text:
Where does extra blood come from to fill your muscles during exercise?
Let's say I go to the gym and lift some weights an hour.  During this time my arms will grow due to the "pump" -- the extra blood rushing in to feed the muscles.  For example, I've measured about 2-3 centimeters increase just in the diameter of the upper arm (bicep+tricep).
But where did this blood come from?  Also, if my arms got bigger, since I'm the same weight that means some part of my body must have gotten smaller, right?

Did you also drink water or a protein shake around the time of the workout?

It happens even if you don't drink anything beforehand.

The blood comes from the body's reservoirs:

spleen (mostly erythrocytes) [1]
liver [2]
veins (probably the most important blood resevoir as they contain 50-60 % of the volume) [3]

In pathological situations, if hypovolemia occurs, blood can also come from:

splachnic vascular bed [5]

But what attracts the blood into the muscle? The phenomenon is called active hyperemia:

Active hyperemia is the increase in organ blood flow (hyperemia) that is associated with increased metabolic activity of an organ or tissue. An example of active hyperemia is the increase in blood flow that accompanies muscle contraction, which is also called exercise or functional hyperemia in skeletal muscle. Blood flow increases because the increased oxygen consumption of during muscle contraction stimulates the production of vasoactive substances that dilate the resistance vessels in the skeletal muscle [4].

References:

The human spleen as an erythrocyte reservoir in diving-related interventions. Kurt Espersen, Hans Frandsen, Torben Lorentzen, Inge-Lis Kanstrup, Niels J. Christensen. Journal of Applied PhysiologyMay 2002,92(5)2071-2079;DOI: 10.1152/japplphysiol.00055.2001
Lautt WW, Greenway CV. Hepatic venous compliance and role of liver as a blood reservoir. Am. J. Physiol. 1976 Aug;231(2):292-5. PubMed PMID: 961879.
Michael J. Gregory, Ph.D. The Circulatory System. Licensed under CC-BY-NC-SA-3.0
Richard E. Klabunde, PhD. Cardiovascular Physiology Concepts. Active Hyperemia. Available from http://www.cvphysiology.com/Blood%20Flow/BF005.htm (accessed 03.08.2014)
Blaber AP, Hinghofer-Szalkay H, Goswami N. Blood volume redistribution during hypovolemia. Aviat Space Environ Med. 2013 Jan;84(1):59-64. PubMed PMID: 23305001.

But veins also bulge and get bigger when you exercise; do you mean that if I exercise my arms it draws blood from the veins of my legs?

@CaptainCodeman the veins that bulge on the surface of the body part you are exercising are superficial veins. Because muscle contracts, profound veins are getting flat and the only way for blood to return to the heart is the superficial colateral venous system. And yes, it will draw also blood from your legs, from the abdominal veins etc.

How does extra blood come from to fill your muscles during exercise?
Blood pumps (blood) and sucks (lymph).
There are many pumps in our body

thoracic pump
smooth musculature
respiratory pump

which work together to provide the blood to the peripheral circulation.
These pumps provide us Pulse, Vasomotor tone and Respiratory waves which when act together can lead to local hyperemia or congestion; see my answer only about these waves here in the thread What does irregular heartbeat mean in simple language.
By Starling law, anything that goes inside the heart goes out from there.
See this answer about elevated position on the venous return which is similar to the the exercise on the venous return.
Smooth musculature accommodates blood to the venous return.
Why your muscle gets bigger during exercise?
There are many reasons which can be explained by Frank-Starling principle and Fick's law.
They lead either to

hyperemia (increased local blood flow) or
congestion

because of

protein intake before the exercise
increased sympaticus (decreased parasympaticus; yes, sympathetic tone in digestive truct and some other systems is down-regulated) and blood flow through the muscle (see the above thread)
unstretched muscle can have congestion during exercise which is felt as hard muscle, also long after the training
too regular exercising without rest can also lead to congestion

in the spaces described in my earlier answers like here about What can cause the swelling in high protein diet of Whey proteins:

where explanations in my earlier answer.
Where does the extra blood come from to fill your muscles during exercise?
From your body (See Cornelius' answer for specific locations)

veins 50-60%
spleen
liver

under physiologic fine regulation where heart is the main pump (positive gradient) while its sucking effect (negative gradient; lymph) keeps homeostasis stable for exercising muscles to maintain hyperemia supported by rapid adaptive smooth musculature, vasomotor tone and respiratory pumps (three types of waves).

If you stand up too quickly, you get a head rush. One way to counteract the symptoms of the head rush is to contract your leg muscles really intensely. This forces blood out of your legs and into the rest of your circulation, including your head. This is actually a tip my family doctor told me that I've always remembered.
As mentioned in the links below working out a muscle group causes excess blood flow to these areas which could cause the blood vessels to dilate, causing the muscles in these areas to swell and appear larger. I now realize this has nothing to do with the head rush item I mentioned above, but still may be a useful piece of advice if you every get a head rush!
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1479005/
http://www.livestrong.com/article/75670-swell-after-workout/

Can you add some references?

Why would pushing blood to your legs and away from your head help with the head rush(orthostatic hypotension)? The dizziness and other symptoms are caused by blood leaving your head. In the short term, flexing drives blood from the muscle group, and opens blood vessels to increase later blood supply to the muscle group.(see also Hick maneuver, a similar leg/torso flex to keep blood in the head for fighter pilots)

thank you I realized I said this wrong, fixing my answer now.


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Genes, chromosomes, base pairs and the 23 pairs
OK so I'm a bit confused. Does a chromosome consist of genes and do genes consist of DNA? What about the 23 pairs in sexual reproduction? I can't remember what the pairs consist of

Please show what you have found on the subject matter so far so that any responses are constructive.

The Wikipedia articles for chromosomes, genes, and DNA contain all the information you need, and are literally the first links of the respective Google searches for those words.

@MattDMo This is perfectly right. But I tend to differ here: Wikipedia is nice but tends to explain things with a lot of words and sometimes in a complicated way which is hard to understand. So I think it is important to answer this kind of questions here as well, even if it is pretty basic.

Wikipedia's articles on things like DNA and Genes are far more friendly to the Layman if you switch to Simple English.  I've found that reading that first, then moving onto the English article is a good way to get a decent understanding.

I will start from the small and go to the big organisational unit:
All of this is constructed by DNA, the sequence of the four bases: adenosine, thymidine, cytidine and guanosine.  They are abbreviated G, A, T and C and are called the letters of DNA.
Genes are organisational units formed by a specific sequence of the four "letters". Genes encode for all the proteins (in fact this is a simple view, but should be enough for the moment) and are the way the information of how the protein sequence looks is conserved.
All DNA is organised in the form of a long string of bases, which would be very long in higher organisms. To come around this problem, the DNA is organised in chromosomes, in which the DNA is wound around special proteins (the histones) and further wound up to get a compact form.  The image below (from here) shows the relationship:

The 23 chromosome pairs are the 23 organisational units in humans, in which our genetic information is stored and organised.  A picture of them looks like this (image from the same website as above):

Please note that the chromosomes are not X-shaped, although they might look like on the image. They are pairs of long DNA molecules, which are not connected.

Pet peeve of mine - chromosomes are not X-shaped! They only look like that at one particular point in mitosis, and not even at the point where they make karyotypes. Sorry, nothing wrong with your answer, I just had to vent :)

They are not, you are absolutely right.

+1 good effort. It is not the first time this kind of basic question raises and it often get closed and we can't find them to point it out to newcomers. It is good if we can keep this post I think.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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How to consider ions charges while calculating ions steady-state equilibrium concentration
i recently tried to find answer for following problem:

"Assume that a membrane is permeable to Ca++ , K+ and Cl- but not to a
  large cation R+. The inside concentrations are [RCl] = 100mM and
  [CaCl2] = 200mM, and the outside concentration is [CaCl2] = 300mM. (a)
  Derive the Donnan equilibrium. (b) Find the steady-state equilibrium
  concentration for Ca++."

when i tried to write space charge neutrality equation, i encounter to a new question,
how should i consider that
a:for each Ca++ there is two Cl-

and
b:each Ca++ has 2 positive charge

in the past i only worked with the ions that had same charge or same number of molecule, for example considering we had only cl- and K+ and some large
cation R+ , this situation is simple but the above mentioned problem is totally different.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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How are babies born without a brain?
In the United States, anencephaly occurs in about 1 out of every 10,000 births. There are several forms of this condition, wherein the forebrain is absent. The forebrain is host to most of the higher functional areas in the mammalian brain. In the most extreme case of anencephaly, the so called holo-form, only the brain stem remains.
In MacLean's model of the brain, the term brain stem is used interchangeably with the term reptilian brain, to designate the most primitive parts of the central nervous system. Many are taught this model.

An anencephalic newborn (warning: graphic content)
  ("An anencephalic newborn", wikimedia, author: Almazi, license: public domain, DOR 27/09/2012)

From my layman's perspective I can't help but notice a reptilian likeness of the anencephalic newborn. Whilst it goes without saying that correlation doesn't equal causation, I would like to know what is known so far about the cause of this condition to yield this particular morphology (as seen in the picture)?
Perhaps someone (eventually) has even some evodevo insight to share as well?

http://www.youtube.com/watch?NR=1&feature=endscreen&v=WMlVNFpzKNI

the autonomous portions of the brain that control breathing and other physiological functions are lower in the brain.  If the newborn is viable it just have just enough lower and back brain function to survive at least in utero.  If a fetus expires in utero it does not go to full term as you probably know.

I think more should be discussion about induction factors, differentiation and transforming factors in the answers. Current answers do not answer this explicitly.

Know your databases! This is just the query fit for OMIM.
http://omim.org/entry/206500

Anencephaly is considered an extreme form of neural tube defect
  (182940), which has been associated with variation in several genes.
  The entity described here is believed to show autosomal recessive
  inheritance.

The genes are those associated with neural tube effects, i.e., VANGL1, T, CCL1, and FUZ. See also folate-sensitive neural tube defects.
http://omim.org/entry/182940
The folate evidence was so convincing that the US/Canada in the 1990s introduced folate supplementation in all bread, flour, and cereal products. Today, US/Canada have a lower incidence of NTD (neural tube defects) than Europe, where folate supplementation is completely left to one's choice (and if women actually care they take it too late).

good catch! I find the formation of the eyesockets striking. I am puzzled whether this is within the range of developmental plasticity as the result from different biomechanical forces due to craniosynostosis (premature skull fusion) OR if mutant genes (and/or pleiotrophies) are involved. OMIM unfortunately shows a practical lack of animal models. On a  sidenote, the related spina bifida is known to interfere with the "eye" (opthalmic) devleopment....

