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Introductory biology text for an outsider
I'm a maths major and I have an interest in learning biology. I know very, very little; I know how babies are made and that's about it. Could anyone recommend a stimulating text to read for its own sake and also to use to learn biology?

What aspect of biology do you wish to learn? (Human biology, plant biology or Zoology? I'm guessing you are interested in human biology from your e-mail). For example are you looking to explore mathematical applications within biology?-e.g. mathematical biology or you just want to study biology in your leisure.

I'm being deliberately vague here; I just want very basic biology and not specific at all. I am deliberately NOT looking for a mathematical perspective, however I would like a generally insightful and interesting view on the topic.

I think Helena Curtis Biology is a quite interesting book. It was written many years ago and so does not involve really recent research but it is really insightful. Another book I would recommend is Campbell - it is both recently written and thought provoking. You should also read magazines like Scientific American to get insight into latest happenings.

I found the Campbell Biology textbook to be quite comprehensive and approachable. I think many introductory biology courses use it.
http://www.amazon.com/Campbell-Biology-Edition-Jane-Reece/dp/0321558235

Yes.  This one. By the time I graduated, I think I had 4 editions.

There are tons of books and it is quite hard to find one that gives such a broad overview. Campbell Biology is a book that basically covered the first year of my Bachelor degree in biology. I am not sure it would be very stimulating though! If there is a specific branch of biology that interests you, let us know we'll be able to give you a better advice.
As a math Major you might enjoy some fields of biology that are highly mathematized. For example, system biology or theoretical evolutionary biology. For the latter, you might like to read Evolutionary Dynamics: Exploring the Equations of Life book from Martin Nowak. But I am afraid it might not be a nice idea to directly jump into some specific subject before having a good overview of the life sciences.
Otherwise you might appreciate some books of popular (but good level) science such as the Extended Phenotype from Richard Dawkins. This book is very stimulating and I think it starts with some basic definitions of biological concepts such those of "alleles" or "phenotype".
I gave you two examples of books from the field of theoretical evolutionary biology. For more recommendations in this field, please have a look at Books on population or evolutionary genetics?.
Hope this helps a bit!

Could you list the book title that you linked to?  The link is now dead but I'd be interested in checking out the book.

@Addem Thanks for highlighting my broken links. It was a link for the Campbell. The same one as suggested in xuanji's answer. See edit.

You should check out Richard Dawkins' book The Greatest Show on Earth: The Evidence for Evolution
It does focus heavily on evolution but it is an amazing book on biology in general.  He covers a wide rage of other topics, from how birds flock so elegantly to dating fossils using dendrochronology.  The chapter on embryology is fascinating.

@xuanji offers a good choice with Campbell Biology  if you want a text solid biology textbook. I've got a copy in my library. I would suggest buying a previous edition if you're trying to save money. However, the book could be a bit dry. Reading semi-popular books on topics you are interested about would probably be better approach.
Both @ebrohman and @Remi.b provide good suggestions with Dawkins. I also like Ernst Mayr's What is evolution on the topic of evolution.
For ecology, check out books by E.O. Wilson or Jared Diamond.
If you want to learn more about environmental toxicology, Rachel Carson's Silent Spring is a good book to start off with.
If you're looking for a mathematical biology book, Linda Allen has two biomath text books, one on deterministic models the other on stochastic models. Murry's also produced some classical mathematical biology books. Most people would consider these books dry, but as a mathematician, you might like them.
James Watson can be controversial but he's written some interesting books. His Double Helix is a good read.
If you provide what specific type of biology and mathematics you are interested in, I will provide more suggestions.

The Bible of biology is the Alberts' Molecular Biology of the Cell:

http://www.ncbi.nlm.nih.gov/books/NBK21054/

The Campbell is also pretty good and maybe easier to read..

Campell would provide a better overview if the OP wants to learn about more than molecular biology.


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Molecular Evolution: Mrbayes never stops?
When I use my own data to build Bayesian phylogenetic trees using the software Mrbayes, after many generations, it never reaches stopping status (namely, the average standard deviation of split frequencies below 0.01).
What should I do to get to this point?
The dtype is protein, 37 taxa were included, the model I used was as follows:
prset aamodel=fixed(wag);
lset rates=Invgamma;
mcmc ngen=100000 samplefreq=100

There are a few things you can try to get better convergence. I'd try the following in increasing order of difficulty/effort/processing time.

