general (at least to some people anyway), wood...

feels Good to know that m not the only with a 10 year old's sensibility ( on farty stuff ;)

Why is it that natural things like farts, poop, halitosis etc., from
  which we are always surrounded smell "bad"; whereas manufactured
  products, such as perfume or glue smell "good" to most of us?
In my understanding, things smell "bad", because they are not good for
  us. But how are farts not good? And shouldn't artificial things like
  perfume or glue, which are relatively new to us, smell "bad"?

Kind of a strange question but here is a quick and rough answer... There are at least three things to think of here.
Firstly, yes often natural things that are good for you have evolved to smell attractive, but not all natural things are good for you. Therefore a fart should not smell good just because it is natural. And it is likely that breathing farts non stop is not good for you.
Secondly, perfumes etc. have been chemically manipulated or designed to smell nice by human manufacturers - the preference for such smells existed before the specific perfume, the manufacturer simply designed a fragrance that was attractive.
And Finally... Not everything exists because of selection. Farts probably smell as a by-product of process of digestion rather than selection for avoiding them. Gas is produced during the digestion processes, the amount and odor (determined by the constituents of the gas) of gas will likely depend the efficiency of digestion and what is being digested. The dominant selection force affecting the odor is then probably related to digestive efficacy and selection against odor would only be (relatively) very weak.
It's better to digest food and fart a bit than it is to not digest but smell nice, digestion is quite important!

Flowers smell good to us. Is there any evolutionary advantage to us or to the flower ?

Generally speaking flowers smell good to pollinators - there are a limited number of possible scent chemicals and/or common arrays of "good" smell receptor in the world so I would suggest that there is likely to be some crossover - but that is pure guess work

Some comments from me: Most substances that smell bad contain some kind of sulphur components - and we are really sensitive to them. If I open a bottle with beta-Mercaptoethanol in a lab (and not in the fume hood) it will only take seconds until someone else starts protesting and opening up windows. Some of these chemicals are highly toxic (for example hydrogensulfide), so it makes sense that we are aware of them. Regarding the flowers: There are some flowers, that smell really awful, have you ever been close to a Ginkgo tree that is blossoming? Not very nice I can tell you...


text:
How is sweetness measured?
Some time ago, I read in a newspaper--though I can't recall the details--a list of (mostly artificial) sweeteners and a list comparing how many times sweeter each was than sugar. How is relative sweetness quantified? Is there a standard method?

Response of the gustatory receptor neurons can be measured using standard electrophysiological techniques, under different conditions(exposure to substances). For example see this article.
However, it is difficult to say if a person feels sweetness or not or how the substance produces complex taste perceptions in some people.

What I had read was the they had even measured the sweetness of something which was toxic (see the question's edit history). How could they have done that? Making a human have toxic material?

Please mention the source of this information. Toxic can also mean potentially toxic over continued use. They could have tested this in mice. To say anything we need to investigate the real source. Relying on newspapers for scientific facts is sometimes like playing chinese whispers. The reporters hear something, understand half. Add some of their interpretation and end up reporting erroneous information.

Hard to tell the source of it. Just remember reading and being amazed by the fact.


text:
Can we say that microevolution and macroevolution is fundamentally the same thing over different time scales?
This Wikipedia article states:

Macroevolution is evolution on a scale of separated gene pools. Macroevolutionary studies focus on change that occurs at or above the level of species, in contrast with microevolution, which refers to smaller evolutionary changes (typically described as changes in allele frequencies) within a species or population. ... macro and microevolution describe fundamentally identical processes on different time scales.

My question is: Is this a valid claim? Can we say that creating the genetic information for a feather is not qualitatively different from changing the colour of that feather?

This question about the difference between macro- and microevolution might be of interest.

You are mixing up two different things in your question:

the mechanisms (processes) that cause micro- and macroevolution, and
the genetic basis for different types of traits.

The processes of evolution (selection & drift acting on genetic variation) are the same for both micro- and macroevolution, and this what the Wikipedia article is stating. The second question is dealing with the amount of cumulative genetic change that is needed for different types of traits. This naturally differs dramatically between traits (the accumulated genetic change that is), and is also reflected by the different scopes of micro- and macroevolution. Macroevolution is usually studying problems above the species level, and therefore often larger morphological changes, while microevolution is dealing with smaller changes within species and populations. The macro/micro division is also artificial and should be seen as a continuum.