From what I've read and I know from my Biology classes, during the formation of the embryo a whole bunch of things may go wrong. In these cases, during the neurula stage, in which the brain is supposed to begin its development, something goes wrong while the neural tube is forming.
The causes? Some people argue that a lack of folic acid may lead to defective brain development. Studies seems to show that most factors don't affect the formation of the neural tube, which include age of the mother, occupation, and exposure to chemicals.


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Punnett square and hybrid cross
A plant breeder crossed two plants, one with red flowers, and the other with white flowers. Red is dominant. Calculate the phenotype and genotype ratios of the F2 generation of this cross.
Is this a monohybrid or dihybrid cross?

In the problem, is this simple dominance? In real life, isn't this trait incomplete dominance?

I've voted to close because this question shows no effort to come up with an answer - this is not in one with the biology SE homework policy.

Unfortunately, that isn't a very well-written problem, but I think I can help. If we assume simple Mendelian genetics, this would be a monohybrid cross, as you're only examining one trait (flower color).
You have a pure-breeding white flower and a pure-breeding red flower. These make up the P (parental) generation. Their offspring will be the F1 (first filial) generation. A cross of two plants from the F1 generation produces the F2 (second filial) generation.
Since each P-generation plant in the has only one possible allele to give, each of the F1 plants will inherit one red and one white allele. Because red is dominant, all F1 plants's phenotypes will be red.
When you cross two F1 plants, each has a 50% chance to pass on either the red or the white allele.
Using Punnett Squares:


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Below which temperature human muscles don't work?
When one exposes theirs body parts to cold environment (especially foot and hands), they may be numb, with temporarily blocked both muscles.
What is typical body temperature below which human muscles don't work properly?
Moreover, what is the mechanism behind it?
EDIT:
Interested in case when muscles almost cease to work (e.g one is not able to grasp a cup), not just in small perturbations to strength.

If you dissect striated muscle out of most-any organism, the actual contractile apparatus works over a wide range of temperatures. So that's at the single-muscle-fiber scale. The muscle itself continues to work at all (thawed) temperatures below body temperature -- the problem comes with its regulation.
The shivering response -- a centrally controlled  involuntary contractile pattern -- overwhelms voluntary muscle control. So the mechanism behind loss of muscle coordination in hypothermia is the same as the shivering mechanism. When the core temperature drops, the midbrain starts over-riding voluntary control of the muscles. When the core temperature drops far enough; around 32C, the shivering often slows down or stops. Voluntary movement becomes compromised probably because the brain simply isn't working; neuron firing rates are so slow that sensation, processing, and motor responses are all critically impaired.
The feeling of numbness does not actually directly accompany a loss of muscle contractility. You can walk pretty much indefinitely on frozen feet if you can keep your balance (and you keep your core temperature up.) Lots of people survive severe frostbite of their feet (their feet do not often survive, however.) The reason why it seems your hands don't work when they get cold is that you can't feel what you're doing (note; your hands can be much colder than your core body temperature.) But the muscles themselves work right up until they freeze solid.
UPDATE:
 Here's a paper that directly addresses the scenario posed by OP -- the decrease in grip strength with temperature.   Figure 1 of that paper illustrates their experimental setup; they measure the contractile strength of the index finger while manipulating the temperature of the rest of the hand. They show that contractile function is impaired with temperature and look at temperatures as low as 12C.
They measure as much as a 50% impairment on twitch tension upon cooling to 12C. It's interesting that they review results suggesting that some of this effect is intrinsic to the muscle fiber (not neurological), showing that I should refine what is meant by "continuing to work" in my opening paragraph. (I meant having an ability to generate contractile force when equilibrated in solution containing sufficient ATP and Ca$^{2+}$, not the ability to contract optimally.) For fun, I linearly extrapolated the final arm of Figure 5 and found that the 'voluntary tension' approached 25% at 5C. This suggests that total failure of the voluntary contraction happens somewhere below the freezing point of water (muscle would freeze at a temperature lower than 0C because of colligative effects.)

http://www.jacklondons.net/buildafire.html

Thanks, especially for the last link. (I thought also about possibility that capillaries contract to much at lower temperatures, to support demand of muscles.)

Regarding the capillaries, you're right they that they greatly constrict, but the muscles have enough blood supply to continue functioning. Muscles are also good at tolerating anaerobic conditions (lactic acidosis.)

Was going to write an answer based on shivering, interesting read!

This seems complicated, but I found a reference that might answer these questions (if its right).
Sports physiology common wisdom is that human muscles regularly work in the range of 37C to 40C which is basically body temperature.  Since the muscles generate quite a bit of heath when they function, they are usually not functioning in colder temperatures and hyperthermia starts setting in.
Thomas et al. put this to the test by cooling down some muscles in volunteers!
They say that the core body temperature is more important than the peripheral temperature in restoring muscle strength (torque produced).  Hypothermia makes the victim weaker and weaker apparently and it sets in below 37C pretty quickly apparently.  They speculate that the cooling might actually impair the nervous system from activating the muscles, which might be an answer to your question.
This is probably not the final word, but its as far as I got...

Nice, but a quick skim says that they showed only small deviations. I am the most interested when muscles strength is only fraction (say, <25%) of the maximal one, or they are not working at all.

@Piotr As you can imagine, a specfic study of this nature might be difficult to get past an ethics review.  There probably are some case write ups of individuals, but they would tend to be anecdotal "then I couldn't move my arms!".  Perhaps someone can find a clinical review.. but there will usually be cause to complain when you are reviewing the limits of human physiology.

I am not talking about anything damaging, rather about a common experience for anyone doing winter sports, or even hiking in the rain.

If bulk or major muscle groups have an internal temperature of much less than 37C these authors imply that this is not a common experience - the circulatory system and the functional heat of the muscles will keep the temperature stable.  you will still feel uncomforatable, but until hyperthermia or frostbite sets in the main tissue temperature will be stable.


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Chiral (a)symmetry of curly hair (and fur)
Some people have curly hair, as well as fur of some animals can be curly.
However, shapes which are curly are not mirror symmetric, much alike screws or chiral molecules.
The question is whether curly hair in a given species (say, humans, but I don't stick to this example) are in the same proportion left-handed and right-handed?
One can easily imagine that chirality of molecules (e.g. keratin) gives rise to macroscopic chirality of curly hair. However, it is far from obvious whether this effect is strong enough.
EDIT:
I am interested mostly in data. It might be easy (yet misleading) to convince oneself that there should (or there shouldn't) be relation of microscopic to macroscopic mirror symmetry (or lack of it).
(E.g. in some other cases there is such effect - e.g. with left/right orientation of body organs like heart, or asymmetry of left and right brain.)

curliness of hair is not because of an enantiomeric form of keratin. It is dependent on the way keratin is packed in the intermediate fibers.

@WYSIWYG a link might help the OP...

Please refer this research done by L'oréal on keratin organization and hair texture and shape.
I believe one can also find an answer in classical textbooks like MBOTC-Bruce Alberts. This is a commonly asked question in cell bio/protein structure exams.

Plus.. all amino acids exist as L-enantiomers in proteins. Few exceptions in  cell wall peptides of gram +ve bacteria

@WYSIWYG Here keratin was only a guess. Chirality of  intermediate fibers equally interesting to me. However the main question is: is proportion of left- and right-handed curly hair 1:1 in humans?

This is a great question. I am betting there is no data or precious little. You suggested a mechanism and I think that has led to confusion in the answers. Maybe just edit it down to the essential question? What is the ratio of L-/ R- chirality of curly hair? +1.

@daniel You are right that suggesting an answer was distracting. In any case, it seems there is no data. Maybe I should run a survey among friends or so. :)

Microscopic chirality is not at all necessary to explain curly hair (or other objects).  All that is required is flexibility. Once hair gets long enough, it collides with itself, and is pushed off to one side or another, forming a chiral curl.
For some anecdotal evidence against microscopic chirality, find someone with large diameter hanging curls in their hair. Those seem to often curl straight back on to themselves. A more compelling anecdote is that curled objects, including hair and telephone cords (if anyone still remembers those) can be pulled through themselves and chirally inverted. Sometimes there will be some resistance, but that could be the keratin or plastic or whatever having set in its shape over time, rather than being preferentially formed that way.
These are obviously both anecdotal though, and the idea that there is some slight chiral preference isn't ruled out. I'm not even opposed to the fundamental idea of transitive chirality through several orders of superhelicity (look at DNA), but it just hasn't been my empirical experience. As Ryan points out, if it were a strong effect, all hair would curl the same way, and straight hair wouldn't exist at all.
Just to provide a bit of data, this paper demonstrates that hair curvature is based on the distribution of 4 different cell types in a follicle. The keratin (and many other proteins associated with) intermediate fibrils were associated with curvature, but only to the extend that their compositions were different in the 4 cell types. But the curvature was based on the distribution of the cells themselves.  Chirality wasn't specifically studied in the paper, but I think (given that they were staring at individual fibers with an electron microscope) that they would have noticed it had it existed.
Cortical cell types and intermediate filament arrangements correlate with fiber curvature in Japanese human hair
http://www.sciencedirect.com/science/article/pii/S1047847708002980

Naturally straight and curved human scalp hairs were examined using fluorescence and electron microscopy techniques to determine morphological and ultrastructural features contributing to single fiber curvature. The study excluded cuticle and medulla, which lack known bilateral structural asymmetry and therefore potential to form curved fibers. The cortex contained four classifiable cell types, two of which were always present in much greater abundance than the remaining two types. In straight hair, these cell types were arranged annularly and evenly within the cortex, implying that the averaging of differing structural features would maintain a straight fiber conformation. In curved fibers, the cell types were bilaterally distributed approximately perpendicular to fiber curvature direction with one dominant cell type predominantly located closest to the convex fiber side and the other, closest to the concave side. Electron tomography confirmed that the dominant cell type closest to the convex fiber side contained discrete macrofibrils composed of helically arranged intermediate filaments, while the dominant cell type closest to the concave side contained larger fused macrofibrils composed of intermediate filament arrangements varying from helical to hexagonal arrays approximately parallel to the longitudinal fiber axis. These findings concur with the current hypothesis of hair curvature formation and behavior.