Be satisfied with a higher standard deviation of split frequencies. The MrBayes manual says "A rough guide is that an average standard deviation below 0.01 is very good indication of convergence, while values between 0.01 and 0.05 may be adequate depending on the purpose of your analysis." Especially if you are interested only in the best supported parts of the tree, this is a viable option. 0.01 is only a guideline.
Run the model for more generations. Maybe it is on the way to converging, but it hasn't gotten there yet. 100000 is not really that many. Try 200000 or 500000 and see if the model space is still being explored. You can examine the .p files using Tracer. You may already be doing this, and this is why you know it is not converging. If you look at the plots of the log-likelihoods, they will become relatively stable when the run has reached the optimal location.
Try running with a different amino acid model or without the inverse gamma rate prior. If you can get a simpler model to converge, then
Increase the number of chains to 4 or 8. If you have the ability to run in parallel, this will greatly speed up your analyses.
Try iteratively changing the heating parameter by setting Temp to a lower value, which will increase the likelihood of a swap. By default, Temp = 0.1. You can watch the progress of the analysis in the command line and see which are the heated chains and which is the cold chain.

Many thanks, kmm! These are very useful suggestions, and with these information, I really got good results. There is also another question: the model I selected was based on the results of model test program ProtTest, so although it is difficult to converge, is it the right way to choose a simple model for the analysis? (I mean this operation will produce good results, but the results may be controversal.)

And if all what kmm suggests fail, it may be time to fiddle with finer tunings, such as concerning the proposals that are used to modify the Markov chain.

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Are the brains of any herbivorous animals capable of utilising ketone bodies as an energy source?
I ask this question because earlier today I heard from a lecturer at my university that a sheep's brain cannot utilise ketone bodies as an energy source and hence with insufficient glucose supply for their brains they die.

link I think this link provides some relevant information.

My answer is limited to sheep.
Background
The metabolites referred to as ketone bodies (which I will refer to as ketones from now on) are acetoacetate and β-hydroxybutyrate. In humans these are produced in the liver when the amount of acetoacetyl CoA being produced exceeds the capacity of the TCA cycle. These acetyl groups are instead used to produce acetoacetate, and this can be reduced to β-hydroxybutyrate.
The production of significant amounts of ketones occurs during fasting (diabetic ketosis will not be considered here). Once glycogen has run out, the bodies requirement for glucose has to be met by gluconeogenesis (mainly in the liver) - glucose is synthesised from various carbon skeletons including glycerol and the products of amino acid catabolism (coming from muscle protein turnover). This means that in the liver the function of the TCA cycle shifts almost entirely to supplying oxaloacetate for gluconeogenesis, via the activity of phosphoenolpyruvate carboxykinase. Thus there is no oxaloacetate available for citrate synthase, so acetyl CoA cannot enter the TCA cycle. However, because fasting also results in fat mobilisation the level of acetyl CoA in liver cells goes up (acetyl CoA is the end product of fatty acid breakdown).
So what is going on here? During fasting the fuel economy of the body has to switch from being heavily glucose-based to one which uses carbon from fat and from protein. The ketones are the manifestation of this, and many tissues become heavy users of ketones during fasting as blood levels rise to 5 mM within a few days. This means that the glucose being produced by the liver can be directed towards tissues which are more dependent upon glucose. The classic example of such a tissue is the brain, but in humans even the brain begins to use ketones heavily during fasting.
In ruminants the situation is entirely different. Ruminants rely upon the bacteria in the rumen to metabolise carbohydrate in their diet and this results in large amounts of alimentary ketones entering the blood directly. For their glucose supply ruminants rely entirely upon gluconeogenesis, and the substrate for this is propionate, another end product of bacterial metabolism in the rumen: a lactating dairy cow will synthesise over 3 kg of glucose per day.
So, when I read this question my reaction was that the statement must be incorrect - surely it would make sense for sheep to use ketones in all tissues. However my intuition was wrong - according to

Pell JM.& Bergmane N(1983) Cerebral metabolism of amino acids and glucose in fed and fasted sheep. Am. J. Physiol. 244: E282-E289

cited in

Heitmann RN et al. (1987) Hepatic ketogenesis and peripheral ketone body utilization in the ruminant. J. Nutrition 117: 1174-1180
"Although there is some oxidation of ketone bodies by the brain tissues of humans and rats during prolonged fasting, Pell and Bergman ,using an elegant in vivo preparation, have shown no significant uptake or oxidation of ketone bodies by sheep brain."

