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Why does looking at bright light trigger sneezing in some people?
Why does looking at bright light trigger sneezing in some people?
Are there any recent studies that have found a cause for this Photic sneeze reflex? The Wikipedia article only references studies pertaining to the effect, stating that the cause is unknown. The article also states that "the condition affects 18–35% of the population", which seems to be quite a large percentage.
What could have lead to the development and persistence of such a genetic trait in humans? Are there any evolutionary advantages to this?

You are talking about the photic sneeze reflex.
The mechanisms are not entirely understood, but it affects 18-35% of the population.
According to Wikipedia (although this passage is not sourced):

The probable cause is a congenital
  malfunction in nerve signals in the
  trigeminal nerve nuclei. The fifth
  cranial nerve, called the trigeminal
  nerve, is apparently responsible for
  sneezes. Research suggests that some
  people have an association between
  this nerve and the nerve that
  transmits visual impulses to the
  brain. Overstimulation of the optic
  nerve triggers the trigeminal nerve,
  and this causes the photic sneeze
  reflex.

And, it could  be advantageous:

On the other hand, some people with
  the trait feel that it is
  advantageous. In the event that nasal
  discomfort occurs, but to an extent
  that is insufficient to induce a
  sneeze, intentionally seeking and
  finding a light source facilitates the
  sneezing process and is in turn a mode
  of relief.

Also, anecdotally, as I too photosneeze, I can see an advantage: should the atmosphere become weaker in the future, and allow more light to enter than we are accustomed to, it would discourage looking directly at the sun.

“not entirely understood” clashes with the explanation you give just below. The mechanism is entirely understood.

@Konrad That is just one of many possible explanations. It is not known how the specific trait causes this, and why it persists to today.

This happens to me every day. Someone told me once that it's because the 'light rattles the nerve in your eye'

@Konrad: Just because a phenomenon is "not entirely understood" doesn't mean that people don't have any ideas. The reverse is also true; in fact, I can think of very few things that are entirely understood.

In high school biology, we had to read a book called "Survival of the Sickest". In this book, the idea is presented that this reflex evolved during humankind's "caveman" days. The author presented the anthropological induction that after spending periods of time in a dark, dank cave, mold spores begin to accumulate on the human body and inside immediate and open orifices. The nose, being moist, open, and pulling air in, would then be prime nesting ground for mold. Some claim, then, that humans evolved this reflex as a way of clearing the nose of mold and other impurities upon exiting a cave and entering the brightly lit outside world.

This trait might be correlated to other traits not necessarily be or ever been under selection. I think the first step would be to understand the mechanism behind this connection and whether people from different population have the same rate of appearance of this trait (e.g. in northern population should be  more frequent)...

I agree, but the question was regarding why we evolved this trait, not how the body does it. And that's anthropology; we take the most likely and feasible conclusion from a sea of other likely conclusions. I just wanted to add a new dimension to the existing responses. You know, providing another path in which people can direct their research. Regarding correlating rates of expression and geolocation, I don't think northern populations would inherently show more expression, and I believe the author introduced some evidence of this type, but I cannot recall and I no longer have the book.


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How Do Adherent Cells In Culture Attach To A Plastic Dish?
I am particularly interested in MC3T3-E1 cells (mouse fibroblasts), which are adherent cells. Are hemidesmosomes involved in anchoring the cells to the plastic dish? What (if any) other molecules are involved? What happens at the molecular level?

http://jcb.rupress.org/content/88/3/473.full.pdf

I doubt that hemidesmosomes are much involved in 3T3 adhesion, just because they are characteristic of epithelial cells and fibroblasts are mesenchymal.
You're on the right track, though. It's going to be the same basic processes as adhesion to the extracellular matrix. The major factors will probably be integrins and focal adhesion assemblies.
You're also raising an important point for in vitro work, which is that adhesion to plastic is a very imperfect substitute for ECM, and this probably has implications for the behavior of the cells. If you're interested in ECM-dependent processes like migration, adhesion, and invasion, consider coating your plates with collagen or Matrigel.

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In which order did the cells of the immune system evolve?
Thinking about how complex the interactions between different types of immune system cells (T-helpers, T-Killers, Phagocytes, B-Cells etc.) are, it's fascinating how they all combine to get the desired effect.
However, I assume that they didn't all evolve simultaneously!  Is there any way to tell which immune cell developed first or any theories to that effect?  Perhaps that question is too specific, in which case was it humoral or cell mediated immunity that developed first?
You may find this paper helpful - unfortunately I'm still months off a campus so can't access it.

As I'm lucky enough to have access to that article, I'm going to extract whatever I can find to answer your question.
To begin with, innate immunity must have evolved first - we can see it at almost all stages of evolution. According to Cooper & Herrin, ever since aerobic respiration gave rise to multicellular organisms which in turn needed protection from invasion by single-cell organisms.
They state that around 500 million years ago, the first adaptive immune systems evolved in vertebrates, but do not explain how although they attempt to. Instead, they explain why we are not able to discern at the moment how this evolution came about. The main reason given is that it is unknown when some key cells evolved (namely natural killer cells and dendritic cells) Additionally, mice and humans evolved two different kinds of natural killer cell receptors relatively recently while sharing a common ancestor only quite a long time ago.
Apparently jawed and jawless vertebrates have also evolved two different kinds of adaptive immune systems. They both seem to rely on the same mechanisms but on a different molecular and genetic basis. Cooper & Herrin conclude that at the current level of research, we are not able to determine the evolution of our immune system.
Source: How did our complex immune system evolve?
Personally, if I'm allowed to give in to the temptation of speculation a bit, I would go by a similar strategy as the evolution of Krebs cycle - look which bits make sense even without the rest. There is of course the major obstacle that the cells of the immune system require an entirely new branch in haemopoiesis: all innate immune cells (aside from natural killer, NK cells) derive from the common myeloid progenitor, whereas all adaptive immune cells (and NK cells) derive from the common lymphoid progenitor.
I think this may even be a first hint: NK cells are innate immune cells but they derive from a different lineage at the highest level - they may have evolved as the first lymphoid cells after the myeloid innate immune cells. The next closest related cell is the cytotoxic T cell (CD8+, aka Tc), which utilises the exact same killing mechanisms (perforin+granzymes and Fas ligand) and attaches to other cells in almost the same way as the NK cell (immune synapse). It is also independent and can kill on its own, as long as it recognises its specific antigen. This is the main difference and also a very large step - the generation of the specific T cell receptor. Once the specific T cells receptor is developed, the step to helper T cells (CD4+, Th) is not far, although these perform a relatively bystander-like role in the immune response, steering the other immune cells from behind the scenes and not directly effecting any killing of the pathogen. Therefore I would guess that before helper T cells, B cells evolved, which are capable of producing antibodies. Antibodies themselves are very similar to the T cell receptor (not in gross structure but in the underlying genetic domains and their processing), so a 'detachable' antigen-specific T cell receptor may have evolved and ultimately caused the development of a new cell type. Once all these components are present, it is necessary (or beneficial) to control which cell types are the most active and in which way they act at the site of infection. This is exactly what helper T cells do, by steering the local immune response either into a Th1 (cytotoxic) or a Th2 ('humoral', anti-parasitic) response direction.

I talked about this to one of our professors; he mentioned that this sort of information is hard to find because funding is hard to find for these sorts of projects because they have little chance of being applicable to medicine :)

i dunno, I think it's a very interesting question... I'm in medical school and I find evolution to be a useful tool to help me understand a lot of concepts (anatomy, obviously, but other stuff too)... I guess big picture is frowned upon, since it doesn't follow some linear thought, even though nature may not use the same line of thinking we do...

To add to this, "To begin with, innate immunity must have evolved first ... since aerobic respiration gave rise to multicellular organisms which in turn needed protection from invasion by single-cell organisms."
I remember reading somewhere that the first TLR receptor began in Sponges...

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0051657

Information being interesting or useful for medical students doesn't necessarily make it applicable to medicine ;)

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What are key factors when evaluating and comparing miniprep columns?
I'm looking to comparing different protocols for minipreps for plasmid DNA purification. What factors should I be looking at? A few things come to mind:

Cost
Yield
Time per step
Replacement with other reagents
Spin vs. vacuum
Color and caps or lack thereof

Shopping advice is generally off-topic on all SE sites, and a question about the current price of columns is very localized in time and geographically.

I think this is a perfectly valid question.

I would recommend re-framing this question in how to objectively evaluate columns for making your own column-based purification kits. I have some good advice for you if this question gets re-opened.

I would not focus on awesthetic aspects like colour and caps. They don't influence the overall process or yield, and are just nice marketing aspects. The real things to consider are purity of extraction, quality of column resin, % yield, salt removal, flexibility of kit reagents and overall time and relative costs.

Storage conditions and shelf life are some of the things that you should consider in comparing columns.

Seems like you have covered the essentials here. I can't think of anything else.
Since the Qiagen patent on spin prep columns ran out, these kits are very cheap - $0.40 each?  In the 3 or 4 kits Ive used, they all seem to use the same protocol and about the same buffers, so there might be differences in quality or yield but if so, they are small.
You can even make your own buffers as the recipes are on open wet ware.  None of the kits i've used has suggested that these buffers can't be used.  They even usually call the buffers by the same names.
So your application would have be pretty discriminating to differentiate.  Even if this were the case, the quality could probably be improved a lot just by washing the column more.  Can you provide more details about how a few percent one way or another might be an issue?

I guess that it really doesn't matter. I guess we need to form a community wiki.

Congrats shigeta on being the first user to reach 5000 reputation!