I know that microscopic chirality is not needed to explain curly hair. The question is whether it plays any role, e.g. in shifting the ratio of clockwise and counter-clockwise curly hair from 1:1. (Thanks for the link, anyway; too bad for me that it is under a paywall).

Keratin's handedness does not directly give rise to the curls of hair. One has to cross many many length scales to move from the keratin scale to the whole hair fiber. There's an animation here that shows those many length scales. But here are some other arguments if you're inclined...
If the superhelicity of keratin effected the curling of hair, all hair would twist in the same direction, because the keratin superhelix always twists in the same (left-handed) direction (for the naturally occurring proteins.) But that isn't the case. At least not for my hair!
Or you can ask, if the keratin superhelix gives rise to curly hair, then how is this effect mitigated in straight hair? The structure of keratin isn't directly giving rise to the long-range patterns of hair. The keratin filaments are being arranged in particular ways, and the long-range behavior is independent of the short-range superhelicity.

Orders of magnitude difference of scale is not itself and argument against (see edit of my question).


text:
Abiogenesis: Beyond the research journals as a lead in to discussions on evolution
I just came across this abstract:

Aminoacyl-tRNA synthetases (aaRSs) are responsible for creating the pool of correctly charged aminoacyl-tRNAs that are
  necessary for the translation of genetic information (mRNA) by the ribosome. Each aaRS belongs to either one of only two
  classes with two different mechanisms of aminoacylation, making use of either the 29OH (Class I) or the 39OH (Class II) of the
  terminal A76 of the tRNA and approaching the tRNA either from the minor groove (29OH) or the major groove (39OH). Here,
  an asymmetric pattern typical of differentiation is uncovered in the partition of the codon repertoire, as defined by the
  mechanism of aminoacylation of each corresponding tRNA. This pattern can be reproduced in a unique cascade of successive
  binary decisions that progressively reduces codon ambiguity. The deduced order of differentiation is manifestly driven by the
  reduction of translation errors. A simple rule can be defined, decoding each codon sequence in its binary class, thereby
  providing both the code and the key to decode it. Assuming that the partition into two mechanisms of tRNA aminoacylation is
  a relic that dates back to the invention of the genetic code in the RNA World, a model for the assignment of amino acids in the
  codon table can be derived. The model implies that the stop codon was always there, as the codon whose tRNA cannot be
  charged with any amino acid, and makes the prediction of an ultimate differentiation step, which is found to correspond to the
  codon assignment of the 22nd amino acid pyrrolysine in archaebacteria.

Granted, this is a few years old, but I often find myself having to admit that "I don't know" when at the root of discussions on evolution.  That is, once abiogenesis has occurred, we can go on and explain the rich diversity of life, but sadly we really don't know much before that critical step.  Generally, those satisfied with "magic" as an answer posit their myths and fables, whereas I'd rather try to actually find out what happened.  Sadly, as the abstract shows, you actually need a level of education to understand papers such as this that is generally well beyond those who would deny the reality of evolution.
Does anyone have a collection of papers on abiogenesis that are more accessible and understandable to laypeople?

The fascinating field of abiogenesis is, as Nick Lane put it, "a wild west of ideas, theories, speculations, and even data". The stories we have involve a plethora of assumptions, there is no hypothesis where all or most of the pieces would fit together. Usually scientists agree it was RNA that played central role in the process, as the molecule could both carry the genetic code, necessary for hereditary natural selection, and catalyze basic biochemical reactions. Where the energy came from and how it was harnessed to maintain RNA (a rather unstable molecule) and perform work is still debated. A fermentation in a 'primordial soup' or a primitive form of respiration, perhaps through a thin iron-sulphur membrane, have been proposed as possibilities. The second gave a start to the iron-sulphur world hypothesis. Iron-sulphur minerals could catalyse the first organic reactions to synthetize sugars, amino-acids and nucleotides, and eventually RNA world, where natural selection could take over. Theories abound.
Usually reviews will give you a sound and approachable picture of the current thought on the matter. Take a look into Nick Lane's book and these articles, too.

Lane N., Origin of Life in: Power, Sex, Suicide: Mitochondria and the Meaning of Life. Oxford University Press, 2005. p. 94-104.
Russell, Michael (2006). First Life. American Scientist 94 (1):32.
Van Noorden R., RNA world easier to make - Ingenious chemistry shows how nucleotides may have formed in the primordial soup. Nature 2009
Check Hayden E. A never-ending dance of RNA - The recreation of life's origins comes a self-catalysing step closer. Nature 2009.
Cech TR. Exploring the New RNA World. Nobel Prize articles
Müller UF. Re-creating an RNA world. Cell Mol Life Sci. 2006 Jun;63(11):1278-93.
Lazcano A, Miller SL. The origin and early evolution of life: prebiotic chemistry, the pre-RNA world, and time. Cell. 1996 Jun 14;85(6):793-8.


text:
Why have humans evolved much more quickly than other animals?
Humans have, in a relatively short amount of time, evolved from apes on the African plains to upright brainiacs with nukes, computers, and space travel.
Meanwhile, a lion is still a lion and a beetle is still a beetle.
Is there a specific reason for this?  Do we have a particular part of brain that no other animal has?

I don't understand your last question; evolution is largely directed by genetics, a modified organ doesn't pass itself along (just as amputees don't have limbless children).

-1 for starting with "it seems to me". Can we try and be a bit more quantitative (or at least back up your observations)?

@Poshpaws--"it seems to me" has been removed.  Thanks for leaving the comment.

http://en.wikipedia.org/wiki/Bifurcation_theory, think of genetics as the parameters, nukes, computers, and space travel as variables. There's no reason to believe we're evolving "faster" in a genetic sense.

on a genetic level we have evolved at the same rate, but we have evolved differently - we have evolved the ability think and act intelligently, communicate information, and learn from our peers far better than any other animal. So much of what we know is learned rather than innate - we did not evolve the ability to make a nuke rather we evolved the ability to learn and teach how to make one etc. Take away the evolved ability to learn and communicate knowledge and we wouldn't be all that different from an ape.

Related: Are we “more evolved” than present-day bacteria?

"Meanwhile, a lion is still a lion and a beetle is still a beetle.", I liked most in that post. As time goes by,  a kiss will be a kiss, but fundamental things apply as time goes by. To my mind, our minds as once made, contrary to the answer that I marked, will not evolve any further. As a lion remains or vanishes, man as he and she  have  - present perfect - evolved will stay so (or vanish). As it is, it should go on for more than a little while, in my opinion. Climate change might continue being "fun-amentel", though, not in casa biancas only  :)(

People here dont really have an answer for "why humans evolve faster than animals". They will beat about the bush saying humans didnt evolve faster, just differently - if its different how can its speed be comparable? and isn't brain part of body?; or say its culture that developed better not body - culture development cannot be independent of body development, brain, hands, legs are all part of body; say it depends on population - ants are more numerous than humans. See, the truth is, evolution dont happen. Plain logic can lead you to this conclusion. You are on right track.

We have the Human Accelerated Regions (HARs) which are some of the most rapidly evolving RNA genes elements. While heavily conserved in vertebrates, they go haywire in humans and are linked with neurodevelopment.
Thanks to @Nico, the following paper compares the human genome with that of the chimp and identifies genetic regions that show accelerated evolution. The most extreme, HAR1 is expressed mainly in Cajal-Retzius neuron cells which hints at its important role in human development.
 Pollard KS, Salama SR, Lambert N, Lambot M-A, Coppens S, Pedersen JS, Katzman S, King B, Onodera C, Siepel A, et al.. 2006. An RNA gene expressed during cortical development evolved rapidly in humans. Nature 443: 167–72.

Would be better to link to some original papers like: An RNA gene expressed during cortical development evolved rapidly in humans.

This would be the effect of our rapid evolution in that area and not the cause, right? So even if this is interesting, it does not actually an answer the question at all?

Just wanted to "+1" this answer again after 10 years :).

This question appears to address at least two distinct concepts:

the "speed" of evolution
whether there is some "end goal" that evolution seeks

I will provide an explanation of each separately below:
The Speed of Evolution
The speed at which a species evolves—that is, the speed at which it acquires new heritable characteristics—can be affected by numerous factors. Among the most obvious which come to mind are:

existing population size
reproductive cycle rate
number of offspring
offspring survival rate
environmental demands

That said, have humans evolved faster than other species?
On the whole, I do not feel that I could say without a doubt that humans have evolved significantly faster than other organisms. Considering the above factors (we have a slow reproductive cycle, few offspring, etc.), it seems unlikely but this is where a zoologist would know better. The answer provided by bobthejoe may provide insight as well.
I would just raise a word of caution before leaping to the conclusion that we have evolved rapidly without looking into it, because while we often study human evolution quite extensively in biology classes and thus are more aware of changes like upright walking and opposable thumbs and increased brain size, that doesn't mean other animals didn't evolve that much as well (we just don't learn about them in as much detail). Being a psychologist and not a zoologist, I do not have the knowledge to say with any surety that other species did not evolve in their own ways to the same magnitude as we have in the last 3-4 million years, so perhaps someone else can help you there.
But you ask whether we have a particular part of our brain that no other animal has; the answer to this is no, but the parts of our brains which we do share with animals are often much larger than as seen in those other species.
The "Goal" of evolution
I would like to point out here that human technology has nothing to do with evolution. Not only have all of our notable technological achievements occurred in the last couple hundreds years when human evolution was at its slowest (early human evolution as we know it today dates back at least 5-7 million years, and it was during this several million year period when all the genetic evolution you speak of happened), I would argue that human spaceships and computers are no more sophisticated to us than a mushroom garden and ventilation system are to a termite. I could be wrong here but it seems as if you are under the impression that evolution is striving towards something... That humans are somehow intrinsically better than lions or sharks or beetles. On the contrary, each of these creatures is not significantly more or less adapted to their environments as we are to our own, and in many ways these creatures possess features which are beyond our own.
I shall leave you with one of my favorite quotes:

"We need a wiser and perhaps a more mystical concept of animals. We
patronize them for their incompleteness, for their tragic fate having
taken form so far below ourselves. And therein we err, and greatly
err. For the animal shall not be measured by man. In a world older and
more complete than ours, they move finished and complete, gifted with
extensions of the senses we have lost or never attained, living by
voices we shall never hear. They are not brethren, they are not
underlings. They are other nations caught with ourselves in the net of
life and time, fellow prisoners of the splendor and travail of the
earth."

