text:
How is eye color in humans inherited?
In high school we studied the inheritance of eye color, as it was explained to us in the most simple way: blue eye color is a recessive, monogenic, autosomal trait. Now I know that it is a bit more complicated than that; there are several genes which determine the inheritance of eye color. That's as far as I my knowledge goes.
Which are these genes and what do they encode for? How is the eye color trait inherited? Provided that a man with blue eyes and a woman with brown eyes have a child, can the probability of their child to have blue eyes be calculated?

It is mainly determined by the OCA2 gene, but it also likely involves several other genes, including TYR, TYRP1, HERC2, and several others. To complicate things further, it is not a "mutant/wild type" trait, but multiple normal alleles can be found in the population, and it is believed that the sum of these single nucleotide polymorphisms (SNPs) determine the final phenotype.
I took the info from a 2004 review by Sturm and Frudakis and a more recent paper from Liu et al, 2009

This answer is so close to be good... why don't you expand a little on what those genes do and how they influence color? I know you linked the papers but it would be much nicer if the answer were self-sufficient. For instance you could say that OCA2 encodes for the P protein, a (supposed) Tyr transporter that allows Tyr, a precursor of the brown pigment melanin, to get into the cells.

@aleadam Thanks for your answer, it really looks promising, but I was about to ask you the same thing as nico did: can you please expand it and make it more clear and easy to read and understand?

omim might also be helpful: http://www.genome.jp/dbget-bin/www_bget?omim+227220

There is a nice page that tries to explain this:

The known Human Eye color genes are: EYCL1 (also called gey), the Green/blue eye color gene,
  located on chromosome 19 (though there is
  also evidence that another gene with similar activity exists but is
  not on chromosome 19). EYCL2 (also called bey1), the central brown eye
  color gene, possibly located on chromosome 15. EYCL3 (also called
  bey2), the Brown/blue eye color gene located on chromosome 15. EYCL3
  probably involves mutations in the regulatory region just before the
  OCA2 gene (which produces a protein that is expressed in melanocytes).
  A second gene for green has also been postulated. Other eye colors
  including grey and hazel are not yet explained. We do not yet know
  what these genes make, or how they produce eye colors. The two gene
  model (EYCL1 and EYCL3) used above explains only a portion of human
  eye color inheritance. Both additional eye color genes and modifier
  genes are almost certainly involved.

There is even an interactive calculator available.


text:
How many human proteins are very well characterized?
Following up on How many human proteins have a solved 3D structure?,is there a list of very well characterized human proteins / protein complexes?
My criteria for "very well characterized" includes, at least:

a high quality 3D structure
known activity in vivo
known associates in its activities in the cell
kinetics of its activity
regulatory elements for expression
etc..., and
(probably most importantly) a general consensus among experts that it is well described

This list would most likely include such proteins or protein complexes as:

P53,
polymerase alpha, and
the nuclear pore complex,

to name a very small number.

Don't you think that this question is a good match for bioinformatics community at SE, biostar.SE?

Sure, and I'll go see what's over there, too.  However, if there were a curated list of the kind described in the question, the answer to this question would fall squarely outside the domain of bioinformatics, except for whoever makes the list.

To address your list:

a high quality 3D structure: this you can easily get from PDB, using the answers to the question you linked as starting point. However, it is become increasingly clear that intrinsically unstructured proteins also play important roles in the cell, and for these you won't get a good 3D structure.
known activity in vivo / known associates in its activities in the cell: interaction partners can be found in databases like STRING, although just knowing the partners doesn't mean we understand what's going on :)
kinetics of its activity: I know of no good resource on this one except BRENDA for enzyme kinetics. But of course there are also kinetics to protein–protein interactions that would be interesting to know. (Update: There is AffinDB.)
regulatory elements for expression: there are databases like TransFac, but ChIP-Seq experiments show that we only know a tiny part of the regulation.

But, I think the key to a good answer lies here:

(probably most importantly) a general consensus among experts that it is well described

I would check how often the genes are described in the literature. The GeneRIFs from NCBI may be a good starting point, because these are snippets from the literature that are curated and shown on the NCBI Gene pages. E.g. p53 has >3800 of these. The length of the summary could also be a good proxy. (Or, the length of the Wikipedia page?)

Many of these questions can be answered by UniProt:

around 4,600 proteins with some 3D structure (this query)
of these 3,800 with annotated function in the Gene Ontology (this query)

source: Stack Exchange

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sort: votes


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If D1 receptors stimulate adenylate cyclase (through GPCRs) and D2 receptors inhibit it, then why do mutations in both have similar effects?
D1 and D2 both refer to specific types of dopamine receptors.
I'm sure it has something to do with the fact that the D1 receptors are in regions different from D2 receptors.
I know that adenylate cyclase usually triggers a signal transduction cascade that leads to increased cAMP+calmodulin, resulting in increased gene expression of proteins that help promote long-term potentiation of postsynaptic neurons (presumably lowering the absolute value of the voltage threshold that's needed to trigger another action potential, which increases neuron excitability).
But an increase in dopamine is going to cause more neuron excitability in postsynaptic neurons in some regions (those that have D1 receptors), and less in others (those that have D2 receptors). What then explains the fact that increased expression at all dopamine receptors can help modulate attention span?
I know that D3 and D4 are also involved, but they have to be either excitatory, inhibitory, or neutral.

Could you please split your questions into several ones? You currently ask 3 questions within the text and the question in the title seems to be the 4th question unrelated to the previous ones.

okay I've deleted the separate questions for now.

There are two problems with your hypothesis: 1) you cannot assume that the same receptor will be involved in the same process all over the brain and 2) you cannot assume that something as complex as attention span be the result of the action of only one receptor.

Okay - that's true. I think that would serve as the basis for a follow-up question about where D1 receptors are expressed relative to D2 receptors - I've asked it http://biology.stackexchange.com/questions/752/which-brain-regions-are-d1-dopamine-receptors-expressed-and-which-brain-regions.
That's also true, but changes to one receptor most certainly do affect attention span.

@InquilineKea: they probably do, but the result may be indirect and dependent on other factors. I do not know enough about that to give you a proper answer though

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text:
How do dopamine agonists like amphetamine/methylphenidate affect acetylcholine signalling?
Do they increase it, or is the effect mostly neutral?

In its current form, this question can be answered in one sentence by a simple Google search. Can you be more specific and expand your question?

Amphetamine and methylphenidate are not (direct) dopamine agonists.
Dopamine agonists are the substances that would specifically bind to dopamine receptors and activate them, thereby mimicking the effects of dopamine release.
Amphetamine/methylphenidate are so-called indirect sympatomimetics. This means that they stimulate the simpatyc nervous systems (with neurotransmitters noradrenaline and dopamine in CNS), but in indirect way: they don't bind to the receptors. Rather, they promote the massive neurotransmitter release from the presynaptic part. The released transmitter (DA, NA) then just diffuses to the postsynaptic membrane and binds to its own receptors.
There are some works done on investigating the effect of these substances on parasympatic system with acetylcholine as neurotransmitter.
Sympatomimetics like amphetamine generally lead to increase of acetylcholine release throurout the nervous system: in hippocampus and caudate nucleus, nucleus accumbens and generally in forebrain and cortex.
This effect of amphetamine is indeed in many cases mediated through dopamine receptors. Same time some direct dopamine receptor agonists were found to supress ACh release in some brain regions.


text:
How do I get the current "camera position" in PyMol so I can reuse it in scripts?
I have a few protein models I want to take pictures of with various ligands bound.  It would be nice if I could do it from the same "position", but the only way I can figure out to repeat the same view is with zoom resi. 64, 152, 150 or the like, which isn't framed that well.
How can I manually position the viewport, capture it's parameters, and repeat it in the script?