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What happens to dextrorotatory amino acids in humans?
As indicated by this question, most of the amino acids in the human body have the L-chirality. As enzymes also have handedness, what happens to the D-amino acids that end up within the human body? Are they simply excreted? Are there enzymes (perhaps not in humans) that convert a D-amino acid to a L- one?

For the most part they are not used.  there are amino acid racemases, which interconvert L- and D- forms of some specific amino acids, which may be used in some particular biosynthetic or metabolic pathways.
In particular I'm thinking of firefly luciferase which uses D-Cysteine as a re-dox reagent to regenerate the luciferin substrate that the light - generating enzyme consumes.  see slide 4 here.
Nonribosomal peptide synthases often use D amino acids too.
I don't believe that d- amino acids are really incorporated into proteins though.

Don't most viruses rely on the availability of some amino acids that humans don't need or use? For example it is to my belief that the herpes virus relies on the availability of a amino acid that is not used by humans and is commonly found in chocolate?

Its pretty rare to require a nonstandard aa at all and a fast growing virus would be strongly inhibited by such a requirement.  The viral proteins I know of don't require a special amino acid.  I'm sure there are exceptions, but they are rare I believe.

You may also be interested in D-amino-acid oxidase (EC 1.4.3.3), a flavoprotein  (FAD) highly specific for the D-form of amino acids, which was discovered by Hans Krebs in 1935 (see here), and which has a wide distribution (including in humans).
The enzyme has been very thoroughly investigated, in particular by Massey & co-workers (see here for example)
D-amino-acid oxidase (EC 1.4.3.3) catalyzes the reaction which results in the following transformation

D-amino acid + H2O + O2 = 2-oxo carboxylate + NH3 + H2O2

2-Oxo-carboxylates are what used to be called α-keto acids.  For example, pyruvate is produced from D-Ala.
The product of the enzymatic reaction is the imino-acid which is nonenzymatically
hydrolyzed to a-keto acid (see Pollegioni et al., 1994, and references therein)
An excellent review

D-Amino Acid Oxidase: Physiological Role and Applications
by S. V. Khoronenkova & V. I. Tishkov,
Biochemistry (Moscow) is freely available from here

These authors have some intersting things to say about D-Serine, D-Proline and D-Alanine, and much more.
Additional Reference

Pollegioni L, Fukui K, Massey V. (1994) Studies on the kinetic mechanism of pig kidney D-amino acid oxidase by site-directed mutagenesis of  tyrosine 224 and tyrosine 228.  J. Biol. Chem. 269, 31666-31673. [pdf]

many D-amino acids are not used at all, although some have rather elaborate metabolism, both synthesis and utilization: D-alanine for example.

This sounds interesting. Is there any chance you could add some details (and/or links) to your answer?


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Why do men have nipples?
I'd be tempted to call nipples in men vestigial, but that suggests they have no modern function. They do have a function, of course, but only in women. So why do men (and all male mammals) have them?

I concur with one of the answers in that it is evolutionary not very important to remove features that are not used, specially in the case of female/male traits. Another more dramatic example is that of fish that live at the bottom of the ocean, that have developed new sensory organs to adapt to life without light, but they still have eyes from when they where living in shallower waters where light was present.

This is a typical case of if a trait is not advantageous, why does it exist.

Human male nipples are sexual markings, just like eyebrows, they are used to communicate. Also DNA has to be compact, so to program a complex body part like a chest, the same gene is used in both sexes. The same gene is used for hands and feet, also, which is why they are so similar with same number of toes in all animals except for bats and birds. Hooved animals get the same 4 limbs, exactly, because the same genes code for all limbs to be compact. I don't think that males can keep a newborn alive, but the nipples stay a bit big in males because they are visual markers like eyebrows.

In case you haven't noticed, male nipples function as an erogenous zone.  In humans, anyway.

@com.prehensible do you have a source for nipplesbeing used in communication, because this is the first I have ever heard of it.

Figuratively speaking. When I am walking along and I have my phone in my shirt pocket, it has happened that my nipple writes a text message and sends it to someone in my contacts list.

The two key concepts here are:

sex-specific selection, and the fact that
males and females share the majority of genes

1) sex-specific selection
Obviously, any population where females lacked nipples would be in trouble. Men, on the other hand, have no evolutionary need for them, but they don't pay much either - there is no strong selection against men with nipples. So at first sight, it seems that nipples are positively selected in females while seem to be quite neutral in males.
2) Males and females share the majority of genes
If you consider two separate species where the two species undergo different selection pressures, you will just see one species evolve toward one optimum while the other one will independently evolve toward the other optima.
However, males and females are not independent entities. The vast majority of our genes can be found in one sex as well as in the other sex. In other words, most male phenotypes do not evolve independently of female phenotypes. As a result of this interdependence, you can end up with the trait that is selected in one sex present in the other sex.
Evolutionary equilibrium
This is all much more rigorously defined in terms of selection coefficients and evolutionary pressure. Without going into the math, the questions of who has the highest selection coefficient and How differential is gene expression for this trait are important questions to predict the equilibrium trait value in both sexes.
Lack of a strong selection pressure
Finally, any trait that is seemingly not-useful has to have a significant disadvantage on the fitness of the organism to be selected out (Why do some bad traits evolve, and good ones don't?). Even if a trait is useless for both males and females it may persist. The case of females needing the trait just makes its elimination in males even more difficult, as explained above. However, in some mammalian species, the males do lack the nipples (Evolutionarily, why do male rats and horses lack nipples?).

I believe it is for this reason: the female body plan is the default one. Males are a variation upon that, in humans at least. Nipples are part of the basic body plan. For a man to not have them, he would need to actively evolve something that would prevent nipples from developing. There is no selective pressure for the development of such a thing, so it hasn't happened. Keep in mind that the code for the general body plan is shared between males and females. The Y chromosome modifies the development of that body plan so the person becomes male.

I think your answer makes sense from the 4th sentence on. As for the first three sentences: why would you define the female body plan as the "default" when half the population is male? Consider the opposite stance: given that the Y chromosome has fewer genes, it seems just as reasonable to say male is "default", female a modification. The point isn't that either is default, only that referring to either as default is subjective at best.

Female is default because organs first develop as female in the embryo and fetus, then transform into male. Also bear in mind that both sexes have X but onlymale have Y.

@Shep: Preece and Armatus are right, 'default' refers to sex determination. At the beginning of development, the cells have bipotential state. Then, the Sex-determining Region of the Y chromosome (SRY gene) express a transcription factor that initiates male development. In absence of Y chromosome, the human embryo develops as 'default' into a female.

@Armatus, that is true, but suffers from the ergo hoc proptor hoc logic fallacy. It's reasonable to say that the process of organ development is simply a hold over from the trajectory of how mammals have evolved.

@leonardo I was explaining why he would call it 'default', which is really just a word definable however we wish, like all other words. More importantly though, I kept it short because it's extremely annoying to type on SE on a phone.

Consider this. If a boy is born without the receptors for androgens, they will develop physically as a female. Check it out: http://en.wikipedia.org/wiki/Androgen_insensitivity_syndrome

Yes, I read it: "The gonads are testes regardless of phenotype due to the influence of the Y-chromosome. A 46,XY female thus does not have ovaries or a uterus, and can neither contribute an egg towards conception nor gestate a child." This means that if you have XY chromosomes, you will never be a normal woman, even if you insensitive to androgens.

That the female form is the default, and that there's no selection for removing some default trait, isn't enough to explain male nipples without  more information about the developmental sequence.  If nipples developed late in the process after sex determination, then the default status of female traits would be irrelevant to male nipples.  So the hypothesis should include the suggestion that nipples arise early in development.  Another possibility is that, regardless of what sex is the default, nipples are generatively entrenched.

No one has mentioned the Neutral Theory of Evolution, which explains mutations that are not necessarily motivated by increased "fitness".
Similarly, (and more to the point for this question) there is no selective pressure with regards to men's nipples.
Men have nipples because they find a purpose on women, but for men, there is no reason to not have them. From an evolutionary standpoint, it is simpler for men to have them. The more complex situation (women have nipples but men do not) would most likely only occur if there was some selective pressure for men to not have nipples.

@Shep And yet it misses the most crucial piece of information, while simply restating other things that have been said. In fact, his second point is almost an exact restatement of something I said. The female body plan is the default one, and that fact is the heart of a real answer.

No Preece, it is not saying the female body plan is the default one.  It is saying that if a trait is necessary for one gender, it is simpler to have it for both genders as well, unless it hinders the gender that doesnt' require it.

I agree that males probably have nipples just because there is positive selection in females for having nipples while it is neutral in males (there is gender specific selection coefficient for having nipples). However, this is not exactly what the Neutral Theory of Evolution states! This is probably why no one mentioned the Neutral Theory of Evolution. Therefore, the answer seems a bit misleading.

Also, the sentence mutations that are not necessarily motivated by increased "fitness" should better be replaced by the existence of alleles present at high frequency even though they don't confer a selective advantage (that is, they don't confer higher fitness to the carrier).

I'm astonished that this answer has 20 upvotes and was accepted. The correct answer to this question has nothing to do with the neutral theory of evolution (which, as Remy notes, is not the same as observing that some traits are neutral) and everything to do evolutionary constraint (in this case, with the timing of sex determination in the developing embryo).

This answer is wrong. The most active users of Biology.SE are considering the problem here.

Sorry to spoil the fun here, but male nipples are not completely useless. With stimulation and hormones, they can be used to make milk. I don't have a great peer reviewed source for this, because it is sort of common knowledge. I heard about it at a Le Leche Leage meeting when my son was small.
Here's another article

This is interesting: are there any documented instances of males (in any mammalian species) actually providing nutrition to their young this way?
Don't get me wrong; I certainly don't want to oppress men by suggesting that they shouldn't breastfeed if they want to, I've just never heard of them doing it. Maybe a question for SE.Parenting?