–Henry Beston, in The Outermost House
I don't have a dog in this fight, and I could very well be falsely assuming that you think this particular way when you in fact don't (you only wrote 4 lines after all, it's hard to glean much from that), but I wanted to make sure that these concepts were clear either way, particularly for any future visitors who might get the wrong impression. :)

-1.  While I appreciate your contribution, it completely misses the mark in answering the simple question.  There was no assumption or innuendo in my question.  The premise was simple: as a species, humans have clearly evolved a set of cognitive abilities and motivators that have lead to technological feats.  By comparison, I do not know of any termites that purchase Trane AC systems for their homes or pilot jet aircraft.  My question pertained to the "why" behind that.  bobthejoe has provided the best answer to that question.  I am voting this answer down because it is tangential.

@MatthewPatrickCashatt it seems like you're coming at it from a fairly anthropocentric view which stoicfury is trying to address

@NickT--Since I asked the question and am the only being capable of dictating my intention, and therefore the correct response to the intention manifest, in the words of the giant-of-thought George W. Bush, "I'm the decider". ****And yes, that was said tongue firmly in cheek whilst grinning.

@MatthewPatrickCashatt: Just because your question is posed with few words does not mean it is "simple". Evolutionary biology is a vast and complex field which you—based on your question and subsequent responses—appear to grossly under-appreciate. With all due respect, I think you misinterpreted my answer as a personal affront and typecast the entire response as nonsense when in fact it is quite relevant. :\  Based on your personality profile it is unlikely you will change your (public) position on this though, even if you were to (secretly) agree with it after rereading it more fairly.

Just to be clear though, you write in your comment above "There was no assumption or innuendo in my question." This is false. The question "Why have humans evolved much more quickly than other animals?" assumes at least 2 things: that humans have evolved and that humans have done so faster than other animals. The context of your question suggests you think of evolution as a linear progression towards an "advanced state"; as if there is a "beginning" and "end" of evolution. This, as any biologist will point out to you, is false. That's all I was attempting to clarify. :)

@stoicfury-- I have no argument with your point of view or your explanation of concepts.  The reason for the down-vote was that a great answer existed already and, judging by the up-votes garnered by that answer, it seems validated.  This is how the Stack Exchange sites work.  I lose points if I vote your answer down, but it was important that I did so for the sake of ensuring that the most appropriate answer to the question remains at the top.  It's nothing personal.  I found your insight, quotes, point-of-view, etc interesting, just not a direct answer to the question.

"The reason for the down-vote was that a great answer existed already and, judging by the up-votes garnered by that answer, it seems validated." Downvotes are for answers which are not useful, i.e. irrelevant or false. If SE downvoting was designed the way you suggest, it would not make sense to be able to upvote more than 1 answer. In other words, while you can have only 1 accepted answer, there can be more than 1 useful answer, and in fact there are badges for when "merely useful" answers outscore accepted answers, to highlight the fact that the first is not always the best. :)

I wish I could give this answer a hundred +1 votes!  I find myself in 100% agreement with stoicfury on every point.  Well done sir!  Bravo.

It seems to me that humans have, in a relatively short amount of time evolved from apes on the African plains to upright brainiacs with nukes, computers, and space travel.

The question covers changes of two sorts: biological evolution and cultural evolution.  The other answers speak to biological evolution, but I want to point out that much of the most striking changes ("nukes, computers...") are due to the evolution of our culture.
By 40,000 years ago most of our biological evolution to the present had happened (perhaps the most notable exception being changes related to our coevolution with disease organisms).  Yet although we had achieved upright brainiac-hood by the apparent evidence, we were not strikingly different from other large animals.
We had sharpened rocks and sticks, and made better use of the surroundings, particularly in non-food categories, than other animals.  We had been successful enough to spread throughout much of the old world.  Nevertheless, the overall contrast with other animals seems rather muted when viewed by the differences with the modern world.
Most of the visible changes since then are due to evolution happening outside our genes and bodies in what can be called culture.  Other animals have culture but our nature gives us many times the cultural capability.  We build upon the culture we find ourselves in and make it more effective.  The cultural presevation and advances come not just from aping ('monkey see, monkey do'), but from language, and from mechanisms of cultural distribution and preservation, most notably from the invention of written language.  These things have driven the cultural evolution of the largest visible changes, those of the last few millenia.

Very interesting!  And don't forget memes that use our social interaction as a vector for survival, evolution and preservation.

The ability to walk on two legs was hugely significant in human evolutionary development. This led to the hands being freed up to develop into precision tools rather than having to be durable for walking on rough terrain.  Increased dexterity in the hands led in part to the leap forward in human development.
~ The Human Body (Prof. Robert Winston - BBC Documentary 1998 (BBC Text Summary)

This is from a documentary I recently watched, I'll find some proper references when I get back in :)

Was that the one that also talked about our jaw muscles being weaker, thus allowing our brain to grow more?

@Brightblades I don't recall it mentioning that, it was a fairly recent BBC offering?

@Brightblades apparently not as recent as I thought, I've added the reference =)

Cool.  I will have to look that one up.  As for the jaw muscle theory, that one was mentioned within the past few years anfd had something to do with the sagittal crest:  http://anthro.palomar.edu/hominid/australo_2.htm

What you are talking about is genetic vs memetic evolution. While both are important in our species, the memetic evolution is responsible for the changes you are citing (mostly technological advancements and "culture"). There are some interesting situations where memetic evolution is actually "cancelling out" genetic evolution. For example medical technology has largely allowed many (at least in the developed world) to survive in spite of genetic handicaps (lack of resistance to a pathogen, insulin, glasses, etc).
Despite this I would argue we are still evolving rapidly in the genetic sense though not for the reasons you imply. In most vertebrates (any slow-reproducing creature), there is an ongoing selective pressure against pathogens. If their immune systems don't continually change (and antibiotics don't intervene), pathogens will wipe them out. While not as glorious as developing bipedalism, this is still evolution. We are also now a very transient species with people migrating extensively compared to the recent past. This leads to new genetic combinations and thus potential selection.
It could be argued (as others have) that the selective pressures for brain development (especially for language ala the FoxP2 gene) have brought about the rise of language, technology and culture. However I would argue that these evolutionary changes largely occurred, at minimum, the last few tens of thousands of years.
As others have also noted, crazy genius isn't THE end goal of evolution, it is merely ONE possible outcome. The real goal is genetic perpetuation (which we do seem to excel at) ;)

Many animals have actually reached an optimal solution to their evolutionary path.
That means that from where their genome is right now, pretty much all changes are harmful to expected reproduction. Over time such species start to have less variability within their genome and start to evolve less. Evolving is simply not sensible anymore.
Humans on the other hand are in an extremely open evolutionary path, that means there is much variability within the human genome that leads to greatly varied expected reproduction.
That is why humans are evolving so fast.

Very interesting!!

Well, at least they might have achieved local optima. One can probably always imagine traits that would actually benefit a species but where the it's highly unlikely that a evolutionary path can get across the gap.

Interesting and thought provoking. Though I am curious why you wouldn't think plants and animals are conscious. Maybe they aren't self aware like you are, but if a lioness preserves herself to tend her cubs, is she not aware of the fact that things can exist or no longer exist? That life can be lost? No matter at what level you may perceive, this realization in her will trigger an emotion ( chemical reaction) which in turn will give her the fortitude to continue to survive, or as we sometimes see in nature, to not. How are we different? I hate this cut off that I see. " if it doesn't do it on the level that we do it then it don't do it at all". That's silly, if you believe in an evolutionary development of genetic material how can you not believe that emotions and awareness have levels of development too? Sounds a bit like the "chosen one" complex. Once you take that road, you're a hop skip and a jump from the creationist and 6000 year old earth.

I think you misunderstood the question--and made several assumptions about my way of thinking at that.  The question isn't about consciousness.  It is about evolution.  A lioness may preserve her cubs to the best of her ability--in the same way as it has been done for a few hundred thousand years, and yet a lion may still come along and eat them.  Not once in the course of evolution has it occurred to the lioness to develop, say, rule of law to prevent this.  I simply want to know why.  I am about the farthest thing from a creationist, by the way--I am asking a question about evolution.

I believe that it is significant that we spend so much of our brain-power on deciding who we want to mate with. For lions it seems like choosing a partner is much less based on rational thinking. The weakness of this theory is that I do not know how humans behaved earlier, and whether mating was strictly regulated by cultural rules to ensure that mating was not based upon convenience, but rational thinking about what who is the best partner in the long-term.
The reason for me believing that this is so important, is that a well-functioning couple in a well-functioning community, will have the time and energy to educate their children, who again will make wiser decisions on who they will choose as their partner.
I would love to get this theory tested (and hopefully rejected, as that is the way I learn the most) by this community.

I really doubt if most people make their mating decisions based on rational thinking. But indeed, sexual selection may played important role in evolution of human brain. Anyway, I think answers should be based on facts rather than personal opinions.

Is there a specific reason for this? Do we have a particular part of
  brain that no other animal has?

Because you are human. So every minor change in appears looks important from skin colour, to the length of a nose, to the sounds we regularly make. If you were a lion, such minor difference would be noted but hardly commented upon. Think about this, all male lions have manes right? That is the essential display of maleness in lions. However male Tsavo lions have no mane. this is the equivalent of a tribe of people where the women have no breast.
There is no special part of the brain that is unique to humans. The structure of the brain in a mouse is essentially the same as the human. The big difference, is how big each section of the brain is.
In fact elephants and dolphin come close to matching human in cerebrum complexity. And the long-finned pilot whale, has actually  more neocortical neurons than any mammal studied to date including human.
So why are us humans the guys with the guns?
Environment... no matter how smart a dolphin is, they will never master fire, because living in water does that to you. (also no hands, imaging trying to make rope with only your mouth to work with.)
And why elephant and man not waged war upon each other...(we have just not warfare were both sides used spears and swords) well them elephants have at best one hand with two fingers. No elephant, no matter how dexterous will ever learn how to knap a flint tool. Elephants never evolved hands... and us human got our hands from our ape ancestors that lived in the tree and needed limbs that could grasp.
Humans are special... but not in the way you would think. It is not because we are the most brainy animal out there, the long-finned pilot whale is more brainy. No because we are talkative social animals.... elephants talk too and they do talk to herds tens of kilometers away, maintaining decade long relationship made as calves.. Not because we use tools, birds and dolphins use tools too. Not because we have hands... many animal have hands... even non primates... like raccoons.
We are special because we can do all these things at the same time. We are brainy, have a pair of hands, tool using, social animals that live on dry land.
But that said... even with all those features.. the human species have been around for about  200,000 years. Civilization for 10,000.
Nukes, computers, and space travel.. strange as it is are very recent inventions. There are still people alive today who remembered the Wright brothers touring their new invention, the airplane. There are people alive today who saw the start of space race and the coming of the first PC (personal computer), the first nuke, the first mobile phone.
Go back just 200 and an LED flash light is tech so beyond bleeding age technology, it might as well it be science fiction (first light bulb invented in 1801. First commercial light bulb 1879).