I have found get_view, e.g.
PyMOL>get_view
### cut below here and paste into script ###
set_view (\
     0.590180993,    0.670941532,    0.448923886,\
    -0.507570565,    0.740831316,   -0.439937204,\
    -0.627747774,    0.031782545,    0.777776182,\
     0.000000000,    0.000000000, -417.497009277,\
     0.741809845,    7.078243256,   16.473480225,\
   329.157806396,  505.836212158,  -20.000000000 )
### cut above here and paste into script ###

but this doesn't work in a .py script, where I need to modify it to cmd.set_view(...), as it complains it wants just (or up to 5) arguments, not 18.  The wiki is vague about it, it just says

PYMOL API
cmd.set_view(string-or-sequence view)

Try to pass the matrix as a String containing 18 floats separated by commas, e.g. like
cmd.set_view ('''
     0.590180993,    0.670941532,    0.448923886,\
    -0.507570565,    0.740831316,   -0.439937204,\
    -0.627747774,    0.031782545,    0.777776182,\
     0.000000000,    0.000000000, -417.497009277,\
     0.741809845,    7.078243256,   16.473480225,\
   329.157806396,  505.836212158,  -20.000000000 ''')

cmd.get_view() seems to return a tuple, so you'll have to convert that to a String if you want to pass the same position to cmd.set_view().
I tried it in Pymol 1.3 on the command line (not in a script though) and it seemed to work.

Ah, I guess if I translated the "command line/interactive form" of the commands into the API version, I should have also kept those parenthesis that get_view returns so they're really nested (so you do pass it a tuple).  Would look like cmd.set_view((1,2,3...))

Note that you might also want to make use of get_viewport and viewport in case you do not only need the same perspective, but also the same paddings to the outer boundary.

I should add that get_view seems to be undocumented at the moment. It works for me with PyMOL 1.5. Looks like this or a related command does not work reliably in all situations. You might also want to read https://www.mail-archive.com/pymol-users@lists.sourceforge.net/msg08419.html


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Is the protein in teardrops still attached to cells, or is it released and free-flowing?
A ScienceDaily article says that the protein in teardrops can kill bacteria.
But how does it reach the bacteria?

I am not sure I understand your question.
According to the article you mention the proteins in teardrops kill the bacteria which are invading the eye (e.g. also present in the teardrops):

"Those jaws chew apart the walls of the bacteria that are trying to
  get into your eyes and infect them,"

EDIT: These proteins are enzymes called lysozymes. Those are free-flowing proteins of the human tears. These proteins are actively produces in the lacrimal glands and actively secreted into the lacrimal liquid.

Basically, I'm wondering: are these proteins in teardrops free-flowing? Or are they still attached to cells in the teardrops?

I added information about these proteins into the question.


text:
How are chromatids correctly segregated during mitosis?
In my book this is described as happening by kinetochores depolymerising from their attached microtubule spindle, then being dragged towards the spindle's centrosome by a dynein protein. I can understand this, but what it does not seem to answer is how different copies of chomatids beome attached to the correct spindles in the first place (i.e. spindles connected to opposing centrosomes). How does this work?

It's a spatial constraint.  As the DNA is replicated, the two resulting chromatids are kept stuck together by cohesin proteins.  The DNA sequence that corresponds to the centromere then coalesces the kinetochore.  It seems that the DNA-protein interactions at the centromeres creates a particular structure along the chromosome.  Since the two chromatids have their kinetochores pointing in opposite directions, when a spindle microtubule attaches to the kinetochore, it is nearly impossible for another microtubule from the same spindle to attach to the opposing kinetochore.


text:
Does current evidence support the use of resveratrol as an anti-ageing drug?
A while back there was a lot of noise about resveratrol, a naturally occurring phenol which was touted as a potential anti-aging drug due to its role in regulating the SIRT 1 gene. A number of studies suggested that it could extend the lifespans of model organisms such as D. melanogaster and C. elegans.
Has there been any follow up on this? Have there been any human trials?

It's worth noting that earlier this month a large body of resveratrol research was retracted:

The University of Connecticut, in what clearly seems like an attempt to get ahead of damaging news, has announced an “extensive”
  investigation into research misconduct involving one of its
  scientists, Dipak K. Das.
According to a press release, the university has notified 11 journals
  that published Das’ work about the alleged fraud. One area of interest
  for Das, a government-funded professor of surgery and director of the
  Cardiovascular Research Center, has been resveratrol, a substance in
  red wine that has allegedly been linked to improved cardiac health.

Retraction Watch's coverage has been pretty thorough and includes comments and citations:

UConn resveratrol researcher Dipak Das fingered in sweeping
misconduct case
So how peripheral was Dipak Das’ resveratrol
work, really?
Resveratrol fraud case update: Dipak Das loses
editor’s chair, lawyer issues statement refuting all charges

Yes, that was huge. Nevertheless, I know very honest people (in other institutions) that have found interesting results using resveratrol both in vitro and in animal models. Although a revisit of the literature will be needed, the field should not be ignored by the acts of one rotten lab.

I'm hesitant to upvote this answer. Much of the discussion on Resveratrol and proof of concepts of its pharmacodynamics don't come from Das's lab.

@bobthejoe someone needs to outline the evidence from other groups here as an answer then. I'll upvote a well sourced answer

rocken use of news sites.

If you search clinicaltrials.gov (maintained by the NIH) for "resveratrol", you'll find 44 clinical trials, many of them ongoing or not yet started.
A recent review by Smoliga JM et al states in the abstract:

"Although the supporting research in laboratory models is quite substantial, only recently data has emerged to describe the effects of resveratrol supplementation on physiological responses in humans. The limited number of human clinical trials that are available has largely described various aspects of resveratrol's safety and bioavailability, reaching a consensus that it is generally well-tolerated, but have poor bioavailability. Very few published human studies have explored the ability of resveratrol to achieve the physiological benefits that have been observed in laboratory models, although many clinical trials have recently been initiated."

Resveratrol has recently been shown to induce cellular senescence (at least at high concentrations, see here) which has the potential to accelerate ageing.  Senescent cells display and highly inflammatory phenotype which could damage tissues if not removed.  However, Resveratrol itself is rapidly metabolised and it may be these metabolites that have health benefits, but this needs to be researched further.

oh good point nice way of showing how it is counterproductive but may become actualized through metabolism


text:
Does AMP/ATP ratio affect lifespan in vertebrates?
The reference below says that a higher AMP/ATP ratio is associated with lower lifespan in C. elegans.
Is this finding also generalizable to vertebrates as well?

Reference:
Apfeld, J., O’Connor, G., McDonagh, T., DiStefano, P. S. & Curtis, R. The AMP-activated
protein kinase AAK-2 links energy levels and insulin-like signals to lifespan in C. elegans.
Genes Dev. 18, 3004–3009 (2004). PMCID: PMC535911.

Interesting, but I am not sure how useful studies into many of these processes  which shorten lifespan actually are. There are many drugs/poisons which have deleterious effects on organisms, but they don't tell us much about  longevity or the aging process. Better to focus on drugs/interventions which extend lifespan?

There are many papers suggesting a link between AMPK (the major cellular sensor of the AMP/ATP ratio) and lifespan.  As with most of these sorts of experiments, I think it is currently unclear precisely what the mechanism for this is, but AMPK regulates TORC1 and autophagy, both of which are also important for lifespan regulation.  Here is a PubMed link to search results.


text:
Which brain regions are D1 dopamine receptors expressed, and which brain regions are D2 dopamine receptors expressed?
This is a follow-up question to If D1 receptors stimulate adenylate cyclase (through GPCRs) and D2 receptors inhibit it, then why do mutations in both have similar effects?.
As a further question - I'd like to ask: do D1 dopamine receptors have the same (excitatory) effect everywhere in the brain? And do D2 dopamine receptors have the same (inhibitory) effect everywhere in the brain?