I don't have access to the Pell & Bergmane paper so I cannot explain what they actually did. What is clear from the review by Heitmann et al. however is that fasting ruminants respond in the same way that we do, switching to hepatic ketogenesis, and presumably they also maintain gluconeogenesis, using not propionate, but amino acid carbon skeletons. The context of the statement quoted above suggests that even in the fasted state the sheep brain doesn't use ketones.

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Why is a nicotinamide-tryptophan combination used to treat affective episodes in a few older clinical trials?
At least one of the journal articles that reported on such clinical trials allured to the nicotinamide-tryptophan pathway that I assume must be related to the metabolism of tryptophan into serotonin since at least one of these journal articles placed some emphasis on the serotonin hypothesis of depression.


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Virus titre and copy number of integration
If I need to preform a genome-wide high throughput screen using pooled shRNA library infection followed by deconvolution by deep sequencing, how would I determine the optimal infection rate at which the majority of cells only be infected with single copy of shRNA? Thanks!

Do you mean infection, transduction, or transfection?  If you mean infection, what virus are you using?  Several viruses you can use an MOI of 1 to get that result, but others wouldn't produce it with an MOI of 10 (good example of the later is RSV).  Presumably you are using a lenti system?

I also don't know what cells you're using.  If your lab has never done lenti infections before, I recommend pLKO.1-puro optimization (or an analog) before trying shRNA library.  That should give you a ball park MOI, but a good guess is between .5-3

Yes I am using Lentivirus in human melanocytes. I need to get MOI of 1(one copy per cells) for majority cells for the purpose of later sequencing. I just need to determine the infection rate to achieve MOI of 1(is there asomewhat methematical model for this?)

Oh, are you wanting to know how to titer lentivirus to get the molecules or TU per mL? I didn't get that from your question.  Calculating MOI is easy with the titer information.  You have the number of particles/PFU/FFU/ELISA/RT-PCR readout per mL of virus stock.  You then take the amount of virus you added to your cells (in what ever units) and divide by the total cell count.  Perhaps I'm still not clear on what you want, but transduction optimization and titering are different things.

I did lentivirus infection before using pLKO system and I know the  infection rate judging by GFP or puroR. However, we don't know the copy numbers of virus in each cell. The copy number of virus per cell is important when we are doing a pooled library screen-I don't want  cells infected with  copies of virus carry different genes. My questions is, by either mathematical  or experimental approach, how we determine the optimal amount of virus added to cells so that the majority of cells will only carry one copy of virus while we still have a  reasonable infection rate. Thanks!


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Why does the heart use lipids (and not glucose)?
Fetal hearts use glucose as their primary metabolic substrate.  Adult hearts use free fatty acids, which are less efficient (require more $O_2$ to synthesize the same amount of ATP); however, during cardiac failure, the heart can switch to glucose utilization.  Why doesn't it just use glucose all the time?

The heart uses lipid and glucose (although the fatty acids contribute a much greater fraction to cardiac energy production - you can experimentally cause damage to the cardiac myocytes if you decrease the ability of the heart to metabolize either glucose or fatty acid fuels

Lipids require more oxygen to burn, but also they are cheaper to store (since they have great calorific power than carbohydrates and they're hydrophobic, thus not requiring water for their storage). The body can store so much lipids that it becomes an almost everlasting energy source (A normal adult have enough energy stored as fat to allow basal metabolism for weeks to months), which cannot apply to glucose. If fat is not present, glucose would have vanished from the body long time ago. Glucose levels must be maintained at a certain level, because it's the main energy source for the brain (which cannot use lipids ). The brain can use ketone bodies (product of fat oxidation) as a last resort.
For all the previous reasons, the heart (and many other organs, like the liver) uses fat while possible. If possible just means when not starving to death and with sufficient oxygen supply. This second condition doesn't apply to heart failure. In this case, oxygen supply fails and the tissue switch to glucose just because they can use it without oxygen (glycolysis and lactic fermentation).

But...most tissues strongly prefer glucose under those conditions (not starving to death and with sufficient oxygen supply), even if you are fat, typically cited as being due to the increased oxidative stress of fatty acid metabolism; the question is why the heart prefers fatty acids instead, despite this.