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Why does wood become darker when it ages?
I have lots of pieces of pine furniture which have different colours depending on how old they are. So, I just wondered why that is. I guess it has something to do with structures and chemical compounds that were already in the wood when it was still alive, so I hope this is not off-topic here.
What processes take place in dead wood when it ages?
What determines the colour it will have? For example, pine and spruce wood looks very similar when freshly cut, but will develop very distinct colours afterwards.
Is there also wood that does not become darker?
Is it something to do with the processing of wood, or will that happen to any stick you leave lying around in your room (so it doesn't rot)?

Not sure- but maybe because of accumulation of resins and other secondary metabolites.

While most wood we see comes from stain or oils, wood left on its own will darken.  As far as this article suggests, this is caused by the polymerization of polyphenols from lignin into tannins which are dark red or brown in color when they are highly polymerized.
The specific content of the lignin in different woods will affect the density, strength and color of the wood.
This woodworking reference shows that intense UV exposure to wood will darken it to give it an aged look.


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Opposite results between Blomberg's K and phylogenetic signal in Phylocom (AOT)
I've been trying to test for significant phylogenetic conservatism in some plant traits. So far I used R-package picante (Blomberg's K) and AOT in Phylocom. So far these two methods yield completely opposite results for the same traits, and I'm confused. Is it possible to get such very contrasting outputs from these two methods?
For example, one trait shows Blomberg's K = 0.2892 (P = 0.001), suggesting that the evolution of this trait overall has not been greatly constrained by phylogenetic relatedness. In contrast, for the same trait AOT yields variance of standardized contrasts across tree = 0.006, significance of contrast variance relative to null model (low rank) = 1, and significance of contrast variance relative to null model (high rank) = 1000 (i.e., P = 0.002), suggesting that treewise phylogenetic conservatism is significantly greater than the expectations of random tip swapping.
I've just started looking at these phylogenetic signals, so I may be overlooking something critical. I will greatly appreciate if you could kindly give me directions, thank you very much!

I think I figured. Someone told me that the above results are the same. The absolute value of K = 0.29 indicates the magnitude of the signal is less than expected under a Brownian motion process, but it’s still more than random expectation (according to the P-value,P = 0.001). So both methods suggest that treewise phylogenetic conservatism is significantly greater than random expectations.
Actually the meanings of K statistic and P-value were clearly stated in the original paper (Blomberg et al. 2003). I should have looked at it first... but anyway, I think it is solved now.


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What's the difference between protein and DNA behaviour during agarose gel electrophoresis?
I'm planning a science project about gel electrophoresis, and I'd like to know if there are any measurable, quantifiable (for example, things I could represent in a graph or chart) differences between the behavior of protein and DNA during agarose gel electrophoresis.
Detailed inputs and useful links are greatly appreciated.

Proteins are usually not run on agarose gels since the pores of the gel are too big to have a good separation. A 1% agarose gel has pores of around 150nm, poly acrylamide (which is usually used) have 3-6nm depending on the degree of polymerisation and gel strength. You will only use agarose gels for really high molecular weight proteins otherwise you won't see much separation of the sample. DNA samples have such a high molecular weight and can thus be separated on agarose gels.

@Chris One of the requirements of the project is to run several simultaneous experiments while changing one variable only (in this case, it's the protein/DNA). I'm separating proteins in dyes, which would explain the use of agarose.

What do you mean by "separating proteins in dyes"? Another thing: While you can't separate Proteins nicely on agarose, you can use low percentage polyacrylamide gels to separate DNA.

@chris Excuse the typo. I meant that electrophoresis will be run on food coloring dyes... you know... which are made of proteins

which food coloring dyes will you be using? Most of them are based on small molecules, not proteins.

Thats in interesting question. I think so too, that these are mostly not proteins, since most proteins are not colored.

As already mentioned, you don't use agarose for proteins, they're pretty much exclusively run on polyacrylamide gels, typically as an SDS-PAGE. I've never seen anyone run an agarose gel of a protein.

@MadScientist I'm fairly new to this (I'm only a high school freshman) and so haven't done adequate background research on the subject. I was just asking this question to see if such a project fits the required criteria and thus actually conduct a research. I'll consider polyacrylamide, though it's way more expensive and harder to find (I doubt I'll have access to the school lab or that they even have it).

I'd recommend to simply focus it on DNA and ignore proteins. You should also find out what equipment is available, you need a gel electrophoresis chamber (and they are different for agarose and PAA), power supply, the gel material itself (+ APS and TEMED for PAA), buffer, loading dye, something to stain the DNA or protein, and in the case of DNA also a UV lamp.