As to your main question, I imagine the Paul Allan Brain Atlas has what you're looking for. In 3D even.

Human Brain Map
D1 Receptor
D2 Receptor
Also comes in mouse flavored.

Offhand, I cannot be of assistance for the second question.

To your second question, from what I remember the activity of each receptor is the same, it is the balance of the frequency of activating and inhibitory receptors that summate temporally and spatially that give the overall effect.


text:
What are the trajectories of flying insects?
Many flying insects tend to have very jagged trajectories. For moves of a fruit fly looks like a random walk.
Is there any research on the properties of trajectories (e.g. their fractal dimension or mathematical models producing similar behaviour)?
Besides the path of a single insect, I am also interested in the interaction of a small number of insects (e.g. 2 or 3).
I am aware of the research in flocking and swarming (e.g. Tamas Vicsek, Anna Zafiris, Collective motion 2010) and of techniques of obtaining such trajectories (e.g. Danping Zou, Yan Qiu Chen, Acquiring 3D motion trajectories of large numbers of swarming animals or an open access pdf, 2009). However, I haven't found within them an answer to my particular question.

I'm curious what is your purpose in consideration of insect movements in isolation of their function (avoiding predators, looking for prey, finding new habitat patch etc.)

@MartaCz-C: Abstraction sometimes helps (I am a physicists). And properties of the trajectory are very likely in a close relationship both to optimizing certain actions  (avoiding predators, looking for prey, finding new habitat patch etc.) while being bounded by constrains (physiological, energy, ...).

Quick search - Some articles that may interest you:

Random walk model of insect movements

Kareiva P. M., Shigesada N. (1983). Analyzing insect movement as a correlated random walk. Oecologia 56(2-3) 234-238

Artificial life model of flying insects and its comparison to real insects navigation strategies.

Dale K., Collett T. C. (2001). Using artificial evolution and selection to model insect navigation. Current Biology 11(17) 1305–1316

The last one is not about insects, but it's a trial to practical usage of the mathematical analisys of invertebrate movements.

Shimizu N. et al. (2002). Fractal analysis of Daphnia motion for acute toxicity bioassay. Environmental Toxicology 17(5) 441–448

This is not an answer but a list of references. Whether accepted by the poster or upvoted by the hoi polloi, it should be edited to provide an explanation (unlikely after ten years) or converted to series of comments and then deleted by the mods.

Dickinson (2005) has a good review of insect flight, including behavior, biomechanics, electrophysiology, and neural control with links to more of the primary literature. What follows is a general summary thereof.
The jagged trajectories you mention are called saccades in the insect flight literature. In Drosophila, saccades are ~90° turns accomplished in approximately 50 ms. Because flies can't move their eyes independently of their heads, saccades are though to allow a relatively constant visual field most of the time, interspersed with rapid reorientations during which the fly is "blind."
The actual turn begins with the generation of a torque, which starts the fly turning. Shortly thereafter, the halteres sense this change and a counter-torque is produces, which stops the turn.
Rather than random turns, Drosophila are turning away from visual expansion as they near objects. So as they move closer to an object, it expands in their visual field, and they turn away from it.

Thanks, a good and informative answer. However, I am interested not only in saccades but the whole patterns of movement (so also structures at different time scales, e.g. minutes).

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text:
Is it correct that the body only responds to the most painful stimulus?
I'm rather ashamed to say that this question is partly based on an episode of House.
I have previously heard that, if there are multiple simultaneous painful stimuli, the mind will only feel the sensation of pain from the most severe injury.  A large amount of googling has turned up nothing and PubMed searches are proving tricky as I cant find the name of this effect (if it exists).
If it does exist, is the mechanism solely effective for pain signals or would we for example only feel cold at our coldest points (i.e. from the face or the hands rather than both) on a frosty morning?

"House MD" is one of the best series as regards the veracity of the medical observations. Whereas many cases are normally so rare that it is just improbably that House comes accross them, they all are usually ultimately correct as regards the symptoms, the course etc. The only series with a better medical background  is "ER", but with every new season the proportion of the medical part was decreasing so dramatically that I just gave it up in the middle.

When I get hip pain, it is so excruciating that the lower back pain goes away. As soon as my hip pain is relieved, the lower back pain comes back.

Pain is an associative cortical phenomenon, not a peripheral sensation. As with any cortical associative event, the experience of pain is dependent on attention, memory and prior experience. I may write an answer to this, but I'll have to dig a bit to find the relevant references. The way I like to think about it comes from Patrick Wall. I never met him myself, but Eric Kandel and John Brust have both quoted him to me as saying something like: pain is a need state that has more in common with hunger than somatic sensation or vision.

Your question statement is a little bit incorrect or, better say, imprecise.
First of all it is not clear what you mean by the "body response" here? Pain is sensed by peripherial receptors (several types of receptors, mostly purinergic, are assumed to play role in pain preception) and then this sensation is propagated into CNS. So, the local "response to pain" (like swelling, increase of the blood perfusion) is not the response to the pain stimulus, but rather a methabolic response to the cell injures and release of many humoral factors like interleukins, "wound hormones" etc.
And this is true that out of many different pain inputs the one with highest intensity seems to "outshine" all other inputs and ultimately the pain perception is constrained to a single body part. However, if you consciously focus your perception on other parts of your body you may be able to percieve the pain originating from these parts even if this pain is lower.
This principle is known as a smaller particular case of a more general principle known as "the dominance principle of Ukhtomsky". Wikipedia has only the Russian language version about this principle (as well as about Ukhtomsky, a prominent Russian physiologist) and it seems to be not really known outside of the Russian scientific community (this is the only page I found about him in English).
The more general principle of Ukhtomsky postulates the following: one certain input may lead to the formation of the dominance center in the cortex. The domaninace center is characterized by the higher level of nerve cell excitation, whereas the rest of the cortex undergoes an inhibition so that different, even unrelated inputs converge here, helping this center to exist for longer time. The only way how this center can be ceased is to form another dominance center by a extremely high stimulus (for example a startle sound). Here the most insensive pain leads to the formation of such a center and all substantial pain stimuli just contribute to the persistence of this center: the pain is however percieved to originate from the place where the first stimulus, responsible for dominance center formation, originated from.

Is there any evidence that Ukhtomsky's postulate actually occurs?

@yamad Do you mean if the postulate has ever been proved or if it is applicable to this particular case with pain perception?

I mostly interested if the postulate has ever been shown to be true in any case. Of course, I would also be interested if it happens to be applicable to the case of pain perception.

@yamad In Russian physiology this theory is considered to be proved. There is a classical book by Ukhtomsky (last edition was published in 2002) which describes his experiments with dogs which were used to prove the theory. There are numerous publications mentioning dominance principle in pubmed, but they are mostly in Russian.

So would Ukhtomsky's principle apply for other sensations such as the feeling of cold?

@RoryM Not every input leads to the formation of a dominant center,  the input has to fulfill certain criteria -- and if those are met then every input (cold, burn etc.) can do it. Pain is an example where it is true in most cases due to the nature of this input, but Ukhmomsky showed also other inputs in his experiments on dogs.


text:
Why is a lack of oxygen fatal to cells?
In animals temporary anaerobic respiration leads to the breakdown of the pyruvate formed by glycolysis into lactate.  The buildup of lactate in the bloodstream is accompanied by a large number of protons causing lactic acidosis, which is detrimental to the health of the organism.  This is one of the main suggestions I have come across for why a lack of oxygen is fatal to cells, however the LD50 for lactic acid as referenced by the COSHH MSDS seem awfully high (even if the route is by ingestion rather than directly into the bloodstream) for this to be a cause of cell death:

Toxicological Data on Ingredients:
  ORAL (LD50): Acute:
3543 mg/kg [Rat (Lactic Acid (CAS no. 50-21-5))].
4875 mg/kg [Mouse (Lactic Acid (CAS no. 50-21-5))].