The usual explanation is that glucose is potentially dangerous because there is always a chance glycolysis will run too fast and produce lactic acid.  While lactic acid buildup is no big deal for a skeletal muscle, lactic acid build up in the heart can affect the ion channels and hence the heart rhythm.
Fuels for the heart are fatty acids, ketone bodies, and lactic acid taken from the blood.  Evidently when the source of lactic acid is the blood, the heart does not take it up any faster than it can convert it to pyruvate (and then to AcCoA, etc.)
Since aerobic metabolism is so important for the heart, is has a high content of mitochondria.

Welcome. Could you add sources to your answer? As a scientific stack we appreciate, and factually demand answers to be backed up by references.

Why will glycolysis run too fast? Any reason?


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Adaptability in immune system
I read somewhere that recently some people are trying to use harmless bacteria that live symbiotically in humans to express some portions of antigens of the harmful ones. Some people have raised concern that continuous exposure to the same antigen may lead to adaptibility of immune system to that epitope and render it useless when the germ actually comes.
Can't we use the same procedure for exposing some parts of MHC of the donor to the recipient before transplantation, so that, by the time the real transplant is done it may become adapted ? How much time would it take for this to occur ?
I can already see one drawback : In emergency transplants, this can not be used due to time factor. Can you see any other drawbacks ?

A patient needing an organ transplant, even if it is not an emergency, is usually seriously ill. Triggering a potentially severe immune reaction is not a good idea for them. If you would manage to trigger an adaption in some patient, this does not mean that it will always work. So you need a (error save) method, to check for adaption, because non adapted patients will need immune repression before transplanting the organ.

I don't know how long the adaption process would take, but it will only be possible for transplants from living donors, because it will sure take a lot longer than an organ can be kept alive.

@skymninge I am saying that this can be used complementary to the "traditional" way. If patient gets adapted, then good otherwise go with the conventional way.

@skymninge I like the first point in your comment - triggering an immune response in the already sick patient will be not so good.

Do you have a link to the place you read that?

@Amory I don't have a link but I read that in a book - Good Germs, Bad germs by Jessica Snyder Sachs

No. MHC works differently from any other antigen. MHC is involved in the maturation of T lymphocytes in the thymus. Forming lymphocytes need to recognise the MHC with a certain affinity (lymphocytes with too much affinity for the MHC are destroyed). In all this process there is no intervention of foreign antigens, so the system you propose won't work because the lymphocytes would search the MHC of the graft and they would attach them with abnormal affinity. This would trigger autoimmune response.
What you propose is the main functioning of allergy vaccines. You expose the immune system to low dose of antigen during long time, and that would make the body to not react aggressively to the substance. However, this phenomenon is based in B lymphocytes, which recognaise soluble antigens and little cells (humoral immune system) instead of whole cells (cellular immunity).
In the domains of science fiction, however, it would be technically possible to transfect thymal cells in order to express the MHC of the donor, since it would express both. Actually, this should be theoretically easy (The thymal cells seems to express almost any protein in the body, in order to prevent autoimmunity), but it face the problem of thymal degeneration.

Angel Naranjo Oritz : Just wondering, why are lymphocytes with too much affinity for MHC destroyed ?

Could you explain the first paragraph more elaborately ? I am not able to understand your idea.Thanks !

@biogirl If there is too strong of an affinity for the MHC complex, the lymphocytes may be able to bind outside of the specific MHC:antigen context; in particular it may allow them to react to self-peptides, resulting in autoimmunity.

@Amory I may be wrong but what I understood is - If lymphocytes bind too strongly to new MHC , they may also trigger autoimmunity ?????

Exactly. MHC function is to "show" internal peptides to the immune system. When this peptids are alien, the lymphocyte assumes that the presenting cell is infected by a virus or a bacteria, and try to destroy it. There is a double check that ensures the lymphocyte attach the MHC and also that it can separate. If an alien peptide is present in the system, the second check doesn't trigger, and instead the lymphocyte will induce apoptosis.

@biogirl Yes.  It's a Goldilocks process.  If they don't bind strongly enough to MHC, they're useless and are destroyed.  This is called positive selection, and occurs first.  Next, lymphocytes undergo negative selection, where they are selected for moderate binding, lest they always bind MHC, even in the context of self-antigens.