I remember seeing a male breast feeding in a discovery documentary long time ago. Though I was very small then and don't remember the name of the program.

It seems like it is more common in people and domesticated animals, but here is An Article about a bat that regularly suckles its offsrping, Here is a recent general article about this topic

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Why do stars disappear when I look at them?
I've noticed that when I'm out at night stars seem to vanish when I focus on them. I assume the reason is physiological and not astronomic. Why does this happen? I would expect that things would be more clear when I focus on them.

You might also notice this phenomenon while lying in bed, e.g. the dim glow from the illumination of a digital clock or small LED is often visible only if you look away (using peripheral vision).

When there is little light, the color-detecting cone cells are not sensitive enough, and all vision is done by rod cells. Cone cells are concentrated in the center of the eye, whereas rod cells are very rare in the center (image source):

When you focus on the star, the light is projected close to the center of the retina, where it will hit few rod cells. Thus the star appears to vanish.

citation for figure?

it's the link before the figure, I've added "image source" to the link


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Does red light preserve your night vision?
A number of companies have started marketing LED lamps that can be switched to a red mode. The claim is that red light is less harmful to one's night vision. Given that our eyes are less sensitive to red light, though, I'm not convinced that that red light is any better than dim white light. So if "equivalent" luminosity is defined where it's equally easy to, say, read a book in both light types, is there some physiological reason that red light is better than the equivalent white light?

This is a very good question.  Red light is routinely used by scientific laboratories to do low light dissections of retinas, and of course it is used in other low light contexts such as printing plate development.
In both of the above contexts, you have a clear subject: the retina being dissected or the printing plate being developed.  In the case of the printing plate the film has been designed to be specifically non-reactive to red light, so red light is used because your eyes can see it, but the film doesn't react to it.  Similarly in some scientific settings it makes sense to use red light during dissections.  Mice lack a long wavelength opsin, and therefore using a dim red light allows the experimenter to have a relative sight advantage compared to the mouse when keeping the mouse dark adapted.
But in the case you're asking about, there is no film or animal to serve as a second party.  So is there any intrinsic advantage to using red light?  As it turns out, there is.  The fovea, which is in the center of our eye and used for high acuity vision, has no rods and primarily L- or red sensitive cones.  Note the high density center area which lacks blue sensitive cones and has 2:1 red to green cones.

So by having red light present, you stimulate this area.  But red light is present in white light, too, why not just use that?  Leonardo's answer comes the closest, but it's a little off.  Red light is used because it preferentially stimulates L cones more than rods, but you are definitely not able to preserve night vision by using red light.  Why not?  Well it may look like it is possible to exclusively stimulate cones from the chromatic sensitivity figure

But that figure is 1) normalized and 2) not indicative of synaptic signal processing.  1000's of rods can converge onto a single ganglion cell, where cone convergence in the fovea can be on the order of a single cone per ganglion cell.  When it comes to perception, in order to compare the black rod line above with the red L-cone line you'd have to magnify it dramatically in size.  Practically speaking, it is nearly impossible to stimulate cone pathways without stimulating rod pathways when using a relatively broad spectrum LED that you're powering with a battery.  Maybe with a high power infrared laser.
So the purpose of using red light is to attempt to balance the activation of high sensitivity (red insensitive) rods with that of the low sensitivity (but red sensitive) cones in the fovea.  While using a similar level of rod activation with blue light, you would perceive a "blind spot" where your fovea is.
Finally, instrinsically photosensitive cells (the melanopsin cells brought up) do not factor into this processing.  These cells are activated only with extraordinarily bright levels of light, and the therefore do not enter into conversations dealing with night vision.

How can I see blue things by the center of my eye?

You're essentially a dichromat in the center of the eye, so you are blue-yellow color blind there.  That means you can distinguish blue from any color, except yellow, over a very small region.  You can find a more thorough discussion of the phenomenon by George Wald here

No, I can distinguish blue from yellow well in the center of my sight.

Center of sight here is defined as 8 minutes of arc, or about 1/8th of a degree of visual angle. It is a very critical angle, though, since it contains your fixation point.

I have no color blindness at fixation point.

Occam's razor be damned, this must be you.

@Anixx, do you have color blindness at the edge of your vision? (Answer, yes, but your brain fills it in)

@Shep I do not know about the edge, I know about the center.

@anixx, the point it that there's a lot more going on in your visual perception than the raw inputs from photoreceptors, ranging from temporal distortions to geometric reconstruction, it's hard to say definitively that you have no color blindness.

Do you disagree with this article recommending green light for night vision? http://www.astromax.org/activities/members/kniffen.htm

A year later, does anyone who understands eye biology agree with the article recommending green over red? :(

Your "2:1" link is now broken.

@endolith one more year later, I've read the article, and to me it does sound plausible. But do note the fact that was repeated there multiple times: the (scotopic) luminance of the chart must be really low, so that you, at the very least, don't saturate rods.

Here is a comparison of the range of wavelength sensitivities for both rod cells (labelled R) to the 3 subtypes of cones cells (labelled S, M and L) from Wikipedia.

If one is exposed to red light (above ~650 nm), it would activate the L-type cones mainly (possibly some M-type activation), but no rod activation. Rods are the low light receptor cells in our eyes, and as such, are very sensitive to the photon density, or brightness, entering the eye.
This is just my speculation, but I think it's plausible that if you were in a completely dark environment with just a red light, filtering out the higher frequencies, night vision could be spared in the sense that we don't activate the rod cells.

so the rods and cones adjust to brightness independently? If so, you may have the answer.

There will certainly be a response by each cell (if they are sensitive to the wavelengths of light), and sensitivity adjustments on a network level. It stands to reason that if you only activate using a frequency the L cones can be activated by, then it would work.

One such cell-specific mechanism, at least, is the direct result of active rhodopsin depletion: when it reacts to light, the rhodopsin pigment photobleaches and must be recycled to reactivate it. This recycling is quite slow in rod cells; Wikipedia says it takes about half an hour for the rhodopsin level to fully regenerate after exposure to bright light. Thus, to retain night vision, it would certainly seem desirable to avoid exposure to light at frequencies that can trigger rhodopsin transformation.

It doesn't quite work like this because the chart above shows the relative chromatic sensitivity, which is very different from the luminal sensitivity.  That means that you can't compare the height of the Rod curve to that of the L-type cone because they've been normalized to peaks with very different sensitivities.

A portion of this post has been incorporated into During night flying, which color lens for a flashlight is most beneficial? on [aviation.se].

Another reason why red lights are now sponsorized for night illumination is because they are supposed to be safer in terms of interference on the circadian cycle. This is not related to better vision, but better health.
The mammalian eye senses the light by the conventional rode and cone cells. However, a third light-sensing cell type has been recently identified. This third light-sensor is based on melanopsin-positive cells. While rod and cone cells respond best to white, full spectrum light, melanopsin cells only respond to a specific bandwidth of blue light, in the range of 446-477 nanometers. These cells connect and regulate brain centers responsible for circadian rhythms. Therefore, during the night, blue-light exposure might interfere with circadian rhytms facilitating the onset of depression and other metabolic derangements associated with circadian cycle see another SE question. White light contains also blue light, while red light does not. This is apparently the rationale to claim that red light is less harmful. However, no clinical evidence is available to my knowledge, and the threshold of blue light required to stimulate melanopsin receptors is probably over the common night illumination.
References:

 Hattar S, Lucas RJ, Mrosovsky N, Thompson S, Douglas RH, Hankins MW, Lem J, Biel M, Hofmann F, Foster RG, et al.. 2003. Melanopsin and rod-cone photoreceptive systems account for all major accessory visual functions in mice. Nature 424: 76–81.
 Holzman DC. 2010. What’s in a color? The unique human health effect of blue light. Environmental health perspectives 118: A22–7.

Very interesting, so a white light may mess up my sleep patterns? So is the answer to the night-vision question "no", "maybe", or "inconclusive"?

As I understand it, I would summarise this as "probably - maybe not your sleep pattern but your sleep quality will probably be affected".

@Armatus, I agree that it will probably affect my sleep patterns, but this answer says nothing about night-vision, that's what I'm curious about.

Thinking about it, since our eyes are closed - wouldn't any light become red-ish anyway because it would go through our (blood-filled) lids?

@Shep 1) sorry I'm not aware about consequences on night-vision, are companies selling red lamps claiming improvements on night-vision? 2) Red light is the only one passing through our tissues, but lamps are used after sunset when you are still awake.

@GianpaoloR, I don't want to turn this into a camping gear (or advertising) discussion, but yes, they are.

-1, sorry. This is a nice answer, but it's not an answer to the question asked here.

-1 here as well, intrinsically sensitive ganglion cells require an outrageously large amount of light to activate them.  They are not, at all, relevant to a discussion about night vision.

For the negative votes: thanks. I edited the answer to be more on target.

As mentioned in the other answer, red light does not affect the melanopsin receptors in eyes. These receptors not only regulate body rhythm but also regulate the diameters of the eye pupils. Once they are stimulated, the eye thinks that there is enough light around and the pupils get smaller to protect the eye against over-exposition, which reduces sensitivity.

any references for for melanopsin--pupils link?

In the linked article: "In the mammalian retina, besides the conventional rod-cone system, a melanopsin-associated photoreceptive system exists that conveys photic information for accessory visual functions such as pupillary light reflex and circadian photo-entrainment. "

There are multiple ways that pupils can be dilated, and this one only comes into play with very very bright light.