There are two important properties that determine how a molecule will move during gel electrophoresis:

size and shape of the molecule
charge of the molecule

You're applying an electric field, and all molecules will move according to their charge. The gel itself hinders the movement of larger molecules. This means that small molecules will move further than large molecules.
Nucleic acids like RNA and DNA have a uniform negative charge from the phosphate backbone. This means that they will generally separate according to their size and shape (plasmids can be present in different forms like supercoiled, circular or linearized).
Proteins have different charges, some have a positive charge at the pH typically used for gel electrophoresis, some have a negative charge, and some have no charge at that pH. So if you would simply run proteins on a gel, some would move backwards, some forward and some not at all.
To make the proteins separate according to their size we use the detergent SDS to denature the proteins, and to give them a uniform charge (SDS is negatively charged). Proteins are also run on polyacrylamide gels and not agarose as the size of the pores in agarose is a bad fit for the typical sized of proteins.
While I've never seen anyone using agarose for proteins, it seems that it is possible and sometimes used for larger proteins. I found one paper describing a protocol, they used very high concentrations of agarose in the range of 4-5%. I suspect that they won't handle well, but you should try that out yourself. If the proteins you're examining are a bit larger, using agarose should be possible.

Just a small addition.. Agarose pore size is huge for most proteins. However, agarose gel is used for analyzing antibody-antigen interaction. The complexes that form are huge and can be separated by AGE. See rocket immuno-electrophoresis


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Circadian rhythm in birds

Animals can use their circadian clocks to determine direction from the
  position of the sun. In a particular experiment conducted in Iceland,
  a bird, kept in a cage open to the sky, was trained to seek food on
  the western side. Its circadian rhythm was then phase-delayed by 6
  hours and after phase shifting, the bird was returned to its open cage
  at 12.00 noon real time. It was observed to seek food in the:
a. north.
b. south.
c. east.
d. west.

I think that if its circadian rhythm was phase delayed by six hours, at noon, it will feel that it is still 6 a.m. So, the sun will be located in its "east" and it will try to seek food in the "west" but its"west" will be our south. So, answer should be south. Is my reasoning correct ?

I think it also matters when before the phase delay, the bird was fed.


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Evolution- Variations, adaptations and selective advantages
I am trying to understand Variations, adaptations and selective advantages  and how they are all related.
Feel free to add or correct me if I'm wrong- Variations are structural, functional, or physiological differences between individual's within a species that result from mutations.  If the variation provides a selective advantage (genetic advantage) the organism's chances of survival in terms of both survival in a changing environment and reproduction increases. The variation is then considered an adaptation. So basically adaptations are variations which provide a genetic advantage and give some organisms within a species a better chance of survival than those without the adaptations. This survival advantage allows those organisms to reproduce and pass on their adaptation more frequently than those who do not possess these adaptations.

I think you should think about/define the terms more clearly - from what you write I would label your "Variations" as traits (or rather differences in traits between individuals). "Variation" is close to the techical term variance (as in phenotypic trait variance and additive genetic variance), so you risk misunderstandings.

I would define variation as something a little less specific. When talking about evolution I would consider it to mean any phenotypic variation that exists. I say phenotype because that is what selection "sees" but there can be genetic variation without phenotypic variation (see synonymous mutations). The trait could be physiological, morphological, behavioral or a life history trait (a trait which, all else remaining constant, affects fitness e.g. Lifespan or development time). This is also not necessarily just within species too, comparing homologous trait between two species could reveal between-species variation. For example, in one species every individual might day at exactly 100 days old, in another it may be 102 days, there is no variance within species but there is variance between. The phenotypic variation can be a result of genotype, environment, or a genotype-environment interaction.
If a trait positively affects fitness it is an adaptation, it is a trait that offers some kind of benefit over other current or previous incarnations of the trait. The variance for that trait can be zero - a highly adaptive trait is likely to spread rapidly and variation for that trait would zero if it was entirely genetically defined and fixed in the population but that trait would still be considered an adaptation. I would define fitness as the lifetime reproductive success of your evolutionary unit, commonly thought to be the gene. If a variant of a trait increases relative fitness it provides a selective advantage, and any genes (alleles) causing that trait should spread through the population at the expense of other alleles.
It is important to remember that not every biologist will define these in the same way, there is some debate about definitions in biology.