I also wonder if this is a larger problem for an organism as a whole rather than on a cellular level.
The alternative, I suppose, is that glycolysis alone does not provide sufficient ATP for vital cellular processes to occur.  If this is the case, which ATP requiring processes are most vital for the short term survival for a cell?

You're being a bit anthropocentric, plenty of organisms get on fine without, some are even harmed by free oxygen. :P

As a corollary, perhaps, oxygen toxicity occurs at the other end of the scale http://en.wikipedia.org/wiki/Oxygen_toxicity

Here's an illustrated example in neurons:
ATP, of course, is generated by aerobic respiration. The critical biochemical reaction in the brain that is halted due to lack of ATP (and therefore O2) is the glutmaine synthetase reaction, which is very important for the metabolism and excretion of nitrogenous wastes:

The body uses this reaction to dump excess ammonia (which is a metabolic waste product) on glutamate to make glutamine. The glutamine is then transported via the circulatory system to the kidney, where the terminal amino group is hydrolyzed by glutaminase, and the free ammonium ion is excreted in the urine.

Therefore, as you'd expect, under hypoxic conditions in the brain, excess ammonia builds up which is very toxic to the cells. Neurons are also highly metabolically active, which means they generate more waste products. A buildup of nitrogenous waste products in the cell (and bloodstream) can be potentially fatal due to it's effects on pH (screws up enzymes and a whole slew of biochemical reactions).
In addition, the buildup of ammonia will cause glutamate dehydrogenase to convert ammonia + aKG to glutamate, which depletes the brain of alpha-ketoglutarate (key intermediate in TCA cycle). This basically creates a logjam in the central metabolic cycle which further depletes the cell of energy.
This is just one example of many. Of course, there are many, many other critical metabolic processes that require ATP (i.e. the Na+/K+ ATPase pump that regulates neuronal firing and osmotic pressure), but nitrogen metabolism was the first that came to mind :)

Energy production starts with glycolysis, which generates NADH and pyruvate.  Pyruvate goes to the mitochondria to make more NADH (or FADH2, which is similar to NADH) in the Krebs Cycle.  NADH is used to power the electron transport chain, which gives most of the energy the cell uses.  The last step of the electron transport chain consumes oxygen (Complex IV reduces oxygen to water).
If you do not have oxygen, the electron transport chain will not work.  If that doesn't work, the Krebs Cycle slows.  If that's not consuming pyruvate, glycolysis slows.  The cell dies from lack of energy.  It has less to do with the acid buildup as a consequence of lactate as it does with buildup of NADH and the consequent slowing of the central metabolism.
The issue is most pronounced in multicellular organisms  because it's much more difficult to get oxygen to all your tissues, so "think" tissues have cells that are already close to hypoxia already.


text:
How is the effective dose calculated when only part of the body is irradiated?
For calculating the effective radiation dose in Sv, the equivalent dose absorbed by each body part is averaged according to tissue-specific weighting factors, which sum up to 1.
If not the whole body is irradiated, how are these factors used?

Not sure that I understood your question correctly.
The concept of "effective dose" was specially introduced to provide a mechanism for assessing the radiation detriment from partial body irradiations in terms of data derived from whole body irradiations. The effective dose is the mean absorbed dose from a uniform whole-body irradiation that results in the same total radiation detriment as from the nonuniform, partial-body irradiation in question.
What is probably misleading you is the sum of the weighting factors to be 1. This is because we try to liken the partial body irradiation and the whole-body irradiation and the weighting factors represent the relative tissue sensitivity and susceptibility to the radiation. Your radiation should not go over all possible tissues and organs, you just assume the irradiation to be zero at them that cancels their summands so that they can be ignored in the final calculation. In other words, it is absolutely fine (and it is even so "by design") to have only some of the WT*HT factors in your formula.

I don't quite follow. What would x and y be in the following sentence? "A whole-body irradiation of x would be equivalent to irradiation of y of the thumb (weighting factor 0.01)". I suppose x and y could be chosen such that y=100x for some unit (Gy?), and this would mean that those two irradiations would have the same effective dose measured in Sievert? That doesn't completely make sense for me, since Gray already compensates for tissue mass.

@Poshpaws: Sorry, I can't upvote because I'm not registered :( Also, I still don't know what "effective dose" means. hopefully, someone can answer my questions in the comment above!


text:
Are there any examples of sudden leaps in evolution?
As far as I understand, various abilities like flying, sight, hearing etc. were caused by slow evolution, where those with a greater ability to to these things had better chance of survival. (If this assumption is wrong, then I am happy to delete this question).
Are there, however, any documented examples of by evolutionary leaps being made, over the course of just a few generations? I understand, that some abilities have a tipping point where one gets the ability suddenly, but there is not a lot of physiological change made. An example of this would be the ability to climb a tree, which could suddenly be possible if the body weight is reduced with just a few percent. What my question is about, are sudden changes to the characteristics of a creature.

How sudden is sudden enough for you?

@Kevin It depends upon the magnitude of change in the characteristics of the creature.

E. Coli being able to subsist on cellulose?  That was a nice laboratory controlled experiment, showing the 2 mutations change required for that.  Although that was only rapid in chronological time, since it was 40,000 generations of bacteria.

@Brightblades This is certainly interesting, but with this question I was primarily thinking about things happening over the course of tens of generations. On the other hand, what really counts for the survival of the fittest is of course adaptability to adapt in chronological time. How long time did this adaptation take?

@David I don't recall precisely, but it was over a period of years (one scientist doing the experiment).  It's only been going for 24 years:  http://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment

@Brightblades Thank you for the link. It is certainly interesting reading!

I see my memory is failing on several levels...  It wasn't until 2008 that the processing of citric acid happened.  Man, I need a check up I think.  I think the whole idea of Punctuated Equilibrium may fall in to your question of rapid evolution:  http://evolution.berkeley.edu/evosite/evo101/VIIA1bPunctuated.shtml

I believe that the technical term is a "Hard Sweep".

@kmm and @shigeta provided you with a nice observational account of sudden leaps in large organisms. However, if you want to look at where this is the norm and try to build a mathematical theory then you need to look at something much smaller; the prime candidate is affinity maturation.
In the human immune system, when exposed to an antigen B cells produce antibodies. If it is your first exposure to the antigen then the antibodies produced will probably have very low binding affinity. However, after some exposure time, your B cells will start to produce antibodies with much higher affinities for the antigen and thus you will be able to better fight off the disease. The cool part, is that the antigen produced is tuned via an evolutionary process!
There is differential survival, with only antibodies with the highest affinity being able to survive. Variability is introduced by a very high mutation rate in the complementarity determing region (CDR). (Tonegawa, 1983). The length of this evolutionary process is very short, typically a local equilibrium is found after only 6-8 nucleotide changes in CDR (Crews et al., 1981; Tonegawa, 1983; Clark et al., 1985), so you need only a few point mutations to quickly develop a drastically better tuned antibody.
The standard mathematical model for this is Kauffman's NK model. With a protein sequence on $N$ sites, we say that evolution is fast (and we have a sudden leap) if after our fitness landscape changes, we can get to a new local equilibrium in a number of generations that scales with $\log N$. Kauffman & Weinberger (1989) showed how this model can be used to study affinity maturation, and showed that to achieve a sudden leap we need high epistasis and low correlations between pointwise mutants. In particular, their model suggests that typical epistasis in the CDR is on the order of 40 proteins (out of the total 112 proteins in the CDR).