@MiguelÁngelNaranjoOrtiz Thanks ! I get it now.

"...lest they always bind MCH even in the context of self-antigens" surprises me. You mean any naive T cell that binds self antigen on MHC "too strongly" i.e. "doesn't let go" will be eliminated as non self tolerant. However, there are naive T-cells who bind to specific antigen on self MHC which bind and then "turn away"? Highly interesting, as the latter look like good candidates for mounting response against non self, foreign, transplant MHC presenting their specific antigen. Sorry for wondering about such basics.

"....because the lymphocytes would search the MHC of the graft and they would attach them with abnormal affinity. ..." - No need for antigen to be presented on foreign MHC?


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Which part of the brain needs to be shut down to lose conciousness?
Whether it is mechanical (trauma), chemical (anaesthesia) or electrical - which part of the brain is shut down to cause loss of consciousness?

I am not sure but I think it is reticular formation.

This is a very tricky question, since it is difficult to measure consciousness.

Related: http://biology.stackexchange.com/questions/10351/mechanical-cause-of-loss-of-consciousness

I agree with biochick, it's reticular formation The reticular formation has projections to the thalamus and cerebral cortex that allow it to exert some control over which sensory signals reach the cerebrum and come to our conscious attention. It plays a central role in states of consciousness like alertness and sleep. Injury to the reticular formation can result in irreversible coma. http://en.wikipedia.org/wiki/Reticular_formation#Functions BUt again I guess there are a lot of other control mechanisms in the brain on the cellular and bigger levels.

Do u regard speep as non-conscious state?

It depends on what you call consciousness. Is consciousness without emotion still consciousness? Emotion is described as a Mammalian "apomorphy" located in the cerebral cortex (see e.g. Carl Sagan, The Dragons of Eden). That may be part of the answer.

There is no widely-accepted neurological structure that mediates 'consciousness.' Even if some structures have been shown to be necessary for consciousness, they have not been shown to be sufficient. This is true with anesthetic mechanisms as well -- their ability to paralyze and block pain signals is fairly well-understood, but the mechanism of loss-of-consciousness is still unknown.
Still, 'consciousness' has to be there, somewhere between being awake and being dead, states which anesthetics can readily bridge (review):

Nevertheless, at some level of anesthesia between behavioral unresponsiveness and the induction of a flat EEG [indicating the cessation of the brain’s electrical activity, one of the criteria for brain death (22)], consciousness must vanish.

Later in the same review:

The evidence from anesthesia and sleep states (Fig. 2–3) converges to suggest that loss of consciousness is associated with a breakdown of cortical connectivity and thus of integration, or with a collapse of the repertoire of cortical activity patterns and thus of information (Fig. 2). Why should this be the case? A recent theory suggests a principled reason: information and integration may be the very essence of consciousness (52).

This is consistent with my own take. Consciousness itself is the subjective experience of 'brain,' so it can't be lost, just poorly integrated.

@Rayan, very useful reference (Consciousness and Anesthesia). Thanks

"somewhere between being awake and being dead". I think that the gap between the 'dream' and the 'sleep without dreams' is narrower, so the study of sleep and dreams may be closer to the answer than the use of anesthetics.

Consciousness is a difficult term to grasp in a short answer, and the question is as interesting as it is challenging. The reticular formation as mentioned by others before me is crucial, as the thalamus is the gateway of information to and from the brain. Therefore, subcortical structures such as the thalamus, when 'shut down', induce unconsciousness. Mircea Steriade (2005) has an excellent review on this and he is a leader in the field the field of sleep and absence epilepsy, thalamo-cortical interactions and consciousness. He describes there the cortical responses seen in the EEG during sleep: the sleep spindles, or related spike-and-wave discharges (SWDs) seen in the EEG during absence epileptic seizures, where patients temporarily loose consciousness. Sleep spindles and SWDs are highly synchronized responses that basically block out sensory input and cortical output. The blocking of sensory input and blocking of output to the body may be regarded as a loss of consciousness, as one is not able to sense the environment or undertake action in response to environmental stimuli (e.g., Kostopoulus (2000)).
However, since the question is what part of the brain needs to shut down, it is technically the neocortex, as the neocortex holds the key to being aware of one's surroundings, i.e., processing of sensory input as well as driving motor neurons to move, talk and respond to stimuli (see wiki page on neocortex). So the end organ mainly associated with consciousness is the neocortex - as described in a review paper by Nobel laureate sir Francis Crick (1990). The authors also indicate the thalamus and other structures as possible sites involved, but principally it is the neocortex. I hope this helps you a bit further.