Yes red light is useful IF and only if >650 nm. Some of the answers above are close, but they miss the issue because they used the same scale for rods and cones which they are not on. Rods are several orders of magnitude more sensitive than cones and hence why the graphs above make it look like they have no sensitivity out to 700nm, they actually do, just not nearly as much.
Look up photochromatic step. It explains why >650nm works and it is well documented.

I looked up photochromatic step, but I'm not sure what I'm looking for, do you have some link to whatever you're talking about?

When I was in the Navy in 1957, I was an ECM sensor operator on a P-2 Neptune maritime patrol aircraft, originally built in 1941.  We flew 11-hour patrols low over the ocean.  At night all the pilot's Gage's and controls were illuminated with red light.  The flashlights we had were equipped with red lenses.  Most WWII aircraft were equipped the same way!   For some reason, the red light-night vision theory was obviously the belief back then.  Lieutenant Rudy Jopp, USN, Retired.

I think the most logical and simplistic scientific test in this situation would be application.  Buy red yard lamps and white yard lamps. Set up a various objects in the yard that would be increasingly harder to see in the dark (like a vision test where the letters get small but your distance is static.)
Sit outside with no light for an hour, more if you want, and then pick out the objects. This is your constant, what you will compare your results to. Repeat at least three times making note of which objects you can see.
Repeat this with each lamp, exposure for the exact amount of time as you waited in the dark. Both lamps should give you the same level of visibility, for accuracy. Take note of how long it took to be able to clearly see each object. I recommend a buddy out of your vision to keep track of time so you don't spoil the excitement by introducing light source.
Compare the results and you will know which light source affects your night-vision more.


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Could we transmit smells electronically?
We can encode sound and images in radio waves and send them, but presumably there's some physiological reason that we can't easily make a picture or video of a smell. Could we realistically break smells down into "primary scents", in analogy with "primary colors" and encode the information for easy reproduction?

I guess ultimately you could say the reason is the nature of the sense you're trying to reproduce. While seeing, hearing and touch are all senses based on non-material physical phenomena (sound waves, light rays, forces), the sense of smell serves as a tool to sample gaseous chemicals. This is why it's so intimately connected to taste, which is sampling the chemicals in solid and liquid matter.

There are only three kinds of optical receptors in the eye, but more than 900 kinds of olfactory receptors. Thus you can encode pictures with the three primary colors, but there is no small set of primary scents.
To transmit a smell via "primary scents", you'd have to create an artificial nose that monitors the response of each of the olfactory receptors, and then at the other end release a chemical mixture that has the exact same response pattern. (You won't find a one-to-one mapping of chemical compound to receptor.)

I think this is only half the answer. Encoding > 900 different olfactory signals shouldn’t be too big a problem – just create a distinctive signature for each molecule. We have this already in chemistry databases. The problem is actually converting the electrical signal back to a chemical one, since the alternative, plugging directly into the nerves of the nose, would be slightly unpleasant.

@KonradRudolph did you see the 2nd paragraph? ;)

I believe creating mixes of 900 substances could be rather hard. OTOH, electronic neurostimulation - bypassing the receptors and stimulating their respective nerves directly would be more doable (if still difficult).

one question: just how specifically can one stimulate those receptors. The fact that any wavelength of light stimulates all three photoreceptors to some degree has the interesting consequence that it's impossible to mimic the full color space with 3 primary colors. I wonder if scents would have a similar limitation.

In expansion to biocs' excellent answer, I would like to highlight some practical limitations of this. Suppose we did manage to create a huge database of exact chemical mixtures which produce all smells recognisable by humans. You would still meet some complications:

The output device (analogous to headphones or screen) would either need to be able to produce those substances on demand or have a large enough stack of them.

The former would require a whole lab built into one device - even with our miniature technology this would probably end up rather large.
The latter would require you to regularly stock up on all of the substances. You could sell these in an all-in-one package (again size becomes a problem) or in smaller "smell sets" (possibly practicable - but it would take a long time until people would understand what this is about)

The "smell substances" have to get to your nose somehow. At the same time, you probably don't want them in the rest of the room: While sound boxes are no problem because sound disappears rather quickly after being produced, smell can stick around for longer. The solution would be an apparatus that you insert into your nose. Not very practical, but people might do it.

I can't think of more at the moment but there probably are :)

In my view, the reason we can't transmit smell is that we don't understand it. That is, we don't have a solid understanding of how odor information is coded, so it is hard to imagine how to build a system that could reproduce that information.
This is sometimes discussed in terms of a multi-dimensional "odor space," where each odor could be described by its location along each dimension. The problem is that we don't really know what any of the dimensions are. By contrast, we know that visual space can be described by the intensity of a set of colors in a two-dimensional plane; auditory space is described by frequency and amplitude. It is clear that odors are comprised of chemicals, but we don't yet know where those chemicals fit in odor space. Understanding the odor space is a prerequisite to building a system that could transmit messages from it.
Also, to a great extent, how to engineer a smell transmission system is only partly a biological question. For instance, a CMYK printing system does a fine job at generating images that our RGB photoreceptors understand just fine. A telephone wire can transmit sound without a care about how the cochlea actually works. Transmitted pictures and transmitted sounds work because they activate our photoreceptors and auditory hair cells in the same pattern that the original images and sounds would. We can build systems to do this because we understand the nature of the information sensory systems decode, and we don't need a really deep understanding of the physiology to do that. (Of course, I think figuring out that physiology is great fun, but that's another point.) That is, to build a smell system, it's probably not really necessary to know what every one of the many olfactory receptors does. That's a detail of the way the mammalian olfactory system evolved. The important thing is to understand the nature of odor information. Then it really may be theoretically feasible to create a system to transmit odors.

A smell capsule with primary smells, concentrated non runny oils that can be heated up by a code sent to the capsule Then it will release the code, a built in fan will blow it to you from pc or phone, on a pc it could be renewed, maybe plugged in to a usb, Ive been thinking about this lately an have come to the conclusion that a smell Capsule would only need a collection of smells, if you type out banana there is a code behind the keys for the letter to appear, i think a smell program will be needed so that if some one sends you a coded image of a banana from there smell program the soon as you receive it and click on it the code will activate the same code in your program and you will smell the banana i have no idea how many primary smells there are or even if you can mix them but a collection of most common smells will do the job till the primary and mixing is masted,  I believe a pc is missing the smell capability and it will come along just as many other things have, it would be great to smell the ocean while watching ships or even while sailing one on a simulator, a heating of a oil scent will do the job fine, A thin wire sitting in each concentrated thick scented oil and all the different oils in separate compartments with there individual codes inside a complex capsule and a fan to blow out the heated one that the thin wire heated up

Can you add some references?


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Will humans and animals be harmed by frequencies outside their hearing range?
The human ear (for example) is sensitive to frequencies from 20Hz to 20kHz. Any sound beyond that limit would not be heard by us naturally.

Will it harm us (effect our ability to hear) when we hear sound more than 20kHz continuously?
Or...

Will it harm when we hear a 19,999Hz sound (which is upper limit) continuously?

this question needs to be restated to yield a sensible answer, but my explanation as to why became a little long, so I posted it as an answer below. It may actually be easier to answer if it were broken into two questions: Will sounds we can't hear hurt us (our ears specifically)? Will sounds just inside our hearing range hurt us?

The only sensible answer to these questions is "sometimes".
The reason: even a simple monotone must be described by both frequency and amplitude. Any frequency can cause harm with enough amplitude, and any frequency can be harmless when the amplitude is low enough. If you want to actually quantify the damage, you'll need something like an equal-loudness curve, but for damage rather than loudness. As a proxy, you could use the pain threshold of the equal-loudness curve.
As for the second question, there is nothing magical about 20kHz: physical damage will always fall on a spectrum, there is no single frequency and/or amplitude at which damage begins. If you set an oscillator to constant amplitude and slowly turn up the frequency, you'll notice that the sound slowly dies out around 20kHz. The damage threshold will behave the same way.

I am no an expert on this by any means. However, if I recall correctly, everything has a natural vibrational frequency. And, I imagine this would also be true for your ear-drum. So, if the eardrum is only responsive to vibrations between 20Hz-20kHz, I don't see how any frequencies outside of this limit could ever cause damage to the ear, because there would be no way for the eardrum to vibrate.

Hey @Bob. It's true that things have resonance frequencies, but you have to consider that your eardrum (and the rest of your body) can still vibrate at frequencies that you can't hear. The vibration still has to be translated to neurological impulses for you to hear them, and just because the sensory cells in your ear vibrate it doesn't mean they fire the connected neuron.

If you are talking about sound damaging the sound sensing organs in the ear, analogous to an ultrasonic heavy metal concert, I've found an interesting report just on this topic.

For ultrasonic components above 20 kHz, the limits were set to avoid hearing damage in the audible (lower) frequencies. One-third-octave band levels of 105-115 dB were observed to produce no temporary hearing loss, and were therefore judged non-hazardous in respect of permanent hearing damage.