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


text:
Help with the Price equation
The Price equation describes mathematically the evolution of a population of units from one generation to the next.

$\bar{w}\Delta \bar{z}$ = $Cov (w_i,z_i) $+$ E(w_i\Delta z_i)$

I would like to know how to actually employ the equation to some data. Perhaps a simple online "walk-through" type guide of the Price equation would help. It should simply show the calculation of the Price equation using numbers from an example population. For example, I'd like to see how the Price equation is applied to the following scenario:

A population, $P$, of 5 individuals reproduces to produce population
  $P'$.
The trait value of the $i^{th}$ individual is $z_{i}$ where $z_1$,
  $z_2$ and $z_3$ all = 1 and where $z_4$ and $z_5$ both = 2 and $\bar{z}$ = 1.4.
Absolute fitness is $w_i$ for the $i^{th}$ individual where $w_1$,
  $w_2$ and $w_3$ all = 1, and $w_4$ and $w_5$ both = 5.
Relative fitnesses, $\omega_i$, are $\omega_{z=1}$ = 0.077, and $\omega_{z=2}$ = 0.385.
Thus the population $P'$ has $n$ = 13, with 3 individuals where $z$ = 1
  and 10 individuals where $z$ = 2 and $\bar{z}'$ = 1.769.
$\Delta z $ is the transmission bias and is equal to 0 in this case
  (perfect transmission of the trait score $z$)
The value $\Delta \bar{z}$ = $Cov (w,z)/ \bar{w}$ = ....

Here's an R script to create the above information:
# Define two trait values:
z1 = 1
z2 = 2

# Define two fitness values:
w1 = 1
w2 = 5

# Set number of units possesing each trait in P population:
n1 = 3
n2 = 2

# Create data
df = data.frame(c(rep(z1,n1),rep(z2,n2)),c(rep(w1,n1),rep(w2,n2)))
colnames(df) = c("z","w")

df$omega = df$w / sum(df$w)

n_P = length(df$z)
    n_O = sum(df$w)
z_P_bar = mean(df$z)
    z_O_bar = sum(df$w*df$z) / sum(df$w)
omega_z1 = mean(df$omega[df$z==z1])
omega_z2 = mean(df$omega[df$z==z2])

# Parental population size:
n_P
# Offspring population size:
n_O
# Parental mean trait:
z_P_bar
# Offspring mean trait:
z_O_bar
# Realtive fitnesses:
omega_z1
omega_z2

Here is a simple example using your data in which both terms of the Price equation are needed, since the value of the character for $z_2 $ changes in the second generation. I used your suggested change $z_2'=(9\cdot 2 + 1\cdot 3)/10 = 2.1$.
The Price equation or theorem is:
$$(1)\hspace{10mm}w\cdot \Delta z =  \text{cov}(z_i,w_i) + E(w_i\Delta z_i)  $$
While the idea here is just to give a credible calculation using both terms in the right side of the equation, and while the intuition behind the equation is essentially mathematical (or is it? $^1$), Steven Franks' paper, 'George Price's Contribution to Evolutionary Genetics', J. Theor. Biol. 175 (1995), 373-88, is a good introduction. His characterization of the right side may be the best one can do:

"The two terms may be thought of as changes due to selection and transmission, respectively. The covariance between fitness and character value gives the change in the character caused by differential reproductive success. The expectation term is a fitness weighted measure of the change in character values between ancestor and descendant. The full equation describes both selective changes within a generation and the response to selection..." p. 376.

We work with reference to the following data and will define variables below.
$$\begin{array}{c | c | c | }  n_i & 3 & 2  \\ \hline
z_i &1  & 2  \\ \hline
w_i &1& 5   \\ \hline
n_i' & 3 & 10  \\ \hline
z_i' & 1 & 2.1  \\ \hline \end{array}$$
All cites WK are to the Wiki page on the Price equation:

(1) We can write $\text{cov} (w_i, z_i)$ as $E(w_iz_i) - wz.\hspace{10mm}$ WK eq. (7).
Explicitly:
$$ \text{Cov}(w_i,z_i) = E(w_iz_i)- wz = \frac{ w_1z_1n_1 + w_2z_2n_2}{n_1+n_2} - wz $$
$$ = \frac{1\cdot1\cdot3 + 5\cdot2\cdot2}{3+2} - (2.6)(1.4) =\frac{23}{5} - (2.6)(1.4)= 0.96$$

(2) We can write $E(w_i\Delta z_i) = E(w_i z_i') - E(w_i z_i).\hspace{10mm}$ WK eq. (8).
Now $E(w_i z_i') = \frac{1}{n}\sum w_iz_i'n_i\hspace{40mm} $ WK eq. (9a).
$ = \frac{1}{2 + 3}(1\cdot 1\cdot 3 + 5\cdot(2.1)\cdot 2) = 24/5.$
$E(w_iz_i) = 23/5$ from (1) above.
So  $ E(w_i z_i') - E(w_i z_i) = \frac{24}{5} - \frac{23}{5} = 1/5$

(3) Finally we have $\Delta z =  z' - z = \frac{2.1(10) + 3(1)}{13}-\frac{3\cdot 1+2\cdot 2}{5} = \frac{29}{65} $
and $w = \frac{3\cdot 1+ 2\cdot 5}{3+2} = \frac{13}{5} = 2.6$
So $$w \Delta z = (2.6) \frac{29}{65} = 1.16 $$
$$= \text{cov}(z_i,w_i) + E(w_i \Delta z_i) = 0.96 + .2 = 1.16 $$

$n_i$ is the number of elements in group $i.$
$n_i'$ is the same for the filial generation.
$z_i$ is the value of a character for group $i.$
$z_i'$ is the same for offspring of $z_i.$
$w_i$ is a fitness weight, often the number of offspring an element $z_i$ will have.
$w$ is the average fitness for the parental generation.
$z$ is the average value of z for parental generation;
$z'$ is the average of z for the filial generation.
$z_2' - z_2$ (for example) is the average value of $z_2$ in the second filial
  generation minus the average of $z_2$ in the parent's generation.

$^1$ This site condenses some critical discussion of the Price equation. I have not worked through it yet but it addresses some lingering doubts I have about just what this equation means. Strongly recommended.

Thanks - I've worked that out using my R script & got the same answer! I know it was not in the original question but could you help explain the second term on the RHS ($E(wiΔzi)$) which shows the transmission bias. Perhaps if I said that one of the $z$=2 parents has 4 offspring where $z$=2 and one where $z$=3, the other $z$=2 parent has 5 offspring of $z$=2.

This example only furnishes the requested calculation but there is no functional relationship between the trait z and fitness w. A more instructive example would be Wiki's note on 'altruism' at the linked page.

This is a nice numerical walk-through and explanation, see this webpage.
As requested I've sketched out a solution to the specific case above.
A nicer way for caclulations is to rewrite the price equation as:
$$ \Delta z = Cov(w_i/\bar{w}, z_i) +E(w_i/\bar{w}, \Delta z_i) $$
So lets draw out some important terms.
In the current population average for $z$, the average trait value in the second generation $z'$  and, the average relative fitness of the parents $\bar{w}$ are:
$\bar{z} = 1.4$
$z' = 1.769$
$\bar{w} = 0.2002$
So we an brute force the $\Delta z$ by doing $1.769-1.4 = 0.369$. However we shall also show this using the price equation (note for sample data the correction is $n-1$ not $n$ as shown below).
$Cov(x,y) = ((x_1 - \bar{x})*(y_2 - \bar{y})+(x_2 - \bar{x})*(y_1 - \bar{y})+ ... (x_n - \bar{x})*(y_n - \bar{y}))/n$
Using the data provided we can say:
$Cov(w_i/\bar{w}, z_i)= ((3 * (0.077 - 0.2002)*(1-1.769)) + (2 * (0.385-0.2002)*(2-1.769)))/5 = 0.07392 $
This is a per capita change. $0.07392 * 5 = 0.3696$ (rounding error).
Expectation
So the OP identifies a situation where transmission effects are non zero. Lets just consider that the mutation that causes z=2 is a  super-synergistic and causes its offspring to be z=4. The expectation term in this case is:
$E(w_i/\bar{w}, \Delta z_i)= ((w_4/\bar{w})*(z'_4-z_4) + (w_5/\bar{w})*(z'_5-z_5)) /5$
I've ignored the first 3 individuals because the transmission effect will make their terms 0 (1-1=0).

Thanks for sharing @Sanalphatau. Rather than providing a link-only answer, we typically ask community members to provide a brief summary or excerpt of the salient point(s) from the linked material (see http://biology.stackexchange.com/help/referencing). If for any reason your link gets broken in the future, this answer would become useless without any additional info.

Thanks, I'll take a look shortly (@DanielStandage raised a good point so perhaps you would like to elaborate on the answer). I've also edited the question so that it makes a greater attempt to draw fuller answers.

Apologies, not very well versed with the guidelines. I'll read through and update my answer in the coming day or two (so its more stand alone).

Thanks @Sanalphatau - I look forward to it. If you can then it would be good if you could help me solve the above problem, I think this would help me get my head around it, my main confusion is just knowing which numbers to use where

The first part of your calculation agrees with part (1) of my answer above (divide cov by w = 2.6). Your calculation works but I think by definition $\bar{w}= (1/[n_1+n_2])(w_1 n_1 + w_2 n_2).$ If you finish the second part and show the two sides equal I would upvote. OP added the second part after he got the first part.


text:
Why do we squint when tasting very sour things?
Sometimes while tasting a very sour thing (like tamarind, lemon etc.) our eyes squint immediately and involuntarily for a second, but a little later becomes normal again.
Why, and how, does this reflexive movement occur?