It would be great if yo added some references to support your response! As it stands this is more similar to a comment!

This does not provide an answer to the question. To critique or request clarification from an author, leave a comment below their post - you can always comment on your own posts, and once you have sufficient reputation you will be able to comment on any post.

Hi Bez, I am a newbie in Stack Exchange. I will try to improve my answers!

Hello new Chris and welcome to the Biology StackExchange. Yes, that would be fantastic! It simply requires some references added, which are supportive of the response :)

I hope my edits help and please excuse me for my inexperience.

Two structures are required for consciousness: the brain stem reticular activating system (RAS) and one cerebral hemisphere, as stated here.  e.g. a lesion in the RAS or bicerebral injury will induce loss of consciousness.

Some references would be nice.

As mentioned by @Chros (The old Chris that is :) ), this response requires references! As it stands, this is more similar to a comment!


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Why is it beneficial for trees to grow that tall?
Why is it beneficial for trees to grow that tall?
This sounds like a kid's question Mom, Dad... why are trees so tall?
Costs and Benefits
There are some obvious costs:

Need much Carbon and other nutrients
maintenance cost
energy cost (for growing, to bring water (and nutrients) up to the higher leaves, etc...)
Sensitivity to wind
etc...

Potential benefits I can think of:

Competition for sunlight
Better dispersal
protection against predation
Some birds (maybe especially those that are potentially good seed dispersers) prefer to land on high trees (avoiding the cost of regaining altitude). Being high attract these birds which eat the fruits and disperse the seeds.

Are there other potential benefits?
Specific to palm trees
I am currently in Bali, Indonesia looking at palm trees that seem to have a very low competition for sun light (the forest is not dense, the light is intense), there are no tall predators (but being tall might be a protection against climbing predators as well and there are indeed monkeys and other potential climbing predators) and looking at coconuts, papaya and banana I can hardly think that being tall helps to disperse further away (seeds dispersal by barochory). So, why (evolutionary reasons) are palm trees so high?

Tsunami seems to rare. I thought maybe high enough to crack the nuts from the drop that are hard enough to resist being eaten by animals.

Are the palm trees in a natural forest? You might be looking at an artificially grown oil palm plantation, since it sounds like your description is referring to that.

It might be that non-dense forest you are observing the palm trees in isn't the environment they evolved in. http://www.meltingasphalt.com/parable-of-the-redwoods/ explains this quite well.

Beside the reasons you've given I would add environmental disturbance (e.g. flooding) as a evolutionary factor that could explain selection for taller individuals. Many palms also inhabit and thrive in disturbed habitats (Frangi & Lugo, 1998; Salm, 2005), which indicates that this could potentially (i.e. speculative) be an important factor for this taxon. Palms also have the combination of tall height and a relatively low "wind profile" (relative to many other groups of trees), which indicates that they are adapted to exposed/disturbed habitats.
This, along with the reasons you've already given, seems to cover the most obvious evolutionary reasons for selection on tree height. However, these will naturally trade-off against negative effects on e.g. fecundity from investing and maintaining biomass.

Thank you, this kind of speculations was exactly what I was looking for!

The height of tree species varies, of course, as each tree fills a given niche, much like animals do; you might as well ask why blue whales grow so big.  The answer, of course, is that they seek out and successfully get the nutrients they require.  It is advantageous for some trees to be huge and get the most sunlight possible and so some trees do.
In the specific case of palm trees, however, they aren't true trees but rather a grass, which means they are a monocot and (I'm a little shaky on plant physiology but...) that the outside isn't living but the inside is.  Monocots grow straight up, in one main shoot, and palm tree follow the same pattern.  Tons of sunlight, nothing to come mow or it down, and nowhere to go but up means they'll be big.  True trees, on the other hand, have what is called heartwood in the center, which is technically dead tissue.
Another thing to think about is that trees aren't moving, so they only way they can improve their condition is by growth.  An animal, on the other hand, can migrate to follow food; growth, particularly for mammals, also has a huge heat cost.