References
Clark, S.H., Huppi, K., Ruezinsky, D., Staudt, L., Gerhard, W., & Weigert, M. (1985). Inter- and intraclonal diversity in the antibody response to influenza hemagglutin. J. Exp. Med. 161, 687.
Crews, S., Griffin, J., Huang, H., Calame, K., & Hood, L. (1981). A single V gene segment encodes the immune response to phosphorylcholine: somatic mutation is correlated with the class of the antibody. Cell 25, 59.
Kauffman, S. and Weinberger, E. (1989) The NK Model of rugged fitness landscapes and its application to the maturation of the immune response. Journal of Theoretical Biology, 141(2): 211-245
Tonegawa, S. (1983). Somatic generation of antibody diversity. Nature 302, 575.

Zuk et al. (2006) document the rapid evolution of song-less crickets in a population of crickets that previously used song for courtship.
In less that 20 generations, over 90% of male crickets of the species Teleogryllus oceanicus evolved to a novel morphology ("flatwing") that rendered them unable to call to females. They hypothesize that this shift resulted from the presence of an North American invasive "acoustically orienting parasitoid fly."
Basically the flies detect calling males and parasitize them, rendering them unable to reproduce. Were it not for the presence of the parasitoid fly, the flatwing flies would likely not have survived. Non-calling individuals rely on the presence of calling males to bring females near for mating.

Even though it is a nice example of evolutional change, I am just wondering whether the loss of a previously existing ability to produce songs can be seen as an evolution, not devolution or involution?

Evolution is just descent with modification -- adding or subtracting doesn't matter.

@Alexander Galkin: wouldn't you consider evolution a fish evolving into a land animal and losing the ability to breathe under water?

The ability to drink milk by the inheritance of lactase persistence via a single allele change. Sociology and genetic studies have shown that the immigration of a few lactose tolerant people into large non-lactose tolerant populations, the lactase persistence gene quickly spreads through the population, a sign of a dominant mutation and survival of the fittest at work.
Not in the mood to dissect the papers but here are a few commentaries:

http://sciencelife.uchospitals.edu/2011/09/14/lactose-tolerance-in-the-indian-dairyland/
http://news.discovery.com/human/got-milk-drinking-common-ancestor-india-and-europe-do-110914.html

Is lactose intolerance really likely to stop an organism reaching reproductive age and being successful?

There is a good amount of genetic evidence that does suggests so. Examples of natural selection are seen in pastoral communities that shifted from a farming community to a dairy community. Unfortunately I don't know the field well enough to find good sources.

This is selective sweep (i.e. a given allele’s abundance is sweeping through a population via selection). But that isn’t in itself a sudden leap in evolution since the allele is already in existence (= “has already evolved”).

@Konrad: However, the lactase persistent allele itself is the result of a single spot mutation that is believed to be of rather recent origin. (Some studies suggest it happened around ten thousand years ago, which is an eyeblink in evolutionary timescales.) This is another case of evolution via function loss: the mutation that causes adult lactose tolerance basically disables the switch that, in most mammals, turns off lactase production after weaning.

I think that this might refer to evolution in punctuated equilibrium as described by Stephen Gould et al way back in the 70s.  If this is the case, it refers more to the idea that changes and speciations can be quite rapid in time and for long periods you don't see morphological changes or speciation events in the record.
If so, then this is influenced by the study of evolution in cases where there are large changes in the environment very rapidly. The classic case is when there is a bare island and new animals arrive only rarely. This is all very much inspired by Darwin's observations in the Galapagos, but has since been studied quite a bit.  In such cases you see just handful of sets of birds suddenly appear and you find a finch that can scrape bugs out of bark, another that can dig into narrow niches in the rock for food, where in a broader ecosystem two completely different species would be utilizing those 2 food sources.
It should be said that no evolutionary leap should be understood as an acceleration or deceleration of evolution.  Only a change in the rate of adoption of variations because of a wider set of possible advantages those variations can represent.

Even under punctuated equilibrium, acquisition of new traits happens over a period of thousands of generations, not “just a few generations”. It is punctuated on the geological timescale only.

With all due respect, a few of these answers, although good examples of selection at work, were voted too high given the specific question asked: “documented examples of by evolutionary leaps being made, over the course of just a few generations?”
Sometimes we’re better being honest and identifying something as an ‘unknown’ or ‘yet to be observed’ than to list (and have people up-vote) poor examples.  We do evolution a dis-service when we promote poor examples as answers to questions like these.
To expound:
The cricket losing the ability to sing (communicate) examples does demonstrate mutation and natural selection at work, but really only shows the REDUCTION of a capability.  It’s not a good example of evolutionary leaps.  It only happens to be beneficial in one SPECIFIC context.  This would be analogous to tanks on a battle-field which communicate via radio, vulnerable to radio-frequency tracking missiles.  Any tank with a broken radio would not be vulnerable to these missiles.  Although technically ‘beneficial’ in this context, it’s an example of a loss of capability, not a gain of capability.  We need to promote examples of mutations that PRODUCE capabilities.
Lactase persistence example likewise is an example of mutation and natural selection, but not a good example of a GAIN in functionality (as some have pointed out in the comments).  It’s technically the loss of the normal switching-off mechanism of lactase production following weaning.  So once again, a loss, that happens to have a beneficial side-effect.
Regarding punctuated equilibrium, I’m not surprised that was mentioned but was surprised that it got some votes.  It’s a hypothetical explanation for why we see gaps in the fossils, but not conclusive ‘evidence’, or in the case of the question asked not “documented examples”.
Again: We do evolution a dis-service when we promote poor examples as answers to questions like these.  Let’s focus on quality, not quantity when it comes to presenting evidence for evolution.

I disagree. The designation whether a loss of a switch-off is a 'loss', or whether it may be a 'gain' in a genetic switch-on is purely semantic if we don't know about the epigenetic mechanism. Even then, I think it's semantic. I think lactase persistence specifically is a nice case of neoteny. When there is a strong and sudden positive selection for neoteny, and when this becomes stabilized quickly in a large fraction of a population, I think this can be confidently discussed as a case of a gain of function and as 'punctuated', or as OP puts it, a sudden leap. My $0.02.


text:
How do plant galls form?
I am curious how Gall Wasps, bacteria and other organisms induce galls to form.
Specifically, what chemicals induce gall formation?

http://gardening.stackexchange.com/questions/2052/what-is-this-anomalous-growth-on-my-oak-leaf

One type of gall: cedar-apple rust http://en.wikipedia.org/wiki/Gymnosporangium_juniperi-virginianae

I'd like to add to Amy's excellent answer.
Generally, galls are induced by the forced accumulation of plant hormones at different levels to those naturally maintained by the plant, in a localised area. Usually the hormones targeted are auxins and cytokinins which are both involved in the regulation of normal growth patterns; disrupting these patterns leads to disorganised growth, or in some cases a differently organised growth. There are several methods that I know of:

The gall inducer directly synthesising the hormone.
The inducer chemically inducing the host to synthesise more hormone.
The inducer chemically inducing the host to transport more hormone to the site.
The inducer genetically modifying the host to cause synthesis of the hormone in the host cell.