Emphasis mine, from "Damage to human hearing by airborne sound of very high frequency or ultrasonic frequency"

If you are talking about high frequency sound from a explosion, or some sort of sonic cutter with intensities of such a level of compression or a high decibel range that conveys enough energy to physically damage something of course the answer would be 'yes this would damage your ears and the rest of the body too.
Operators of ultrasonic equipment with levels above 60 dB complained of headaches and fatigue, even nausea below 60 dB they felt no effect (reference table 7 in paper).  But they did not seem to have any hearing loss.
One soviet experiment is both informative and maybe also entertaining to read about:

An unspecified number of subjects were exposed for an hour to a tone of 20 kHz at 110 dB. Tests were made to examine shift of hearing threshold over the frequency range 250 Hz to 10 kHz. Pulse rate, body temperature and skin temperature were also monitored. These tests showed no appreciable effect, even when the Sound Pressure Level was increased to 115 dB. These same subjects were given a one hour exposure to a 5 kHz tone at 90 dB: a considerable TTS was found. The 5 kHz tone at 110 dB produced a powerful vascular response.
...
It seems safe to infer an underlying concept: A sound which does not produce temporary
dullness of hearing cannot produce a permanent noise-induced hearing loss.


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What is special about the N3 buffer for Qiagen minipreps?
For those who use Qiagen miniprep columns, they may be aware that the P3 buffer is the acetic acid step to neutralize cell lysis. They may also be aware that the Qiagen P3 buffer cannot be interchanged with the proprietary N3 buffer. It is also known that the N3 buffer is particularly unique since it primes the miniprep columns for binding. I was wondering about that priming step and what chemically primes the columns. Would it be appropriate to use QBT buffer to prime the miniprep columns?

The Qiagen manual for the Miniprep Kit states that buffer N3 contains guanidine hydrochloride and acetic acid. The MSDS for buffer N3 gives a bit more information:

Guanidinium hydrochloride 25-50%
Acetic acid 10-25%
pH 4.3

Buffer P3 uses 3M potassium acetate, the potassium is usually important in plasmid preparations as potassium SDS is used to precipitate the proteins in solution.
This information might be enough to create a buffer that should work with the silica-gel columns.
I also found a patent about a method for isolating nucleic acids that states that silica particles can bind nucleic acids in the presence of chaotropic salts, so the guianidinium hydrochloride is probably the important difference in the N3 buffer.
The patent for this method from Qiagen goes into even more detail, according to this the buffer composition  is:

N3: 4.2M guanidinium hydrochloride, 0.9M potassium acetate, pH 4.8

The two buffers can be exchanged, however using P3 for the miniprep protocol will yield dramatically low yield, so it can be used in a pinch, but is not recommended for a reason. These solutions may also be made up fresh for use with regenerated Qiagen columns.

N3 and P3 are different. N3 contain chaotropic agents. P3 does not.
Mainly there are two types of DNA purification kits on the market: silica membrane (glass fiber) based and DEAE anion exchange based. The silica membrane based method requires high concentration of chaotropic agents (salts that can change the water structure dramatically, GuHcl, GuSCN, NaI, are a few of them) present in the mixture before loading on to the spin column. DEAE based method, on the other hand, bind DNA based on the charge property on the DEAE resin which largely depends on the pH and ionic strength of the buffer. Chaotropic agents are not needed for DEAE based method.
In our lab we make our own kit using components and buffer recipe provided by Epoch Life Science for both mini prep and maxi prep. Their mini spin column and maxi DEAE column can be purchased without buffer. Their mini spin column also works perfectly with buffer from Qiagen and Lifetech. That's how we used up our leftover buffer from our old kits.


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Have any mutations or genetic loci been associated with exceptional longevity in humans?
Individuals that avoid age-related diseases into later life are known as 'exceptional survivors', and have increased longevity compared to their 'controls' (those that were born at a similar time, yet have 'aged' and died sooner). The Leiden Study determined that in these long-lived individuals there is a considerable genetic component contributing to the survival [Schoenmaker et al] (although this could equally be epigenetic - or even more likely, a combination of both).
I have read about studies that have identified genetic mutations that cause premature aging phenotypes (for instance mutations in the WRN gene cause Werner's Syndrome [Yu et al]).
I have yet to discover any studies that determine any genes/regions associated with resistance to age-related disease (i.e. those that age 'well'). My question is whether anyone knows of any such studies?
Arguably studies that have looked into predisposition to age-related diseases have found some mutations - for instance mutations within the 9p21 genetic locus (i.e. p16INK4a/CDKN2A) have been associated with heart disease and stroke independently (2 age-related diseases) [Wahlstrand et al]. Therefore individuals without any of these risk-increasing alleles could be considered predisposed to exceptional survival - but I see this as separate to my question. Are there any protective alleles/genes/loci that increase 'global' survival? Are there a few protective alleles, or many with small effects? Or are the exceptional survivors just without any disease-causing/risk-increasing alleles?
I am interested in published research (of course), but also in peoples general perceptions of the topic; there are plenty of theories of aging and longevity, but few facts - so please state what you 'believe', and explain why this is the case.
Thanks for your time.
p.s. I am aware that you can genetically modify lab models (e.g. C. elegans eat-2 mutants [Lakowski et al]) to live longer. I am interested in naturally occurring variants, specifically in humans (or that at least relate to human aging).

Update (11 May 2012)
I have found a study, published earlier this year, that finds a single genetic polymorphism to be associated (after correction for multiple testing) with centenarians [Sebastiani et al]. The SNP is in TOMM40/APOE (in LD), which is certainly interesting given the previous links between APOE and Alzheimer's (an age-related disease).
However, I am not convinced by the experimental design; they use age-at-death in centenarians as their cases (having genotyped them), and they use alive population controls as the controls. Whilst there is unlikely all these individual will become long-lived, a better design (to gain more power) would have been to use individuals who have died from 'premature' (e.g. between 60 and 70) age-related disease. So I am still waiting for a convincing study, but this does look promising!

i think you might mean 'longevity' rather than exceptional survival.  At different times in history different traits have been important to survival and it would be good if the title were more specific.   This is a pretty difficult question and its probably the case that there are no strong answers here yet.

@shigeta thanks for your observation. What I am getting at is the difference in longevity between individuals - i.e. are there any genetic mutations/loci associated with exceptional longevity, or put another way, have any genetic regions been associated with exceptional survival in humans - survival being simply 'not-having-died-yet'. Any study would naturally exclude accidental deaths, and only consider deaths from age-related diseases (and thus deaths from related to 'aging'). I am interested in the genetics, and therefore the (molecular) mechanism, by which the survival is achieved.

... I would gladly accept references to negative studies, or review papers that discuss the topic (i.e. are there individual SNPs that confer survival, or is it just being dealt a good genetic hand and not getting any deleterious alleles). Thanks.

It looks like you have uncovered the majority of the corpus of molecular genetics related to aging.  There is a follow up analysis just published this year by Sebastiani et al.  Pubmed has a feature that you can look at the publications that reference the paper you are looking at, and there are only reviews.  Nobody else seems to have done another yet.
You are probably right to feel that the power of the study is not great.  The researchers did try though. The Centenarians have long lived relatives and the controls had both parents die before they were 73.  Although the controls were 68 y.o. and older.  Yes not great.  The controls are very difficult because you don't want people who would die from heart attacks, hypertension and all sorts of things that would color the background.  Its a hard study to do.
No single gene will convey a phenotype like longevity.  Its basically impossible as the advantages would propogate through the population v quickly.  We could talk about how this trait is post-reproductive and about the grandmother effect, but I'm setting that aside for now.
The lack of statistical power of the study is also hampered because a mere 800 centenarians probably reflects dozens of different combinations of longevity groups.  (this is another reason all of these people are of specific european ancestry - to keep the number of variations in combinations down).  There are 281 significant mutations they found.   APOE is by far the most significant (fig1) but given the situation, just focusing on that one is not enough.
For example, even in flies it looks like the sir2-1 gene is not a single mutant anti aging phenotype.  When they cross the mutant strain with wildtype, the sir2.1 mutants live 15% longer.  Its at least one other mutation they had not detected in that caused a 50% longevity bump in the mutants.  Its probable that if there were 5 other important mutations, that the average crossover has one or more of these mutations with it too.
In order to try to understand how these loci might work together to expand life span, they created clusters of these SNPs (interestingly half of them are in genes which is relatively rare).  these clusters of genes look like they affect the lifespan together.  the paper is open and all the 281 genes are downloadable, each one of them has a known biological property you can look at.  how they fit together is still to be determined, but their clusters might point the way for now.

Thanks for your views. I do like the SNP 'profile' they determine, as it is much more likely that longevity is inherited via a large number of mutations with small effects - probably with epistatic relationships. And as you rightly point out, traits that extend maximum lifespan are unlikely to be directly selected for, unless they also confer a pre-reproductive advantage. Any lifespan extending SNPs with deleterious effects (comparatively) earlier in life will be selected against - so there is surely a lot of potential for there to be lifespan extending variants that just haven't been selected

@LukeTheDuke y.w.  at this point only so much work has been done.  All GWAS have this problem, but often there are more of them...


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Is there an evolutionary advantage to crying when sad?
It seems as though the act of crying when sad does nothing to relieve that sadness. Is there an advantage to crying from an evolutionary perspective, or is it the end result of a different process? Also, why is there the same physiological reaction of crying when in sadness or in pain?

Purely anecdotally it stirs empathy in peers so could lead to protection from other members of the group when an individual is vulnerable.

Just a note, not every behaviour (or generally phenotype) has to be advantageous. This question just assumes that there has to be one, and while I agree with Rory about the probably effect of this one, it’s not a valid assumption in general.

@KonradRudolph thanks for the specification, I'll edit the question.

@RoryM Yes but why does it stir empathy in peers rather than, say, blinking quickly?

I've seen various odd theories, but most commonly, it's just assumed to be a social signal. There's no inherent survival advantage to turning up the corners of your lips when you feel happy, either, but there is probably an advantage to letting other members of your group know how you're feeling. There may even be specific advantages to having this happen automatically and in ways that are slightly difficult to fake (tears or duchenne smiles).