Maybe it serves to show others that we may be consuming something poisonous. We cry when we are sad to alert others of our distress. There may be better ways to show something is poisonous, but a child doesn't have any real way to alert who ever is feeding it that it may be poisonous. If I was feeding my baby something, and they had that reaction, I would not give that to them again.

This is basically a "just-so story", not a real explanation.

Short answer
Adverse stimuli in general are accompanied by contraction of facial muscles. It is part of our repertoire of emotional expressions.
Background
A disgusted expression and the expression of pain are both accompanied by squinting. Disgusting stimuli include your example of a sour taste, but also include other adverse tastes (bitter) or visual stimuli such as a gross-looking objects. In other words, squinting is likely a common way of expressing adverse stimuli. So the "sour look" may not be easily explained on its own. Instead, it is part of a huge emotional expressive repertoire that makes us human beings. To be able to read these expressions allows us to be empathetic towards others. People with autism and Asperger's syndrome may not be able to do so and are disadvantaged in their social behaviors.
To illustrate the commonalities between sour (#1), disgust (#2) and pain (#3) I would like to share the following web finds.

Sour taste. Source: Getty Images
!
Disgust. Source: Berkeley Emotional IQ test

Pain. Source: Berkeley Emotional IQ test
PS: I am not a psychologist - Consider my contribution as an educated guess.

Squinting is the organism's way to warn us that we are eating something that could eventually be dangerous, acidic or toxic. It's a reflex, developed many many years ago when the ancient people did not know much about the safety of plants, roots and other foods. They used to try them and decide if the object is eatable or not according to its taste.
Also, our tongue has very sensitive papilla, which react to sourness and make the muscles contract.

Do you have a reference, by any chance?

No, actually this particular question was brought during biology lessons a few years ago and I just remember my teacher's explanation.

This is completely unsubstantiated. There was a (now deleted) answer by @Brendon that makes much more sense: fungiform papillae are innervated by the VIIth cranial nerve. Squinting is most probably a side effect of the activation of this nerve. Whether there is an evolutionary advantage to it is debatable, although for sure there does not seem to be any obvious disavantage.

@nico If it weren't advantageous I can't see why it would appear in all (or almost all) of the human population - surely it'd be like the ability to roll your tongue?

@AndroidPenguin: I am just saying that I see no proof that it is there because it has an advantage. It could be there just because it has not be selected against, which is a different thing. The answer gives no proof either way.

This doesn't even make sense.  The sensation of a sour taste already serves as a warning.  How would squinting help?


text:
What species is this large-ish spider?
Last night I came across this spider outside my house (costal Southern California). It was bigger than any I'd seen before, about 2.5 or maybe 3 inch legspan, maybe just under an inch for the body length. It is a brown-gray color, the cephalothorax has two dark brown stripes, and some mean looking fangs. Can anyone identify it?

Yes, it's definitely an adult male Agelenid - one of the funnelweavers.  More specifically, one of the outdoor species known collectively as Grass Spiders.  The nice long exhaust-pipe spinnerets at the back tell you that, and the racing-stripe pattern on the body.  The big boxing-glove palps hanging in front of the face tell you it's an adult male, which is why it was wandering around looking for love.  I'm not familiar with the California species, but this is probably one of the western Agelenopsis species.
https://bugguide.net/node/view/2001


text:
What is the difference between the Ureter and Urethra? also between the Renal papilla and Renal pelvis?
Differentiate between the following:

Ureter and Urethra
Renal papilla and Renal pelvis

It is not given in my book.
Please help.

Yup, it is. But it is not given in my book. So I needed help.

@siddhu99 See our homework policy for reasons your question may have been downvoted.

overall though, homework is okay though.

The ureters run from the kidneys to the bladder whilst the urethra runs from the bladder to exit the body:

The renal papillae are the site where urine drains into one of the minor calyxes of the kidney.   Multiple minor calyxes join together into a major calyx, and multiple major calyxes join together to form the renal pelvis which then drains into the ureter.


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Genetic Epistasis Question
I need help with this practice question.

I'm assuming that would a epsitatic recessive question since the parents are true breeding and then the ratio would be 9.3.4. But I am not so sure.
Any help would be greatly appreciated thanks!

The answer to the third question should be recessive epistasis.

The Magenta variety is pure breeding, and hence must be homozygous at both loci, (Dominant at Gene A and recessive at Gene B), otherwise, in some of the generation along the family line, there would have been a non-magenta flower, which contradicts the pure breeding nature. But the same cannot be said for the pure breeding white variety, as it can still be homozygous recessive at Gene A and heterozygous at Gene B, it would still exhibit white flowers in all of its progeny after any number of generations.
But the fact that all the progeny of the cross between white and the magenta variety turns out to be red, removes the possibility of the white variety being heterozygous, as that would have produced atleast some magenta plants. Since all were red, we can be certain of the genotype of both the parents, and consequently of the F1 progeny.
This solves your first question. The second question needs the extrapolation of the information gathered while solving the first question into a Punnett square and a simple probability calculation. The third question is a factual question, but it must be mentioned, that this particular type of interaction can be classified under more than one type, and hence a single answer would not be possible for your third question.
ADDENDUM
The third question is actually a bit difficult to answer. The phenotypes will be $\text{A*B*}$=Red, $\text{A*bb}$=Magenta, $\text{aa**}$=white. This gives us $9:3:4$ for Red:Magenta:white. Now the fact that recessive at one locus , Gene A, suppresses the phenotype altogether no matter what the genotype at the other locus, means that one of the phenomenon exhibited is recessive epistasis, where Gene A is the epistatic loci and Gene B is the Hypostatic loci. But, the fact that there are two distinct phenotypes with the epistatic gene dominant, means the interaction is not complementary ($9:7$) but is supplementary ($9:3:4$). This distinction is necessary, and it essentially means that the "intermediate" of the elucidated pathway is also coloured. Otherwise, like in Flower colour in Lathyrus Odoratus, the phenotypes of $\text{aa**}$ and $\text{A*bb}$ are same, and hence the phenotypic ration remains $9:7$. For a ratio of $13:3$ you need domianant epistasis and the phenotypes of double recessive and the epistatic recessive must match. Here, it is recessive epistasis, as the recessive condition at one locus suppresses the expression a other, and not dominant. Feel free to seek further clarifications or simplification.

Thanks for the answer Satwik. Really appreciate it but stil for question 3b, i understand that if the F1 are self-crossed then that would yield a 9:3:3:1 ratio I also understand that there are a number of deviations from that ratio depending on the interaction. I'm assuming it might be a 9:3:4 ratio but I'm not sure since others are also reasnable. What deviation do you think is the correct one?

Also, just to confirm for question d, if we cross BbDd and BbDd and end up with BD, Bdd, bbD, bbdd, then those carrying a dd would not be expressed and only those with with Bdd can produce the phenotype concerned, then that would be dominant suppression interaction? is that true and the ratio then would be a 13:3?? Thanks in advance

@ApothemCyte See the addendum in my answer

The way I understood the problem is like this.
a) The parents are said to be pure bred so we can assume that both parents posses homozygous for each of the traits. Hence, the genotype for both are:
P1: Magenta AAbb x aaBB White
So this will result to all F1 consisting of Red flowered phenotypes (AaBb)
-since the absence of gene A will not code for the magenta intermediate, it's fine to activate gene B because this will not work without gene A.
b) the ratio that will be observed on the F2 generation are:
9 red: 3 magenta: 4 white
c) the interaction of the genes pertains to recessive epistasis. The following ratios are constant for each of the epistatic interaction:

Dominant epistasis: 12:3:1
Recessive epistasis: 9:3:4
Double Dominant epistasis: 15:1
Double recessive epistasis: 9:7
Dominant-recessive epistasis: 13:3


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Write the haplotypes of the family
I'm doing old exam assignments to prepare for my finals on Monday and I've stumbled on one assignment that I'm not sure how to tackle.
A family with 2 children is examined for cataracts using PCR with 4 markers, A, B, C and D. The results are seperated on a gel and the genotypes are as follow:

Where Far = father, Mor = mother, Barn = child.
Notice that there was an error with the analysis so child 2's alleles are undetermined.
The question states: Draw a pedigree with each of their haplotypes. What is the most likely haplotype of child 2?
I don't understand exactly what it's asking. I'm not sure what a HAPLOtype is. I know what a genotype is and that is what the answer seems to indicate.
The answer for the father is: 4 3, 1 2, 11 5, 7 4. Now the only difference between these numbers and the given numbers are the re-arrangement of 5 and 11 in marker C?

The first paragraph of the Wikipedia article should help - it's the combination of alleles inherited from one parent i.e. on the same chromosome. It derives from haploid genotype.

I still don't understand the assignment. What do the numbers mean exactly? Are they related to this picture and if so what does each number represent in terms of letters on the picture?
http://i.imgur.com/0yiiBrP.png

all you need to solve the problem is to know they indicate different marker alleles. The alleles could be due to a variable number of repeats at the loci (see microsatellites and variable number tandem repeats on Wikipedia for examples if you are interested), but that information is not necessary to solve the problem. On your picture, the markers could be any of the alleles.

Why do they occasionally switch between the numbers when writing the haplotypes?
In the diagram the father has:
3,4
1,2
5,11
4,7
But the answer for the haplotype is
4,3
1,2
11,5
7,4
Why is the 11 and 5 re-arranged when telling his haplotype? This is pretty much the only thing left that confuses me.