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What is mRNA expression level?
I cannot find a clear explanation of what is mRNA expression level, and how to measure it. I would appreciate if someone explained it or gave a reference.

you can see this post

The RNA expression level is an estimate of the amount or proportion a given gene's RNA found in a sample of cells (such as a tissue sample) or even a single cell.
Expression is used because the RNA sequence is translated from DNA to RNA according to the signals within the cells.
There are various means of estimating this.  They often involve a sequence specific probe - a short length of DNA usually - which will bind specifically to the RNA in question.  The exclusiveness of the probe sequence, which is usually 20-45 bases long, to the RNA in question can vary and so this is a bit of an art sometimes.
Examples are qPCR (quantitative PCR), expression microarrays.  Both of these technologies have  many flavors and variants.
Another category of expression estimation include RNASeq - which will sequence all the RNA polymers in a sample and estimate all the sequences at one time.  The result is similar to a microarray, but RNASeq does not necessarily require the use of specific probes to an RNA to measure it, though it can.
These estimates are usually relative - except for careful qPCR perhaps.  The numbers are not usually interpreted as "X copies of the RNA" in the sample.

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


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Beetroot white skin mould
Does a mould make a beetroot poisonous or inedible ?
Lemon's mould for instance, makes penicillin, but it's green there, and I'm allergic to penicillin, would the white mould produce penicillin too?

Owing to the large number of fungal genera, can you please expand on how the mould developed, its characteristics or maybe a picture? That could narrow the question down.

It was over a month in the fridge :D.

To be honest, whichever the answer, better to stay on the safe side and throw it away.

The term "mold" does not indicate one taxonomic group of fungi. Rather it is a colloquial term commonly any fungus with microscopic-appearance, often sooty or cottony appearance. As  example, slime-molds (no-more being considered as  fungus); are very much unrelated with Penicillium-mold (a member of ascomycetes) and Mucor bread-mold (a member of Zygomycetes).

All species of Penicillium are not good ... some of them produce toxins. Also all-species are not known to produce antibiotic. Some species of Penicillium  used to ferment cheese etc (so likely these do not produce any antibiotics).

It is better Not to eat a beet root infected with unknown fungus. Often they contain fungal toxins (good-name is "Mycotoxin")

From a study titled "Production of Penicillin by Fungi Growing on Food Products: Identification of a Complete Penicillin Gene Cluster in Penicillium griseofulvum and a Truncated Cluster in Penicillium verrucosum", moulds on food items were analyzed for fungi that could produce penicillin. The conclusion drawn was

Among different fungal species belonging to the genus Penicillium that
  are currently used as starter cultures in the food industry or that
  are frequently isolated from cured meat products, only P. griseofulvum
  (in addition to the previously reported P. chrysogenum and P.
  nalgiovense) was found to produce penicillin and possess the three
  penicillin biosynthetic genes (pcbAB, pcbC, and penDE).

Even penicillin should be avoided as the paper states that

The presence of penicillin in food must be avoided, since it can lead
  to allergic reactions and the arising of penicillin resistance in
  human-pathogenic bacteria.

During world war two, a strain of Penicillium chrysogenum was isolated from the mould growing on a cantaloupe (reference) for the development of penicillin. This was after searching through many mould families developing on different food items so penicillin strains do develop but are rare.
The problem faced is that moulds cannot be differentiated from each other through sight nor is all penicillin moulds safe (reference). Whatever be the case, I hope that you didn't venture to try and eat that beetroot.

Actually, I ate it :D, and it's been like 6 months, and I'm still alive :).

I can come up to a conclusion that I need to retest my self for penicillin, cause I went through some body enchantments, I doubled my immune system, perhaps I'm no longer allergic to it.

@That is debatable because there may not have been any penicillin producing moulds at all. Getting a retest is a good thing.

Mycotoxins present in fungus-infected foods are usually not too-drastic. Often they acts like a slow-poison. They often build up cancer, liver-damage etc.


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Why do our limbs and other body parts get numb/feelingless and then they start to tickle?
Why do our limbs (legs, arms) get numb/feelingless when they are under prolonged pressure or when one has crossed his/her leg while sitting for a long period?
After we move it to a more relaxed or natural position numbness goes away and we get the really strange and hard to bear tickles. Why does the numbness go away by doing this and why do why get these odd tickles?

This other post should answer your question (The question had been quite poorly asked I think but well answered!)

It doesn't elaborate the needle sensation and for another it not always happens because of apparent pressure, like I stated, if one keeps his/her legs crossed (like this) even than the foot on the top gets numb.

Keeping feet crossed like in your picture, involves pressure on nerves in both the legs. If one leg applies pressure on the other, it feels the same amount of pressure. (Newton's third law)


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Process of Transcription
During the process of Conversion to Ribonucleoside Monophosphates the various ribonucleoside triphosphates break off their high energy bonds after linkage to the DNA.But the first ribonucleotide triphosphate retains all the phosphates thus chemically distinct from the rest.
Now my question is:
Why does it retain the phosphates?