As for why we use tears rather than some other kind of signal: the "choice" could have been a fluke of evolution (people coordinated around the first good signal that happened to develop). There's also some work suggesting that our physiological and behavioral responses to pain and sadness are mediated by proinflammatory hormones, so maybe it's not a coincidence that being sad superficially resembles having hay fever...

@octern some great comments, would be a good answer.

First, here is a link to an article that discussion the answer to your question:
Why Cry? Evolutionary Biologists Show Crying Can Strengthen Relationships
The original article to which it refers can be found here:
Emotional Tears as Biological Signals
To speculate a bit on Jez's question, crying in adults could be a result of our possible Neoteny. Crying in infant animals is extremely common as a way to elicit attention and sympathy from the mother. If we are neotenous apes, crying could be a left-over behavior that was seized by evolution, instead of being discarded.

It seems to me that your neoteny hypotesis just shifts the question. How did crying evolve in human infants? Animal pups only have the "vocalization" part of it, by the do not shed tears... (also, as Wikipedia reports, human newborns often cry without weeping, probably because of insufficient development of their nervous control)

@nico You're right, it's not a very satisfying hypothesis. I don't have the answers to your questions, but they are good questions.


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Turn off multithreading in pymol
By default, pymol seems to grab the number of cores on the system for rendering. How can I force it to only use one core?
Motivation:
I have a large collection time-series of of coordinate data from a computational protein folding experiment. I'd like batch render the generated pdb files into a movie in a programmatic way. Pymol however likes to eat up as many cores as it finds available. I'd like to retain some control of the computational burden (required for some computational cluster jobs). How can I force pymol to only use one (or n) core(s)?
Solution:
While the question was closed (as it was decided to not fit into biological criteria of the site) future visitors might find it useful to know the answer:
set max_threads, 1

The solution was found in a Biostars question.

I'm all for bioinformatics questions, but this one has absolutely no biological component to it.

@DanielStandage I'm sorry, and I'll happily move the question somewhere else. I don't think this belongs on SO, however. Do you have a good suggestion where?

@DanielStandage I only posted this question since I saw a high voted question here on pymol scripting: http://biology.stackexchange.com/q/732/822 Again let me know if this is not the intention of the site.

Try http://www.biostars.org/.

I think bioinformatics questions can definitely be on-topic for this site, assuming they include a significant biological component (or at least some biological component). The question you refer to includes as least a minimal description of a biological question being addressed, whereas this one focuses entirely on the software aspect.

@DanielStandage I've given some motivation for the question. I think that the question in general might be useful for others working with pymol scripts, so I'm going to leave it up. If the community decides to close, I'll understand.

@Danielstandage, lets take this to the meta.

@Hooked - what platform are you running? Linux?

@Luke Yes, this is on a Ubuntu 12.04 machine. Though I think the clusters run on a non-Debian distribution.

@DanielStandage So on the (fictional) Builders.SE site, "How do I fix my circular saw?" should be closed because it's not about building anything?

@NickT It would depend on what the scope of the Builders.SE site was, as per their FAQ. Our FAQ states: "Questions on interdisciplinary subjects like bioinformatics are also welcome, as long as they focus on the biological part of the subject."


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Why is the Patellar reflex not triggered when the tendon is extended slowly?
I have been previously told that the Patellar reflex (knee-jerk-reaction) exists to prevent the hyper-extension of the patellar tendon.  Yet if the impact to the tendon is delivered slowly - i.e. by pressing down on it rather than striking it - there is no reflex response.  Why is this, as surely the tendon is being extended by the same amount?

This effect you are observing has to do with the nature of the afferent neurons (Ia fibers), which carry a signal into the spinal cord and synapse onto motor neurons directly.  See this text (scroll down to section 1.10) for a diagram.  At their other end, these Ia fibers penetrate into the muscle and wrap themselves around the body of the muscle spindles, "[which] are specialized receptors that signal (a) the length and (b) the rate of change of length (velocity) of the muscle."
Because the main role of these spindles is to monitor the muscles for very rapid changes in length, the neurons have a static range which is optimized for these quick jerks (rather than firing over a wide range of velocities).  When you are stretching the muscle slowly, the Ia fiber is not building up a sufficient depolarization to fire off an action potential.

+1 this explains the mechanism nicely, but it makes me wonder: if the neurons are capable of measuring the length, then why isn't there a need for a reflex based on length? To bring in some teleology: why would the system be optimized only to automatically respond to (b) and not also to (a)?

Presumably because (a) is handled by higher, slower, functions. If nothing is happening particularly quickly the spinal cord can 'wait for instructions' from the brain. Reflexes exist because when things are happening very quickly it's too slow to contact the brain and wait for a reply. If they're happening slowly, that's not an issue.


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Could hydrogen replace oxygen in cellular respiration?
I was wondering what oxygen actually does in the body. I have seen a few answers to other questions that involve the electron chain and I am really not sure what that is. So I was wondering what oxygen does and could hydrogen do the same thing as a substitute?

Thanks for the clarifying edit @MadScientist. I would rescind my vote to close the question if I could, but alas...http://meta.stackexchange.com/questions/915/can-we-have-the-ability-to-rescind-a-close-vote-before-it-closes.

No, hydrogen could not replace oxygen because it has entirely different characteristics. The most important one is probably its electronegativity - oxygen 'pulls' electrons much 'stronger' than hydrogen.
Basics: Reduction potential
Oxygen is the so-called terminal electron acceptor of the electron transport chain in eukaryotes. You can see "reduction potential" as a kind of stored "energy" which molecules have, similar to the power stored in batteries (very similar actually). To make this text a bit shorter I'll call it "RP" from now on.
One maybe confusing detail is that a substance with low RP has "more energy" than a substance with high RP, so it is the opposite way of thinking.
In very generalised terms, metabolism means that molecules with a low RP (glucose) are oxidised (burned) and turn into molecules with much higher RP (CO2). Coupled with this, a different molecule with very high RP (oxygen) is reduced and becomes a molecule with slightly lower RP (H2O). (You may have heard this before - it's called a redox reaction.) *
The important part is that the RP "released" by the oxidisation (burning) is larger than the RP "taken up" by the reduction. The surplus leaves as energy - heat and light if you just burn the glucose. This is a spontaneous process, meaning it will occur just by itself - even if it takes a long time if nobody drops a match on it.
The idea of metabolism is to let that process happen - but use as much of the energy it releases as possible. This works by not just letting it burn, but intercepting that burning process at different stages so that at each step a bit of the RP can be taken off and stored in something else. This "something else" is NAD which I'm sure you've encountered before. Each step that glucose is burned down, another bit of NADH is made, which then has a respectable reduction potential.
NADH (leaving out NADPH here which is a bit different) is channeled into a process called oxidative phosphorylation which retrieves the reduction potential in an actual form of energy.
Basics: Terminal electron acceptor
Finally, the reduction potential I've been talking about all the time is really just electrons, involved in bonds which are "happy" to react. Passing down the reduction potential as I've explained is really a passing down of electrons into more and more stable, less reactive bonds. That's why it's called "electron transport chain". At the end of oxidative phosphorylation, those electrons are dropped onto O2 and make it into H2O. That's why O2 is called the "terminal electron acceptor".
Why Hydrogen can't replace Oxygen
Now to come back to why hydrogen cannot perform oxygen's function in our body. We use glucose as our source of reduction power and oxygen as our terminal electron acceptor. O has a high electronegativity (3.5) so it pulls electrons strongly towards it. H's electronegativity is only 2.1, so it's much weaker. O as a terminal electron acceptor works because it pulls them much stronger than H when they bond, so an O-H bond is almost like giving oxygen an electron. In order for hydrogen gas (H2) to perform the same function, it would need to be possible to drop electrons onto hydrogen in a bond where it pulls them much stronger than the other partner. They do exist, and such compounds are called hydrides. But the catch is: unlike H2O, these are normally strong reducing agents, meaning that hydrogen would rather not be in that bond. This not a feasible option for cell respiration, at least in humans, because it requires a lot of RP input. Making oxygen into H2O does not require a lot, it's a very cheap electron acceptor.
I hope I was able to put this in understandable terms. Let me know if I need to clarify anything.
--
*It works with other molecules than glucose->CO2 / O2->H2O too, many prokaryotes do that and in fact that's how batteries work

There's a small mix-up in your otherwise very nice post. The reduction potential describes the ability of a substance to be reduced. Thus oxygen does not have a low RP. In fact it has a pretty high reduction potential - it is a pretty good oxidizer. Similarly, glucose has a pretty low reduction potential. It is hard to reduce, it would much rather be oxidized. :-) High reduction potential->Strong oxidizing agent. I find it a bit counter-intuitive too.

Hahaha, what a blunder! I managed to let my lecturer's graphics mislead me. It shows a vertical reduction potential scale - but I didn't realise it's inverted with the lowest (most negative) at the top. I'll correct that of course, thanks!

You're welcome, you could always vote up my comment :D

I would say that while you could not just replace oxygen with hydrogen and expect life to just go on normally, it's possible for living things to be energetically provided for by H2 if it were found in the environment in enough plenty.  This is just speculation as Armatus points out metabolism does not work this way in animals, but I think that its quite possible a living organism could live off of H2 as an energy source.
Extremophiles can metabolize sulfur in underwater vents rather than oxygen.
In the soil, anoxic metabolisms reduce nitrogn gas to ammonia.
Photosynthesis uses light to reduce CO2 to glucose.  Atmospheric molecular oxygen is provided entirely by photosynthesis, and at one point there was little or none of it in the atmosphere and living things were found everywhere.  The glucose metabolism came after O2 appeared.
The main point is that H2 stores a reasonable amount of energy even if free oxygen is not available to drive the formation of water from another oxide, or even more exotic chemistry. There's not thermodynamic reason that it couldn't work and biology on earth has proven to be versatile in getting chemical energy wherever it needs to.
Its xenobiology and speculation, but I feel that if microorganisms evolved on a gas giant with a primarily hydrogen atmosphere, they could use the redox energy from H2, which is quite reactive even without O2 present.