I think that is supposed to mean 4, 1, 11, and 7 are on one of his chromosomes, but I've not seen it written that way before (or I don't remember it). I am not sure how you can figure out the parental haplotypes in this case, either. You can figure out which alleles are inherited by each child from each parent (the child haplotypes), but I don't think this would give you the parent haplotypes, unless you are assuming meiotic recombination does not occur. (eta: I haven't worked out the problem yet)

Definition of Haplotype
The concept of haplotype has the default to be subject to several definiton that differs mostly by their complexity to be understood and by their specificity but different definitions also sometimes differ slightly in their meaning.
In simple terms the concept is pretty easy. A haplotype is a porte-manteau word of haploid genotype and it refers to half the genotype.
What the question is asking
The question is asking is Here is half of the genotype of the child, what do you expect the other half to be?. Note however, that for the last two markers, the first haplotype is not indicated so they are just asking for the genotypes here which makes the question slightly poorly phrased IMO.
The answer key
The answer concern the father, which is silly as the question is about the child. So the answer you stated definitely does not answer the question.
The answer
We have to look marker per marker to answer the question and then consider them all together to reconstruct the haplotype. In absence of information on the subject, we are going to assume that the markers are completely independent (unlinked, eventually on different chromosomes). We will also assume no mutation (probably negligible anyway) and we assume no crazy kind of inheritance such as some selfish elements. You will note also that information about the first child tells nothing about the second child.
Marker A
The first allele inherited necessarily comes from the mother and therefore, the second allele must comes from the father. As a consequence the second allele is either 3 or 4 with equal probability.
Marker B
The first allele inherited necessarily comes from the father and therefore, the second allele must comes from the mother. As a consequence the second allele is either 1 or 4 with equal probability.
Marker C
The four possible genotype are [5,7], [5,11], [11,7] or [11,11], that all occur with equal probability. This means that for Marker C, at one haplotype, the probability of being 5 or 7 is $\frac{1}{4}$ and the probability of being 11 is $\frac{1}{2}$.
Marker D
The four possible genotype are [4,7], [4,8], [7,7] or [7,8], that all occur with equal probability. This means that for Marker D, at one haplotype, the probability of being 4 or 8 is $\frac{1}{4}$ and the probability of being 7 is $\frac{1}{2}$.
Whole Haplotype
From the above, you can compute all possible haplotypes and calculate the most likely to occur. However, there are some ties. The most likely genotypes are (3,1,11,7), (3,4,11,7), (4,1,11,7) and (4,4,11,7) that could occur with probability $\left(\frac{1}{2}\right)^4 = \frac{1}{16}$.


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Why is it $q^2$ for the individual count in hardy weinberg?
My understanding:
In Hardy-Weinberg problems the frequency of a homozygous recessive genetic occurrence in a population is $q^2$. So if 1 in 100 people in a population have albinism (homozygous recessive disorder) then we say the frequency is $q^2=1/100$.
We then say, to find the frequency of the allele count $q$ that $q=\sqrt{1/100}= 1/10$.
I don't understand why we say this. Why would the allele count be the square root of the population frequency? There's 2 alleles per person. Why isn't it x2 or /2 instead?
I suppose my problem is understand what exactly is p and q.

p and q are allele frequencies. Did you search anything about Hardy-Weinberg equilibrium.

Yes but I'm having problems seeing why why square them.

Squaring is for genotypes.

This seems a very nice site: http://www.nature.com/scitable/definition/hardy-weinberg-equation-299. I'm not answering this because it's too long ago I took this class, but Nature has awesome basic explanations of a lot of stuff. And it's credible. Check it out!

WYSIWYG you're not understanding the depth of my question.
I think this may actually be too mathematically difficult to answer on biology stackexchange upon further examination.

@paze If you think so,you are dramatically overestimating the difficulty of this question.

Could you answer it then please?

Okay . If p is probability of allele-A then what is the probability of A mating with another A; p×p=p²

First of, let me correct your equation: $q = \sqrt{\frac{1}{100}} = \frac{1}{10} = 0.1 ≠ 10 $.
From allele frequency to genotype frequency
Imagine you were to randomly sample an allele from a population of allele where the allele A is present at frequency $q$. What is the probability that you draw allele A? Answer: $P(A) = q$. Now, put this allele back in the pool and imagine you have to draw two alleles. What is the probability that the two alleles are A. Well it is the probability that the first allele is A times the probability that the second allele is A, it is $P(A) \cdot P(A) = q \cdot q = q^2$.
From genotype frequency to allele frequency
Therefore, under Hardy-Weinberg conditions, if the allele A is at frequency $q$, then the homozygote genotype AA is at frequency $q \cdot q = q^2$. Now let's denote the frequency of the genotype AA by $f_{AA}$. You know that $f_{AA} = q^2$ from the above though experiment. If you take the square root of both sides, you get $\sqrt{f_{AA}} = \sqrt{q^2} = q$. In words, the frequency of the allele A is the square root of the frequency of the genotype AA.
Recessivity and dominance
Btw, you'll note that those calculations tell nothing about the patterns of dominance/recessivity of alleles (Hardy-Weinberg principle assumes no selection anyway).

also 1/100 != 1/10

Ha ha oops. I forgot the square root. Thank you!

To understand population genetics and the Hardy-Weinberg equilibrium you first need to clearly separate genotype frequencies (the frequency of individuals in a population having a genotype) and allele frequencies (the frequency of an allele in the population gene pool). In your question p and q represents allele frequencies, while p2, q2 and 2pq represents genotype frequencies (if $p=P(A)$, $p^2$ is $P(AA)$). Genotype frequencies can be thought of as the probability that two particular alleles are located in the same individual, and the calculation of these probabilities is a simple application of the multiplication rule of probabilites for independent events.
Therefore, if the allele frequency p is 0.2 the probability of having two copies of this allele is $p \times p = p^2 = 0.2^2 = 0.04$. If there are only two alleles in the population, q has to be 0.8, which means that the other two genotype frequencies are $ 2pq = 2\times0.2\times0.8 = 0.32$ and $ q^2 = 0.8^2 = 0.64$. As you can see, these genotype frequencies also sum to 1, since they represent the genotypes of all individuals in the population,

In Hardy-Weinberg problems the frequency of a homozygous recessive
  genetic occurrence in a population is q2.

Sort of but not quite. If the locus has two possible alleles, $A$ and $a$, the frequency of each allele in the population is $p$ and $q$ respectively. If the population size ($N$) is 500 diploid individuals, there are 1000  loci ($2*N$, because of diploidy) which each could have either $A$ or $a$, and each of the 500 individuals could have the genotypes $AA$, $Aa$, or $aa$. If we know that the population of loci has 100 copies of $A$ then $p = 100/1000 = 0.1$, and $q$, the frequency of $a$, must then be $1-p = q = 0.9$.
The value of $q^2$ tells us how many individuals in the population, under the assumptions of HWE, will be of the genotype $aa$ - it says nothing about the recessivity (or dominance) of the allele, nor the phenotype. In the example above, $q^2 = 0.9^2 = 0.81$ - under assumptions of HWE 81% of the population will be genotype $aa$.
In terms of math it is simple probability theory. If we have a bag of coloured marbles, 5 red and 5 blue, the frequency of red ($p$) is 0.5, and blue ($q$) is 0.5. If we draw one marble from the bag, the probability of the marble being blue, $P(blue)$, is equal to the frequency of blue, $q$, which is 0.5. If we then return the marble to the bag and make a second draw, the probability of drawing a blue marble is again $b$, 0.5. The probability of both of the drawn marbles being blue $P(blue) * P(blue) = 0.5 * 0.5$, or $q^2$. The probability of drawing one red and one blue is $2 * p * q$, and probability of two red marbles is $p^2$.


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Gene frequency problem
1/330 of white people in south Africa have a disease called Porphyri.
What is the frequency of the gene if it is inherited autosomal recessive?
This one I understand. The genotype frequency is $q^2 = 1/300$ so the gene frequency has to be $\sqrt{1/300}$ as it is inherited aa.
What is the frequency of the gene if it is inherited autosomal dominant?
Here's where I run into trouble. So if $p$ is the dominant allele and $q$ is the recessive allele the allele frequency has to be $2pq+p^2$ right? As we can either see them as $Aa$ or $AA$
But my book says it is $2pq+q^2$ and then solves it algebraically by pretending $q^2$ is so close to 0 that it's not in the calculations. I strongly disagree that $p^2$ is very small if I am right with my assumption. Which one is right and why?

I think you pretty much nailed the problem. If I understand correctly, you are just confused about the approximation that your textbook does, an approximation that is correct but not needed. Let me restate the solution to the problem first.
Resolution of the problem
As you said the frequency of sick people $\frac{1}{300} = 2pq + q^2$ in this case, where $q = 1-p$ is the frequency of the (dominant) allele causing the disease. It is a simple quadratic equation with one unknown so one doesn't even need to make any approximation to solve for $q$ (or for $p$). Rearranging the equation and expressing $p$ in terms of $q$ (p=1-q), you'll find that $q ≈ 0.00167$.
Are the results intuitive?
Note that the frequency needed to create a frequency of $\frac{1}{300}$ sick individuals is $\sqrt{\frac{1}{300}} ≈ 0.05$ if the allele causing the disease is recessive while it is only about $0.0016$ (31 times less frequent) if the allele causing the disease is dominant. It shows that indeed a lower frequency of a more dominant allele is enough to create more sick people.
Is the $q^2$ term negligible?
Given that $q ≈ 0.00167$, the term $q^2 ≈ 10^{-6}$, while the term $2pq ≈ 10^{-3}$. So, indeed the term $q^2$ is rather negligible compared to $2pq$.

You write 1/300 = 2pq+q^2 like my book. I say that it's 1/300 = 2pq+p^2 because p is the dominant allele and 1 out of 300 people has Aa or AA. 2pq + p^2. I don't understand why you have +q^2 in the end as we're not counting the recessive aa's ?

It is just a matter of what you want to call q and what you want to call p. They are totally interchangeable. In my example, I called q the frequency of the dominant allele causing the disease. But if you feel more confortable the other way around, you can call p the frequency of the dominant allele causing the disease.

Ah, okay, I thought it was the norm in literature to denote p as the dominant allele and q as the recessive allele, but I guess I am wrong. Thank you.


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Do women have testosterone?
In a documentary on fitness I saw it was stated that women can't get big like men because of their low concentration of testosterone. If it is true that women have testosterone, where is it made? Why do some women, especially later in life, develop facial hair (though obviously not as much as men)? Do men also have "female" hormones in their body?

Yes, they do. The ovaries produce both testosterone and estrogen. Relatively small quantities of testosterone are released into your bloodstream by the ovaries and adrenal glands. Sex hormones are involved in the growth, maintenance, and repair of reproductive tissues [1].
The serum testosterone level in women with no acne, hirsutism, or menstrual dysfunction is 14.1 +/- 0.9 ng/dL (nanograms per decilitre) [2]. An average adult man has 270-1,070 ng/dL serum testosterone [3].
Men have female sex hormones too. For a prepubescent male, estrogen levels are expected to be between 1 and 3.7 ng/dL. During puberty, normal levels fall between 2.3 and 8.4 ng/dL. Levels for an adult male should be between 2.5 and 5 ng/dL [4].