You've tagged this DNA, but really it is about RNA (although the same principles apply).

There is a useful diagram at this site.
During RNA synthesis in vivo the 3'-OH oxygen atom of the growing chain reacts with the α 5'-phosphate of the incoming ribonucleotide (nucleophilic attack), displacing the β + γ phosphates as a pyrophosphate group. This results in a 3'-5' bond between the prexisting oligoribonucleotide and the incoming ribonucleotide. In other words the loss of the pyrophosphate group is an inevitable consequence of the elongation reaction.
At initiation, however, the first ribonucleotide has not been the subject of a nucleophilic attack, because it is first in the chain. Its 3'-OH will carry out the nucleophilic attack descibed above when the next ribonucleotide is added to the chain.


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A basic example of the interactions of 2 or more non-identical alleles leading to an advantageous outcome for an individual organism
Could someone help me out with a basic example of the interactions of 2 or more non-identical alleles leading to an advantageous outcome for an individual organism? Based on empirical research OR on a theoretical model.
An example of 2 or more non-identical alleles cooperating across replication iterations/generations between individual organisms would be even beter. I somehow find this more spectacular :)
Please let me know if I'm not mentioning enough elements to answer the question. It's a very broad question and I accept very broad answers - semantically and across scientific branches.
All the best,
Flo
Personal background: I am new to the scientific field of biology. I think I caught up on some of the basic principles of genetics, allellomorphs, loci and DNA replication and I've gotten interested in the workings of alleles.

I don't fully understand your question for two reasons. 1) When you say an example do you mean an empirical observation or do you mean a theoretical (mathematical and/or logic/intuitive) model? 2) You're interested about a case where 2 alleles cooperate. You mean, you have two bi-allelic (to keep it as simple as possible) genes and for each gene one allele is causing the individual carrying it to produce a helping behavior?

Or a helping behavior only restricted toward individuals that carry the right allele of the other gene? Or do you mean, if two genes, A and B which alleles are A1, A2, B1 and B2. If one individual is A1B1 then this individual has a high fitness advantage. Any other combination does not provide any fitness advantage. Something like this? Or do you mean anything else? Could you please give a better description of what you mean by "allele that cooperate".

Thank you for revealing some of the ambiguities of my question to me. I admit my question is open to different interpretations and not well specified. I have edited the question to address your comments, although not to the full extent.

Reading your updated question, I think you are interested about epistasis. Let me know if I am mistaken.
The concept of epistasis might be confused with the one of pleyotropy, so I will define both terms.
Pleyotropy occurs when one gene influences multiple phenotypic traits. Note: the phenotype, to make it simply is what a living things look like (its cells, proteins, shape of the face, size of the leaves, etc…). It is often thought in duality with the genotype which is the total genetic information contained in an individual that codes for the phenotype (Be careful, the environment is also an important factor influencing the phenotype, if you make sports you will have big muscles!)
Epistasis is when the effect on the phenotype of one gene depends on the presence of several (or only one) other genes. Wikipedia gives this (simplistic) example:

Here, two bi-allelic genes are involved. One gene that determines the hair color. The two alleles influence the phenotype such: one allele gives red hair and the other allele gives blond hair. Now There's another bi-allelic gene coding for baldness. One allele causes the bearer to be hairy and the other one causes the bearer to be bald. Therefore, if an individual carries the allele "Bald" in the "Baldness" loci, what this individual carries on the other loci is not important because it will result into the same phenotype anyway, he is bald. Now if in the baldness loci, the allele is "Hairy", then the expression of the other gene "Hair color" matters and therefore if the allele is "blond", the bearer has blond hair and if the allele is "red" the bearer has red hair.
The "Baldness" gene is called a modifier. One can also say that the expression the "Hair color" gene depends on the genetic background of the individual.
Now cases of epistasis are not always that easy and if they influence the fitness, this kind of epistatic interaction might have implications for their evolution.

awesome - it looks like a fitting example - I'll study epistasis and pleyotropy in the near future (added to my to do list)

;) Great! I would recommend to avoid using the word "cooperation" for such interaction. Cooperation in evolutionary biology is linked to the concept of altruistic behavior. Therefore, cooperation is a word that mostly stand for relations at higher level, between individuals (or between cells) and not between genes. The evolution of altruism is a big field of evolutionary biology (social evolution, evolution of multicellularity, level of selection,…) that is still on debate.