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How did the human brain evolve?
A common question posed is, "how did the eye evolve?", because the eye is so complex.  However, this has been answered rather clearly and there are several examples around the world of animals in which the eye has evolved independently.
The human brain, however, only seems to have evolved once in the history of life on Earth - a brain which is capable of advanced speech, predicting the future given information on the past, producing art, imagining advanced abstract concepts such as algebra, creating advanced tools, etc.
How, then, could the human brain have evolved?  What stimulus was there for progressive Homo individuals to have brains that were slightly more advanced than the previous one's?  I've heard Richard Dawkins summarize it as "big brains are sexy", but that's a comment made in hindsight (and not even shared by all members of the human species today!)  At the time, why would a human female choose a male with a slightly larger brain, so slightly larger that the increased intelligence probably wouldn't be noticeable?  Or why would such an individual have an evolutionary advantage?

You should't confuse "big" with functional. Brain size is a side-effect.

Strongly suggested reading: The Accidental Mind by David J Linden

Hi Jez & a belated welcome to the Biology part of SO! This is a well written & well-received question. I think that it falls in the same trap as the eye question. Either the answer to the question "how did the human brain evolve" is "little by little and over large time scales", or as @nico points out, easily fills a book (or 20000 related research articles). The current answers here focus on a small part of a complete answer or lack detail for a complete answer. I do not think stack exchange will produce a wholly satisfying answer to this interesting question :(

New work suggests a prominent role for genes in the SRGAP2 family, as explained here. Data suggest a mechanism where incomplete duplication - most likely at SRGAP2C - created a novel gene function some 2–3 mya, which is a time corresponding to the transition from Australopithecus to Homo and the beginning of neocortex expansion. Further, in the mouse neocortex, Srgap2 promotes spine maturation and limits spine density, supporting sustained radial migration and leading to the emergence of human-specific features.

Very interesting, and if one gene duplication did indeed result in our brains suddenly getting more sophisticated, it would mean that Dawkins is dead wrong - there really would be one mother who didn't have "high intelligence capability" and a child that did suddenly have "high intelligence capability".  I can see how that's easier to explain evolutionarily than brains very slowly increasing in size.

@Jez, I don't think this means Dawkins was "dead wrong". Just because one gene mutation sets a species on a new evolutionary trajectory, it doesn't mean anything changes overnight. Note that while this mutation produced human-like features in rodents, the rodents didn't get any smarter. The mutation may have allowed human brains to develop, but it certainly didn't cause the jump you're talking about.

You made a few statements in the beginning of your question, I'm just going to focus on the last paragraph (which seems like your question).
When people try to understand evolution, a common fallacy is to assume you're looking at a linear progression, in this case that each surviving child is slightly more intelligent than his parents. This is confusing in part because it's at odds with day to day observation: dumb people have smart kids, tall people have short kids, etc.
It may help to visualize a it as a cloud rather than a line, with the really incompetent people being constantly clipped off the low end and the really competent being, as Richard Dawkins puts it, "sexy". Slowly, genes which tend to land people in the "really dumb" side are weeded out, genes that sometimes produced above-average intelligence are propagated. You can't think about evolution without considering the entire population.

OK, so I ask you the same question I did Preece; if this is such an obvious selection mechanism, why is it so extremely rare in evolution (only ever happened in humans)?  The next-most intelligent animals, chimps, can barely learn simple sign language, and they're on the same twig of the tree of life as us!

no one said it's an obvious selection mechanism. Having a large brain is expensive, for one thing, our brains consume about 20% of our energy, and run exclusively on glucose. In addition, human birth is far more excruciating than most mammals because babies have such huge heads. Our bodies are, in many ways, in a very awkward evolutionary state because the benefits of a big brain have only recently come to fruition.

why would such an individual have an evolutionary advantage?

First thing to keep in mind, is that natural selection will seize upon even very slight advantages and evolve them until the point where evolving them is no longer viable. So, to you a slight increase in intelligence might be unnoticeable, but in a naturally selecting system it would be very noticeable. Don't mix up sexual selection (where the preference of one sex shapes the selection of genes) with natural selection (where fitness to the environment shapes the selection of genes). Sexual selection may or may not have helped shape brain evolution, I can't produce evidence that it did.
But the increased fitness that slight gains in intelligence convey are easier to create evolutionary anecdotes about. It's simplistic to speak of just "intelligence" as evolving. Many different nervous structures evolved through out the animal kingdom, each with a function that directly increased fitness. I get the feeling that you're specifically talking about the evolution of the neocortex, because you reference human intelligence.
So, what I guess you're really asking is what evolutionary advantage does the neocortex convey? The answer isn't that hard, once you understand a little about the neocortex. It is an organ that simply models the external and internal world as perceived by your sensory organs. By external world, I mean modeling things like vision, hearing, touch, etc... By internal world, I mean modeling the actions you can perform, the plans you make, and so on. Increasing the size of the neocortex is essentially increasing the possible complexity of these models. Not only can you find more subtle and complex patterns out there, you can develop increasingly subtle plans and ruses too.
Watching documentary footage of tribal hunters provides a really stark look at just how useful the neocortex is. It frames our intelligence in terms of a situation similar to one we evolved in. It's not hard to imagine why the growth has been explosive. Outsmarting other animals is a great niche that in our evolutionary history was virtually unexploited.

But if it is so easy to see the advantage of our large neocortex, why is it so extremely rare (has never evolved outside of humans)?  Why wouldn't it also be beneficial enough in some other species to evolve to the same extent?

You're imagining that the human brain is unique in some way. It really isn't, we have the exact same structures as almost every mammal, from rodents to apes to dogs and cats. The main difference is that out neocortex is larger. Asking why the neocortex has only evolved in humans is like asking why white fur has only evolved in polar bears. Every mammal has hair, it's not "rare", it's just slightly different in different species. Also, consider that it's possible that intellectual gains are exponential to linear increases in cortical size.


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Finding exons in DNA problem

My attempt:  I looked for the TACs because I thought this would be AUG in mRNA and ultimately Methionine (the start codon). But apparently, that's not how you do this problem.  Im confused because the answer (shown in red) doesn't have any TACs and the boxes seem to start at random places.  I am also confused as to why my professor drew a box around both strands.  I thought only one strand at a time was turned into mRNA?
UPDATE:  It has occured to me that the entire strand is transcribed and then the introns are removed.  So I know why not to look for the TACs.  But now, how can I identify the exons?

look at the polyA which is added after transcription and follow 3'-->5'. The first nucleotide after the polyA is a G then G then A. Can you find back them in the DNA? Yes? As soon as you find a correspondance between the RNA and the DNA you are in the last exon. When the correspondance is lost, you are in a intron, when the correspondance get back, you are in the following exon.

After an RNA has been transcribed, in eukaryotes it is spliced before it leaves the nucleus. This means that parts of the RNA are removed (called introns) and the ends are capped. The parts left over in the mature mRNA after removing the introns are called exons.
The mRNA does not have to start with a start codon. There can be sequences before and after the bit which actually gets translated.
Yes, only one strand of DNA is transcribed into RNA. When you look at the mature mRNA below, read the first few bases and try to find their complements in the original DNA because this is where they were transcribed from. UCAUG is transcribed from the DNA AGTAC (with TCATG on the opposite side).
Now you look for the end of the mRNA. Bear in mind that all the A's are the poly-A tail which is added during splicing and determines how long the mRNA will persist in the cytoplasm. So you look for CUAGG in the original DNA, which must be transcribed from GATCC (with CTAGG on the opposite strand).
As you can see, that's exactly where the two red boxes start and end.
Now since the mRNA you see here is mature (indicated by the poly-A tail and the 5'-cap), that means introns have already been taken out. So any bases that you can see in the DNA between the start and end that we just found but not in the mRNA must have been an intron. Or the other way round: all the bases that are in the mRNA which you can also find in the DNA must be exons.
You will notice that exactly the bit that isn't in the red boxes doesn't appear in the mRNA anymore. Or: All of the mRNA is in the red boxes. The sequence is interrupted by a short bit which you can't find in the mRNA anymore - so this must be an intron.


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How fast does the rotor in ATP synthase spin?
I'm sure the exact frequency varies, but does anyone know roughly how many revolutions per minute / second the rotating center part makes?

According to "Resolution of distinct rotational substeps by submillisecond kinetic analysis of F1-ATPase" (Yasuda et al., Nature, 2001), ATPase rotates at 130 revolutions per second when saturated with ATP.

The rotation rates at various ATP concentrations obeyed the curve defined by a K m of ≈30 μM and a V max of ≈350 revolutions per second (21 000 revolutions per
minute) at 37°C.
Some reported values of very high ATPase activities would predictrapid rotations such as bovine mitochondrial F1 (≈310 rps) (37), yeast mitochondrial F1 (≈280 rps) (38), and E. coli FoF1 (≈300 rps) (39). Much lower ATPase activities corresponding to 10 ≈ 100 rps were also reported in many papers. However, if a significant fraction of  molecules in the bulk solution are in the ADP-Mg-inhibited state or other inactive states, as in the case of thermophilic FoF1, real ATPase activity specific for the working enzymes should be higher, and the rotation rates can be much faster. It is intriguing to learn whether these rapid rotations are really occurring in living cells.