References:

WebMD, LLC. Normal Testosterone and Estrogen Levels in Women.
Ayala C, Steinberger E, Smith KD, Rodriguez-Rigau LJ, Petak SM. Serum testosterone levels and reference ranges in reproductive-age women.
Alexia Severson. Testosterone Levels by Age. Healthline Networks, Inc.
wiseGEEK.com. What Are Normal Estrogen Levels in Men? (Measurements cited in picograms per millilitre, converted to ng/dL)

Two comments. The first is that you gave a good comparison of testosterone in men vs women. But you only gave the amount of estrogen for men and in (slightly) different units from testosterone, thus marring an otherwise great answer.

Healthy young males have estradiol levels in the area of 20-30 pg/ml.
Also, estrogen is a group of hormones, including estradiol and estrone for example. You shouldn't think of any hormones as women hormones or men hormones really, as both genders have them all, albeit in different proportions, and generated often through different pathways/organs.
this link is the best i could find within a few seconds of a google search:
http://emedicine.medscape.com/article/273153-overview
it will really describe where and what hormones are created where and in what quantities, as well as how and where they can convert within the body into more potent steroids.


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Genetic Diversity and Adaptation
I am somewhat new to evolutionary biology, having studied it on my free time as a computer science student.  There is one particular thing that has always bothered me for which I have not seen a good treatment, relating to adaptations to the environment with respect to genetic diversity.  If it is possible for a population to adapt to rapid environmental changes, and they don't have an adaptation for dealing with change directly (such as a complex brain), it seems to me that every generation must have present within them almost every possible environmental adaptation that the population is capable of expressing (including many irrelevant ones and a few relevant to the particular environmental challenge).  Otherwise, it may take too many generations to deal with a change, which may be disastrous for the population.
So my question would be: how does an evolutionary biologist explain the mechanics behind the ability for a population to adapt quickly?  Are most environmental changes slow or gradual enough that the population has a few generations to happen upon the mutations that will allow it to survive, and have generally been successful in this regard for 3.5 billion years?  Or, are a large majority of possible adaptations present in almost every generation, and just serve no purpose or advantage for most of the population if the provided "benefit" is unneeded (i.e., are effectively neutral)?  Or something in between?

Yes, yes, and yes. And a too quick environmental change can kill a whole population, it happens all the time. (we at least hope so when we're infected with bacteria and give them hell)

I like the example of moth species that turned black duing the coal powered industrial age. all the cities were black... the black pheno appeared everywhere within 100 years. simple adaptions can appear in a few generations. The species doesn't change environments suddenly, they push towards new locations and if they change is too extreme, they die, so there is a balance. The planet is full of very stable environments with gradual transition times and extents.

It is a good question. The question is hard to answer though because

The answer is not completely resolved
There are many influential parameters hidden behind this question.

Your question, as I understand it, can be formulated as

Do natural populations have enough genetic variance to directly respond to an environmental change or do they have to wait for this variance to be created through mutations?

To address this question, I will have to assume you have some intermediate level of knowledge in evolutionary biology.
How do we call these two alternatives?
Adaptation can occur through selection on:

Standing genetic variance
De novo mutations

How can we tell them apart?
This section is mainly inspired from Barrett and Schluter (2008).
Adaptation from standing genetic variance and from de novo mutations tend to yield different genetic signature.
In comparison to de novo mutations, adaptation from standing genetic variation is likely to lead to

Faster evolution

Because there the respond to the new environmental is immediate, there is no need to wait for more mutations.
Because the fitness variance associated with the trait under selection is very low even when the first mutation occurs.

Fixation of more alleles of small effects.

Because phenotypic variance is alleles of large effects are likely to be deleterious in the previous environment and would therefore be purged out of the population quite quickly
Because, if adaptation occurs from de novo mutation, it is likely that only few mutation would have occurred that would allow adaptation

Spread of more recessive alleles

Because recessive alleles can reach a relatively high frequency in the previous environment even if deleterious in the homozygote mutant.
Because recessive alleles represent little to no fitness variance at low frequency and are therefore likely and it would therefore take much time for adaptation to occur from recessive alleles if they just appeared through de novo mutations.

You will note that my explanations are non-exclusive and are overlapping. They all boil down to

Loci causing high fitness variance in the previous environment are unlikely to be source of adaptation from standing genetic variance
Loci causing high fitness variance in the new environment are likely to cause adaptation.

If you have a hard time to understand these concepts, then you might want to have a look at Fisher's fundamental theorem, Mutation-selection balance and eventually follow some intermediate level course on the mechanism of natural selection.
Which mechanism is more common?
Do most adaptation occurs through selection on de novo mutations or through selection on standing genetic variance? This question is very hard to answer. It depends on

Type of adaptation
Population of interest

1. The type of adaptation
The answer is likely to differ depending on whether we are talking about

adaptation to a changing environment over the whole species range

How fast is this environment changing is important too as you noted in your post.

A single population that detach from the rest of the metapopulation to slowly colonize a new environment
Adaptation to a universally (independent of the environment) beneficial trait
Coevolutionary process
etc...

2. The population of interest
Different populations retain different level of genetic diversity. This level of genetic diversity depends on

Demographic parameters

such as the population size and its variation through time

Evolutionary history

Such as the number of recent selective sweep

Environment

Such as the diversity of environments present over the range of the species
Such as temporal variations

Genomic architecture

Such as the presence of strong epistasis that could cause large amount of hidden genetic variation (see for example Hermisson and Wagner, 2004) and the eventual "revelation" of this previously hidden genetic variation through new mutation or a new environment (see for example La Rouzic 2008).

Example
Three-spined sticklebacks are present in salt water and fresh water. They occupy several geographically isolated bodies of fresh water (connected by salt water). All populations present in fresh water environments show similar phenotypic traits. We have first thought that sticklebacks have adapted repeatedly to this freshwater habitats (repeated evolution) through de novo mutations. However, some papers suggest that, as the marine population of sticklebacks is so big, that it is possible that there is standing genetic variation for these traits that are selected for in freshwater habitats. Below are some papers of interest

Jones et al. 2012, The genomic basis of adaptive evolution in threespine sticklebacks
Feulner et al. 2012, The genomic basis of adaptive evolution in threespine sticklebacks
Colosimo et al. 2005, Widespread Parallel Evolution in Sticklebacks by Repeated Fixation of Ectodysplasin Alleles

Great question! A lot of things affect how quickly a population or species can adapt to a new environment, including population size, mutation rate, generation time, standing genetic diversity, and selective pressure.
The diversity of life encompasses practically all combinations of those variables. A bacterial population might very well contain enough diversity to allow a portion of the population to overcome a rapid change. In fact, applying antibiotics to a bacterial population and counting the survivors is a common measure of mutation rates.
On the other hand, organisms with small populations and long generation times will be much less likely to overcome a rapid environmental change. This is why there is so much concern over anthropogenic changes to the environment, including climate change.
It's hard to provide a definitive answer, since "rapid change" is a relative term, and the difficulty of adapting isn't known. Some striking adaptations can be caused by a single base pair mutation, such as in beetles and Monarch butterflies that are insensitive to toxic plant compounds.
It's important to point out that natural selection is based on relative fitness. Therefore, an adaptive mutation will spread because it's likely that carriers will be more fit than all of their neighbors. This does not necessarily mean that individuals without the mutation will die or fail to reproduce, only that those with the mutation will do it better.
Likewise, adaptation is not necessarily caused by the environment changing and wiping out all but a few lucky mutants like in the bacteria example. Instead, the environmental change might make things more difficult, but as long as the population can persist, then mutations will continue to enter the population which could confer a selective advantage against the change. So, no, a population does not (cannot) carry all possible adaptations. A population cannot adapt to an environment it hasn't encountered.
Finally, it's worth pointing out that a species can expand its range through migration. A new, unsuitable environment can act as a migration sink (that is, migrants make it there but fail to establish) for a nearby population. If this happens for long enough, some of the migrants may have a mutation allowing them to establish in the new environment.

Selection and the process of adaptation
The genetic variation for fitness is the determinant of how rapidly adaptation can occur. This is summarised within what is known as Fisher's Fundamental Theorem:

The rate of increase of fitness of any species is equal to its genetic variance in fitness

Adaptation is process resulting from two components, selection and genetic variation. The importance of genetic variation is captured by the breeders equation, where the magnitude of the adaptive response, $\Delta \bar{z}$, is the product of selection, $\beta$, and genetic variance, $G$:
$\Delta \bar{z} = G \beta$
If there is no genetic variance in fitness, there can be no adaptation. This is because adaptive evolution relies on the ever changing genetics of a population. If there is no variance in the parental generation, then reproductive variance (different reproductive success among individuals of the parental generation) will not affect the frequency of alleles. Adaptation occurs because reproductive success is connected to an individual's genotype. Selection can produce a response by acting on standing genetic variation, or by acting on novel genetic variation such as that introduced by mutation.
If an environment changes rapidly, a rapid response can occur, so long as there is enough genetic variance to allow a response. For example, a shift in the environment acted on genetic variance in the Galapagos Finches causing rapid adaptation in to multiple niches. Otherwise, when there is insufficient genetic variance, species will struggle to adapt, as is likely to occur with ongoing rapid climate change, and in the future for species which are going through genetic bottlenecks. Any cases where selection is too strong for prolonged periods will result in extinction of the population by a failure to adapt. For example, by application of antibiotics to bacterial infections, if there are no members of the affected bacterial population which carry resistance genes then the population will be wiped out, but if there are resistant individuals then the population will adapt (only resistant individuals will continue to reproduce).
You may wish to read further on Fisher's Geometric Model of Adaptation, including this paper, and Mutation-Selection(-Drift) Balance. Here's a good paper on the quantitative genetics of adaptation.

It is clear that climate-driven evolution has molded plants in deep time and within extant populations. However, it is less certain whether adaptive evolution can proceed sufficiently rapidly to maintain the fitness and demographic stability of populations subjected to exceptionally rapid contemporary climate change.