Some examples of the different methods:
Direct production: The bacterium Pseudomonas savastanoi directly produces indole-3-acetic acid (IAA, a type of auxin). This direct accumulation has been shown to be responsible for gall formation in oleander knot disease. Some key papers: Palm et al. 1989, link 1; Glickman et al. 1998, link 2.
Chemical induction of transport: Root-knot nematode worms induce root gall formation in clover. They probably do so by producing flavonoids which up-regulate transportation of auxin into cells (see link 3).
Genetic induction: As already mentioned by Amy, Agrobacterium tumefaciens is a very well characterised example of induction by genetic modification, however, A. tumefaciens is also known to directly produce auxins in large quantities. Another interesting example of genetic modification is in viral gall-inducers. They are not so well studied as their bacterial counterparts, but in some cases (e.g. white clover mosaic potexvirus) it has been shown that virus infection initially leads to a complex change in the types of cytokinins produced by the plant (e.g. Clarke, 1999; see link 4). It has also been shown that if cytokinins are applied exogenously (i.e. injected into the plant) after viral infection, that the virus cannot replicate well. This suggests that the virus is manipulating the host's hormone production in a complex way.
There is also the interesting case of Rhodococcus fascians, which seems to produce a chemical which is not structurally similar to any known cytokinin, and yet has similar effects (Goethals et al., 2001; link 5).
You specifically asked about gall wasps, but unfortunately this mechanism is, as far as I can tell, not completely known. It is speculated (e.g. in Shorthouse & Rohrfritsch, 1992; link 6) that this involves direct injection of phytohormones. The evidence to support this is simply that other insects, particularly aphids, excrete phytohormones in their salivary sheaths when they inject them into a plant.
Finally, I'll just say that the fact that gall induction is carried out by bacteria, viruses, nematodes, fungi and wasps, and that some mechanisms are shared across all those associations,  demonstrates the ability of evolution to converge on the most elegant solution to a problem. It also shows that plants are so great, everyone wants a piece (but I would say that, because I'm a plant biologist).
References:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC209694/
http://apsjournals.apsnet.org/doi/abs/10.1094/MPMI.1998.11.2.156
http://www.publish.csiro.au/?paper=PP98157
http://www.plantphysiol.org/content/120/2/547.full
http://www.annualreviews.org/doi/full/10.1146/annurev.phyto.39.1.27
http://www.nhbs.com/biology_of_insect_induced_galls_tefno_3838.html

I don't think you're disagreeing with me, all I said is that we don't know much about gall producing insects !

You're right Amy, sorry! Answer updated with some grovelling.

ha ha ha (don't worry, you already had my upvote)

I recently aquired, "“Britain’s Plant Galls, a Photographic Guide.” It expanded upon what you said about insects injecting growth hormones: Sawflies belong with the gall wasps in the order Hymenoptera. The female has a tiny saw-like ovipositor with which she cuts slits in plants prior to laying her eggs. She injects a stimulant when laying her eggs and the galls start to grow before the eggs hatch. Most sawfly galls are solid at first and usually contain a single larva that gradually hollows them out. Mature larvae of most species leave their galls before pupating – often in the soil.

It seems not much is known about how insects induce gall formation (perhaps someone with more of an entomology can jump in).
But we do know quite a bit about Agrobacterium tumefaciens, which causes crown gall in roses, grapes, and other plants. Agrobacterium invades cell tissue and inserts a piece of it's own DNA into the plant cell. The plant cells incorporates the DNA into its genome and begins expressing a number of new genes, including genes that lead to an over production of the plant hormones auxin and cytokinin.  These hormones cause the undifferentiation of the plant cell and uncontrolled cell division, leading to the formation of a tumor-like gall.
More on Agrobacterium at Wikipedia. I can recommend some journal articles if you're interested.

Perhapse the wasp carries the bacteria =)


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).


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How reversible is decerebrate posturing caused by brain stem damage?
This is a follow-up question to How likely would Abraham Lincoln be to survive his wounds today?

You don't have to see a CT scan or autopsy to know if the brainstem is
injured (directly or indirectly), if it doesn't work right.
The description of the first doc at the scene mentioned that Lincoln
was not breathing, and one pupil was dilated (the latter a clear and
unequivocal sign of dysfunction of the third cranial nerve or the
upper brainstem, from where it comes). Unfortunately, the second doc
described the enlarged pupil being the right one (it's extremely
unlikely to have been one and then the other - one of the doc's was
probably mistaken as to the side).
By 3 hours after injury, both pupils were fixed and dilated, and
Lincoln showed extensor (decerebrate) posturing - again, all signs of
profound brainstem dysfunction (but not yet brain death, though pretty
close to it).

Now, what is decerebrate posturing? See http://en.wikipedia.org/wiki/Abnormal_posturing#Decerebrate

Decerebrate posturing is also called decerebrate response, decerebrate
rigidity, or extensor posturing. It describes the involuntary
extension of the upper extremities in response to external stimuli. In
decerebrate posturing, the head is arched back, the arms are extended
by the sides, and the legs are extended.[6] A hallmark of decerebrate
posturing is extended elbows.[12] The arms and legs are extended and
rotated internally.[13] The patient is rigid, with the teeth
clenched.[13] The signs can be on just one or the other side of the
body or on both sides, and it may be just in the arms and may be
intermittent.[13]
A person displaying decerebrate posturing in
response to pain gets a score of two in the motor section of the
Glasgow Coma Scale (for adults) and the Pediatric Glasgow Coma Scale
(for infants). Decerebrate posturing indicates brain stem damage,
specifically damage below the level of the red nucleus (e.g.
mid-collicular lesion). It is exhibited by people with lesions or
compression in the midbrain and lesions in the cerebellum

I think this question needs to be more self contained; the quote needs to be put in context.

Okay - the context is here: http://en.wikipedia.org/wiki/Abnormal_posturing#Decerebrate. I'll add another quote for it.

The decerebrate posturing is a sign of major brainstem dysfunction.
The reversibility of this state (which is considered to be very critical and hardly reversible) depends upon the origin of the brainstem dysfunction.
The primary brainstem dysfunction means that the brainstem was directly damaged (by a bullet) and there is no way that this can be quickly reversed. This is exactly the case here and there are no chances that the brainstem might recooperate with time.
The secondary brainstem dysfunction may be caused by cerebral edema and thereby dislocation of the brainstem towards foramen magnum, where the brainstem is coned. The coning of the brainstem can be reversible if the brain edema is treated quickly and effectively (by administration of diuretics in the intravenal catheter.
With brainstem regaining its normal functions the decerebral posture will eventuall resolve and depending upon the residual brain injury the recooperation of the brain function (and compensation) may be almost entire.


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Do taller people have larger somatosensory cortices than short people?
When we assume that peripheral touch receptor densities are equal in tall and short people, then tall people should have more touch receptors than short people, given the larger amount of skin surface in the former. Hence my question:
Do taller people have larger somatosensory cortices than short people? And analogues to that, what about larger motor cortices in tall people? If tall people need larger somatosensory and motor areas, could this imply that they have less space devoted to other functions, like functions devoted to the prefrontal cortex?

Do you mean mass-corrected size or absolute size? If the latter, then I would say probably due to the laws of scaling.

Absolute size. Mass-corrected size would be interesting too though

If you are interested in the anatomical differences between small and large people, then I'd think you want mass corrected. My brain is larger than my 2-year-old nephew in absolute size, but his is probably larger than mine in relative size.

I would say no.
Your question somehow implies that somatosensory cortex is equally distributed among the different sensory areas of the body, whereas in the reality this is the known "cortical homunculus" concept of how this distribution looks:

If you look at this representation you'll see that chest and legs take only about one third to one fourth of the cortex, thus the changes between short and tall people don't seem to have noticeable contribution to the overall cortex size.
If we just walk away from cortex size and discuss the amount of nerve cells in these areas I would say that these numbers should correlate with the number of peripherial receptor cells that provide input for them, and since there is no known changes in receptor density among different body sizes, even the amount of nerve cells seems to be more or less same.

If there is no change in receptor density, but an increase in body surface area (from being bigger and all) then wouldn't one expect an increase in the number of nerve cells? Basically, I don't understand your last sentence.

I agree with @ArtemKaznatcheev - The core of the question is whether the density of peripheral mechanoreceptors is identical across people of different posture. If yes, a large person (in length, or otherwise) would have more skin receptors and hence a larger afferent input to the cortex, and hence a larger cortical surface needed, as evident in the homunculus.