These are excerpts from:
Ueno, H., Suzuki, T., Kinosita, K., & Yoshida, M. (2005). ATP-driven stepwise rotation of FoF1-ATP synthase. Proceedings of the National Academy of Sciences, 102(5), 1333-1338.
.

Welcome to Biology.SE! In the future please include full reference information for papers rather than just a link — this is because links can break (as can be seen in the previous answer). ——— Please also take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. In particular, it would make a more effective answer if you were to summarize the results from this paper rather than just copying text (including reference numbers that have no context). Thanks!


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Why is selfishness the 'obvious' strategy?
Thinking of behaviours an organism can adapt, at the very base an action can always be either selfish or altruistic (cooperative).
Usually, selfish behaviour is assumed to be the preferred choice and the question is how altruistic behaviour comes about.
But if reciprocal altruism can give both participants a higher benefit than their respective costs (which it usually does), why would selfish behaviour (in the sense of behaviour which reaps benefit at another entity's expense) be what we assume to happen? If evolution tends to optimise things, why does it not optimise this?

What about Symbiosis? In the end you can see every kind of cooperative behaviour as a selfish one if you want to...

Thanks for the comment. You made me realise that the question needs more clarification and at the same time you helped me find the answer to it myself :) I will update the question and add my own answer.

It basically comes down to a question of the unit of selection.
From the common viewpoint, in which natural selection is seen as acting on individual organisms, it's almost a tautology that the organisms favored by selection are those that maximize their own reproductive fitness.  Thus, the possibility that some organisms might engage in acts that help another organism at their own expense may seem like a paradox, or at least a puzzle in need of explanation.
One solution to this puzzle is offered by the gene-centered view of evolution, where selection is viewed as acting on genes, with organisms being merely convenient (and usually, but not always, cooperative) collections of genes that (usually) reproduce together.  From this viewpoint, it is not at all surprising that evolution might favor genes that cause an organism to help other organisms, provided that there's a statistical tendency for those other organisms to also be carrying the same gene.
Other mechanisms for the evolution of cooperation do also exist.  For example, organisms with sufficiently advanced cognitive capabilities may indeed engage in reciprocal altruism, where they help others only if those others have shown themselves willing to help them in exchange.  Such exchanges, being mutually beneficial, do indeed help both participating organisms, and are thus selected for even at the organism level.  However, to persist (in the absence of gene or group level selection effects), they generally need some form of enforcement and/or learning mechanism — if cheaters can keep receiving help without ever helping anyone else, they'll do better than the cooperators and eventually displace them.
Also, in some situations, an organism acting simply to help itself (e.g. by modifying its environment to be more suitable for itself) may also end up helping other organisms that just happen to be nearby.  In such a situation, selection indeed favors cooperative behavior in isolated organisms by default, with the evolution and persistence of "freeloaders" (who spend less effort on improving their surrounding, relying instead on others to do the work) being only possible as long as there are sufficiently many cooperators around.
Of course, none of these mechanisms are mutually exclusive.  Indeed, the presence of some gene-level selection effects tends to be unavoidable in any realistic situation involving cooperative interactions; it's hard to come up with a setting in which no two interacting organisms ever share genes, and obviously the fact that two organisms share a common genetic predisposition to cooperate makes them more likely to do so when they meet.
(However, one not-so-realistic theoretical limit case where that does happen is that of an infinitesimally rare cooperative mutant invading an infinitely large and well mixed population.  The popular use of this simplifying limit assumption in classical models of evolution may be one reasons why cooperative behavior is so often seen as something remarkable and hard to explain by evolutionary theorists.)

This is essentially what I was going to write myself: because there is such a thing as individuals which differ, and individuals who do better (variation and competition due to finite resources), individuals who do themselves best are successful. The biggest exception is probably kin selection since altruism towards relatives can benefit the own genes more than selfishness.

Selfish behaviour is not necessarily preferred. It depends on the game (game theory). For example, in absence of relatedness and reciprocity, we would expect:

All the population defect in the Prisoner's dilemna
Some defect and some cooperate in the snow-drift game
Either all inds defect or all inds cooperate (depending on initial condition because it is an unstable equilibrium) in the stag hunt game.

When there is relatedness (genetic correlation) between individuals, Hamilton's theory of inclusive fitness says that:
$$R\cdot\frac{dw(x,y,z)}{dx}>\frac{dw(x,y,z)}{dy}$$
where the letter d means partial derivative, the function w() is the fitness function and the parameters of the fitness function represent the trait of the focla individual (x), the mean trait in the subpopulation (y) and the mean trait in the populaiton (z). For more information This fitness function depends one the ratio of the fecundity function of cooperating over defecting.
These fecundity functions in the prisoner's dilemna equals the baseline fecundity (usually we write down 1) plus the payoff when the other cooperate times the probability that the interacting individual cooperate plus the payoff when the interacting individual defect times the probability that it defects. It gives:
$$f(cooperate) = 1 + (B-C)x + C(1-x)$$ if the individuals get the payoff B-C when the interacting individual also cooperates and Cwhen the interactzing individual defects. xis the probability that the other individual cooperates.
Usually, the first equation above is written under the form:
$RB>C$
Instead of R, you might as well consider another correlation, a correlation of behaviour due to reciprocity. The equation becomes:
$kB>C$
You might as well consider both, reciporcity and relatedness which give:
$$BR-C+k\cdot(B-RC)$$


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Finding DNA from Amino Acid sequence problem

My attempt: First I took the single letter AA codes and made them amino acids.  So, the first one is Trp which is 5'-UGG-3'.   From this I got the DNA sequence 3'-CCA-5'.  However, the correct answer (shown in red) doesn't have this sequence.  What did i do wrong?

Your approach to translate the AA sequence, codon by codon, was correct. This was a bit of a trick question because to recognize it, you had to read the sequence backwards.
UGG-CAA-GGT-CAC etc is read directly off of the 3'->5' strand of the circled answer, reading from right to left.
The bottom left is a red herring because it starts with a start codon, ATG, but reading beyond the start codon, the sequence wouldn't match.


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Is it true that newborn babies don't produce tears while crying? Why?
Well, I was just going through an article on eye, where in fun facts it was mentioned that newly born (for initial 1 to 3 months) babies do not produce tear while crying. Actually, I have found this true.
Now, I am wondering why is it so? Does any one know the reason behind this?

See my comment here: http://biology.stackexchange.com/questions/2087/is-there-an-evolutionary-advantage-to-crying-when-sad/2100#comment2763_2100 Seems to be related to insufficient development of their nervous control (at least according to Wikipedia)

It is not completely true.  Babies develop the lacrimal system at 42 days, in utero.  The canals and ducts for tears are formed at 60 days [2].

At birth, tear production by the lacrimal gland is minimal. Normal tearing develops several days to 2 weeks after birth.[1]

Some 6% of newborns are born with a tear duct obstruction (in some online articles it stated up to 10%, but I think my source is more reliable).  The child still produces tears, but they can well up on the eyelid [2].
Other more serious abnormalities can cause this problem.  Duct cysts or hemangiomas can also cause tear duct blockages in more severe cases.  Various factors, such as anatomical abnormalities and problems with pumping tears increase the propensity for the disorder in children with Trisomy-21 [2].  As nico has alluded to in the comments, there may be a lag in the development of the physiology of tear production even in non-Trisomy-21 children.

[1] Thomas K. McInerny, MD, FAAP, ed. 2009. American Academy of Pediatrics Textbook of Pediatric Care. Elk Grove Village, IL. American Academy of Pediatrics, p1706.
[2]M. E. Wilson et al. (eds.), Pediatric Ophthalmology, 2009, pp. 276-284.  DOI 10.1007/978-3-540-68632-3_1.

This does not really answer the question of whether newborns cry without weeping. They have a lacrimal system, but that does not mean that 1) it is fully functional and 2) they use it when crying.

@nico I didn't find anything on the nervous control of the ducts other than its pathophysiology in Trisomy-21 patients.  The original question did not ask about full functionality, so I made some presumptions based on the fact that no further anatomical development occurred was noted to occur after birth.  If you find some information on the neurophysiological development, I look forward to reading it!


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Are there any structures in mammals that are used only by males?
There are examples of structures which only serve a purpose in females, but it seems like the opposite could also be true. Are there any structures which exist in both mammalian sexes and only serve a purpose in males?

I would speculate the prostate.

but it seems like the opposite should also be true. Why?

@nico because a structure that becomes vestigial in females and still serves some purpose in males will have evolutionary pressure to remain intact in both sexes. Likewise, a mutation that serves a useful purpose in only half the population will still be a useful mutation as far as the population is concerned.

@Shep: my point is the fact that an example of a shared structure that is used only in females exist does not in any way imply that the opposite should also be true. It could, but there is definitely no causality here.

@nico ah, should --> could, I didn't mean to imply any causality there.

Some researchers consider the neural circuitry responsible for orgasm vestigial in women. I disagree with this for a number of reasons, but here is a book exploring the hypothesis:
http://www.amazon.com/The-Case-Female-Orgasm-Evolution/dp/0674022467/ref=sr_1_1?ie=UTF8&qid=1336286206&sr=8-1

Females of Rangifer tarandus have horns which only used by males in competitions. Other species of deer only have males with horns.
Apart from this, possibly, clitoris and vulvar lips have no purpose in women: the vulvar lips are underdeveloped halves of scrotum, and clitoris has no need to be so sensitive as it is because it plays no role in sexual reproduction in females.