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Are human fetuses more likely to be male?
Question: From a physiological point of view, when sex is determined in a human fetus, is it equally likely to be male or female?
Studies in this area typically measure age at birth, where the data would have already been biased.  There's a slight imbalance in the human sex ratio, in that there's an overall tendency towards males.  However, this could be accounted for in numerous ways, such as abortion.
Fisher's principle suggests there would be an evolutionary tendency towards 50:50 chance.

@Dane Why are you marking the older question as a duplicate though?

@MarchHo Is jan23 earlier than jan11?

@Dane Jan 23, 2012 vs Jan 11 2015?

@MarchHo A great mistake of us.

Hi, as long as the newer question has an answer, it is accepted to close the older question. There are many such instances in meta.

http://meta.stackexchange.com/questions/147643/should-i-vote-to-close-a-duplicate-question-even-though-its-much-newer-and-ha

The Fisher's principle is not applicable to the fetuses because it has been formulated for parental expenditure and basically states that the ratio of male to female parents (implying that both parties have reached the age of fertility) will tend to 1:1.
There are several mechanisms that we can use and that are mentioned in the canonical paper by James (2007):

(a) there are equal numbers of X and Y chromosomes in mammalian sperms
  (b) X and Y stand equal chance of achieving conception
  (c)
  therefore equal number of male and female zygotes are formed, and that
  (d) therefore any variation of sex ratio at birth is due to sex
  selection between conception and birth.

James brings much evidence that none of these conventional beliefs is true. Rather, they are dependent upon many factors: exposure to stress during pregnancy, glucose level etc. He reports that there is an excess of males at birth in almost all human populations, and the natural sex ratio at birth is usually between 1.02 and 1.08. However, the ratio may deviate significantly from this range for natural reasons. (I really recommend reading the paper I linked, it is available for free).
Branum et al (2009) analyze birth statistics in the US taking into account many factors like ethnicity, gestational age and plurality and show that the ratio can increase even more with growing gestational age and has different values among different races.
So, taking everything together, I can say thay YES, the chances for human fetuses to be male are indeed higher.

Note there is a slightly higher mortality rate for males, which tends to bring the ratio towards 50:50 at reproduction age.

"the ratio of male to female parents (implying that both parties have reached the age of fertility) will tend to 1:1" Does this equal to that female parents and male parents would have equal mean amount of offsprings? But this is obvious claim!

The following paper(1) studies the trends in male to female ratios among newborns over the period 1950-1994 in 29 countries (20 major European countries, USA, Canada, Japan, and others). In all countries at any time point, the male to female ratio was always higher than one. In some countries (Mexico and a few northern eastern European countries) the male proportion has been decreasing over the 1950-1994 period, whereas in southern Europe and Australia it has been increasing. Overall, the ratio has remained constant.
The authors mention several factors that could contribute to the decrease of males. Among those factors are:

hormonally induced ovulation
maternal nutrition
environmental factors (like alcohol exposure of the fathers)

On another note, the increased male to female ratio in newborns could be explained with the size of the sex chromosomes. The X chromosome contains ~155 million base pairs, whereas the Y chromosome contains ~58 million base pairs. Thus, the X chromosome is heavier than the Y chromosome, and a sperm cell carrying the 22 autosomal chromosomes +Y chromosome will swim faster and have a slightly higher chance of fertilizing the egg. This explanation is purely my speculation.

Trends in male:female ratio among newborn infants in 29 countries from five continents

Could you provide some reference for the last paragraph, ie. that the ratio might be dependent on the weight of Y & X chromosomes?

@kate The last paragraph is my speculation. I can only support it my the reference I gave for the length of the sex chromosomes.

I see; thank you. It sounds really interesting, though.

@Gergana Vandova: then you should probably state it is just your guess in the answer. Right now it looks like a very (unsubstantiated) bold claim.

there is some evidence that the female reproductive system may also do some gender based selection and skew the chances of one or another outcome depending upon environment, if I recall the snake work correctly.
I found a recent (2002?) review:  West SA, Reece SE, Sheldon BC. 2002. Sex ratios. Heredity 88: 117–24.

Furthermore, in some of these cases individuals appear to show
  extremely precise control of their offspring sex ratio. For example:
  (a) in the Seychelles warbler (described above), females vary the sex
  ratio of their offspring from 90% female to 80% male depending upon
  environmental conditions.

It isn't so easily predictable what the outcome is for a given environmental set of conditions.  To me it is not surprising since sperm competition and selection in the oviducts is common to nearly all animals.


text:
How and where, in the human brain, are memories stored?
Background
I am a computer programmer who is fascinated by artificial intelligence and artificial neural networks, and I am becoming more curious about how biological neural networks work.
Context & what I think I understand
In digesting all I have been reading, I am beginning to understand that there are layers to neural networks.  A front-line layer of neurons may receive, for example, a visual stimulus such as a bright light.  That stimulus is taken in by the front-line neurons, each of which produce a weighted electro-chemical response that results in a binary decision to pass an electrical charge through its axon to the dendrites of the tens of thousands of neurons to which it is connected.
This process repeats through layers channeling the electrical signals and focusing them based on their permutations until ultimately a charge is passed to a focused response mechanism such as the nerves that control shrinking of the pupils.
Hopefully I got that correct.
Preamble to the question ;)
Assuming that I am not completely off-base with my basic understanding of how a biological neural network operates, I am beginning to grasp how an input (stimulus) results in an output (response) such as motor movement or reflexes.  That would just seem to be basic electricity of open and closed circuits.
HOWEVER, what confuzzles me still is how a memory is stored.  The analogy to an electrical circuit breaks down here, for in a circuit I can't really stop the flow of electrons unless I dam up said electrons in a capacitor.  If I do that, once the electrons are released (accessed), they are gone forever whereas a memory endures.
So. . .
How the heck are memories constructed and stored in the human brain?  Are they stored in a specific region?  If so, where?

Regarding pupil size alterations it is the circular muscle of the iris which controls pupil size.  Effectors are always either muscles or glands - not nerves.  Otherwise spot on :)

“the analogy to an electrical circuit breaks down here” – it’s not really an analogy, and it doesn’t break down. This is how the brain works: not an analogy, but rather the actual mechanism. The only part missing is the dynamics in structure.

@Rory - But the nerves control the muscles, no? That is what Matthew certainly means.

What do you mean by "focusing them based on their permutations"? Permutation usually means a bijection of a set onto itself or plainly rearrangement. What do you mean by rearranging electrical signals?

Unfortunately, we are all still "confuzzled" by how memory works. We are far from a complete understanding of how memory is stored and recalled. Nonetheless, we do know a little, so read on.
Your understanding of basic neural function is almost correct. First, an individual neuron will signal through its single axon onto the dendrites of many downstream neurons, not the other way around. Second, I am not sure what you mean by "focusing them based on their permutations," but it is true that neural information can undergo many transformations as it propagates through a circuit. Third, if there is a behavioral outcome of the network activity like a muscle response or hormone release, those effects are mediated by nerves communicating with muscles and hormone-releasing cells. I'm not sure if that is what you meant by "focused response mechanism."
Finally, as you have discovered, the analogy of neural circuits to electrical circuits is relatively poor at any reasonably sophisticated level of analysis. My opinion is that biological systems are often poorly served by being framed as engineering problems. Others will disagree with that, but I think understanding a biological system on its own terms makes many things much clearer.
The key thing missing from the electrical circuit analogy turns out to be one of the keys to understanding information storage in neural circuits--the synapse, the site where one neuron communicates with another. The synapse transforms the electrical signal from the upstream neuron into a chemical signal. That chemical signal is then converted back into an electrical signal by the downstream neuron.
The strength of the synapse can be adjusted in a long-term way by changing the level of protein expression--this is called long-term potentiation (LTP) or long-term depression (LTD). LTP and LTD therefore can regulate the ease with which information can flow along a particular path. As a basic example (that should not be taken too seriously), imagine a set of neurons that represents "New York City" and another set of neurons that represents "My Friend John." If you then happen to be in New York City with your friend John, both of those groups of neurons will be active and synapses between these two networks will be strengthened because they are co-active (see Hebbian plasticity). In this way, the idea of NYC and the idea of John are now bound together.
Where are these neurons that represent NYC and John? We are still not totally clear on this, and the question is complicated because there are many different types of memory. For instance, your memory of how to ride a bike (procedural memory) is not treated the same as your memory of what you ate for breakfast (episodic memory). However, a best current answer is that the hippocampus and its associated regions are important for the initial encoding of memories and the neocortex is where longer term memories are stored. There is substantial communication between these two areas so that memories can be effectively adjusted over time.

Update
In response to Jule's comment asking for some resources, I realize it is important to make the point that the Hebbian model I outlined hasn't been definitively shown. Like with all aspects of neuroscience, there is a lot of good work at the molecular and cellular level and good work at the behavioral level, but the causal link between the two is not so clear. Nonetheless, Hebb's idea is still the mainstream working model for how memory works. Some reading might include:
1) Neves, G., Cooke, S.F., Bliss, T.V.P., 2008. Synaptic plasticity, memory and the hippocampus: a neural network approach to causality. Nature Reviews Neuroscience 9, 65–75.
 A review on hippocampal memory and its relation to LTP/LTD and Hebbian theory. Notes the general difficulty of proving the theory and some ways for experiments to move forward.
2) Lisman, J., Grace, A.A., Duzel, E., 2011. A neoHebbian framework for episodic memory; role of dopamine-dependent late LTP. Trends in Neurosciences 34, 536–547.
 A review proposing an elaboration of the Hebbian model that includes neuromodulatory influence on plasticity and memory process.
3) Johansen, J.P., Cain, C.K., Ostroff, L.E., LeDoux, J.E., 2011. Molecular Mechanisms of Fear Learning and Memory. Cell 147, 509–524.. An excellent review on fear learning and memory with an extensive section on Hebbian theory.
4) Liu, X., Ramirez, S., Pang, P.T., Puryear, C.B., Govindarajan, A., Deisseroth, K., Tonegawa, S., 2012. Optogenetic stimulation of a hippocampal engram activates fear memory recall. Nature. A research article which is perhaps a realization of some of suggestions in the Neves et al review. They use light to reactivate a fear memory. This suggests that activation of the hippocampal network that was active during memory formation is sufficient to elicit the memory.

Do you have a reference to a paper that summarizes the experimental evidence for this theory?

Thank you once again yamad for your thorough answer on this fascinating subject.

For a little more on ways in which the nervous system is plastic, see my answer here http://biology.stackexchange.com/a/1359/72

Memories are not stored in synapses: https://www.scientificamerican.com/article/memories-may-not-live-in-neurons-synapses/

I would like to point out some ways your understanding is wrong. "Neural networks" are usually a computer science term, only very, very loosely based on actual neural networks. The idea of layers in a neural network is pretty much an invention of computer science, it doesn't really reflect the reality. Also, neurons are not binary switches. It isn't so much about on/off, so much as a temporal rate code of action potentials. The actual brain sort of stochastic, and does not really work on the level of the single action potential.
The adaptation of the term "neural networks" by those devious computer scientists is unfortunate. Their work is virtually unrelated to actual neural networks.

I think you overstate the difference from neural networks. For instance, they are often not binary but rather have a smooth transition function (an idea copied from biology), are stochastic (an idea copied from biology) and doesn’t work on the level of a single AP. The adaptation of the term isn’t unfortunate, it’s a consequence of where the inspiration came from. Almost every CS concept has such an inspiration, and many non-CS concepts have as well (ever seen a crane?).

@KonradRudolph They simply don't approach the complexity of an actual neuronal network. Even the computational neuroscientists, who are explicitly trying to model neurons, fall short. It's an unfortunate adaptation of terms because now "neural network" no longer refers to a network of neurons. It refers to a crude simulacrum of a neural network.
The degree to which computer scientists have neglected the biology is disturbing and has stunted the field of AI.

@Preece I agree with all of your comment except the last sentence. Biology isn’t being neglected, it’s simply not relevant: neural networks in CS solve a problem, and that problem isn’t “try to model biology as accurately as possible”, nor is it trying to create a “classical” AI. It’s simply a statistical tool for pattern matching / clustering. That said, modelling the biology accurately would be interesting in its own right; it isn’t done for one simple reason: it’s not computationally feasible.

@KonradRudolph there is more to looking at the Biology then trying to model the nervous system. Neural structures are implementations of algorithms. I think analyzing these algorithms is at the heart of AI research. You don't need to model neurons to model neural algorithms. Trying to get AI without looking into them will (has) provided many interesting things, but the potential of the field is barely tapped.

@Preece But much of the work with neural networks isn’t really done in a context of AI research, it’s simply a tool in statistics, and here people are only interested in statistical properties, and it’s easy to show that a single hidden layer ANN is just as mathematically expressive as any more complex version so more complex versions are not just impractical, they are unnecessary. And on the AI / comp. neuroscience side of things there is a lot of research done in this area.

I can make a rough analogy in terms of digital media storage.
Our memories exist as a relationship between our perceptions and our sensations. Computers store input readily. However, humans store memories perceptually. This means who we are and how we remember an event permanently changes our recollection.
If you look at the progression of lossy video codecs as resolution has increased you'll see the algorithms have changed. Each generation has become accustomed to seeing certain types of video artifacts: from film, to analog static, to vhs, to h.264. Think of the algorithms as individual modes of perception.
We have ancient basal circuits which allow visual and frontal cortex areas to collaborate in the formation of memories. It's not an objective process. We all have our own algorithms.

Another very interesting post from you.  Thanks!


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Is it possible to trace of the ancestry of a person by only using his/her genetic information?
Is it possible to trace the descent of a person only using his/her genome sequence?

I edited your question to make it more clear. You mean the genetic information, the sequencing of the genome, right?

In short, yes, it is possible. There are companies that sequence part of your genome and then can trace it back to your ancestors. All human family trees can be traced back to their African origin 200 000 years ago, but the companies that sequence your genes do not do that. For example, 23andMe sequences only 1 million of your base pairs (single nucleotide polymorphisms (SNPs)). They trace your most recent heritage, which could lead to Europe, Africa, or Asia. They can basically trace which part of your chromosomes (and thus your ancestry) came from your mom or your dad:

Unlike the sex chromosomes and the mitochondrial DNA, which are inherited as blocks, the 22 biparental chromosomes, known as autosomes, are scrambled during reproduction. Through a process known as recombination, each parent pulls his or her paired set of 22 autosomes into chunks, then reassembles a new single set using half the material from each pair. The two single sets of chromomes from each parent are combined into a new paired set when a sperm fertilizes an egg.

You can read more about 23andMe here. There are other companies that are specialized in tracing your ancestry: Genetic Genealogy, DNA Tribes, and Heirlines.

Back when I was doing my PhD, there was a group in the same department as me working on an interesting project exploring the extent to which surnames (generally paternally inherited, at least in the modern west) and Y chromosomes (always paternally inherited) shared their descent.
The answers are always complicated, especially for more common surnames which have multiple origins. There are also confounding factors, such as the rate of non-paternity (which can be surprisingly high, often around 1-2%). It is, however, striking just how much you can tell about a person's heritage, just from a relatively small amount of genetic information.
For more info about the surnames work, see (1) and (2).