Thanks for your answer. It doesn't provide the answer I was seeking though. I was looking for functional evolutionary reasons for a tree to be tall (like the three examples I provided). I know it is a reaction to natural selection, I know the concept of ecological niche. You're saying that tree can improve their condition by growth but my question is why? Or more specifically why growing tall?

For the case of palm trees, saying that they cannot grow wide but only tall is some kind of answer although it still does not answer to why growing tall rather than not growing (and invest more into reproduction)? Hope my comment makes sense!

@Remi.b I tried to say that in my first paragraph, and again in my last.  It's straightforward, and you guessed it: The taller the tree, the more sunlight it can get.  Other factors like soil and temperature can play a role as well.

The taller the more sunlight. Even if there is no competition? For what reason does being tall helps a tree in regards to temperature and various soil factors?

@Remi.b just because a particular individual (tree) has no competitors does not imply that the species evolved free of competition. I would guess that it always comes down to getting more sunshine. For example, a polar bear born in a zoo in Brazil will still be furry and white even though those characteristics don't help that particular individual.

@terdon Ha ha. Ok. So basically the answer is: there is nothing else than competition for sunlight that drives trees to grow tall? And if I can't see any single palm tree on my island that seems to be under competition for light, it is only because I'm unlucky and I observe these trees in an environment which is different than the one who drives the (meta)population to be tall. Are you sure that there's nothing else than "competition for sunlight" that drives trees (with barochorous seeds dispersal) to grow tall?

@Remi.b no, I am not sure at all. I know very little about plant physiology and evolution, it has never been my field, but the sunlight explanation seems sufficient to me. All I am saying is that you cannot extrapolate from the individual to the species.

@Remi.b Additionally, if you remove the competition it doesn't necessarily follow that the species will shrink immediately.  It can still be quite advantageous.

@Armory yes it can be advantageous...but why? That's all my question. Indeed, the trees I've been looking at were maybe not representative of the whole population (in terms of envirronment). Good point Terdon. But I want to come back to my question rather than talking about very basic stuff of evolutionnary theory. Do you have any hypotheses (other than the 4 in my question) to explain what selection pressure make trees grow tall?

@Remi.b And I (we?) are wondering why that's not enough for you?  Trees require sunlight to survive, and growing taller means more sunlight, so why shouldn't they?  A taller tree would have a fitness advantage that would be selected for.  I'm sure in some scenarios predation could play a role but not as strong as the desire for sunlight.

Are you saying that monocots should be more likely to grow tall? I don't understand your argument in the second paragraph.


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How to reduce/eliminate cell clumping in suspension CHO cells, without using an anti clumping agent?
what is the best way to eliminate clumping suspension cells used for transfection. Anti clumping agents interfere transfection and hence can't be used. Though maintaining the cell density low helps, but doesn't help in the long run.

changing the media can help - for example, chemically-defined media designed specifically for protein expression might work better than media containing serum, which can promote the expression of cell adhesion proteins

Thanks for the reply. I am currently using invitrogen's CHO S SFM which, though not completely defined chemically, is serum free.

I had clumping issues with HepG2 cells for a long time, I had to split them every 2 days and trypsanize them for 30-45 minutes at 37C to really break them up. Then I would split them at 2 or 3 to 1 ratios so that they formed a more uniform distribution. Less density seemed to cause more clumping, probably because each cell grew into a clump. These aren't CHO cells, but might be helpful.

After looking around for a bit, I came across a few potential solutions however they are not a definitive answer to your question and requires testing under your experimental conditions to see which works best.
This page contained one excellent suggestion and that is to select for cells that do not clump during the passage, by pooling the cells in 15ml of media in a tube and letting the clumped cells to settle down by gravity for 5 minutes and afterwards taking the top 1ml and passaging it and after 20 passages using the exact same technique, you should be able to get single cell suspension. The main caveat is the heavy selection for non-clumped cells, which might harbour certain properties that might be undesirable for the procedure you are interested in so it might be nice to do some RNA expression profiling to observe the differences and perhaps even publish it! Amongst the suggestions on this page included using different concentrations of Mn2+, Mg2+, and Ca2+ in your (custom?) media since cell adhesion is regulated by integrins, cadherins, and selections and in general, Mn2+ increases ligand affinity, Mg2+ promotes adhesion to cells, and Ca2+ decreases cell adhesion as referened here. You can also try heparin, as tested by this paper on CHO cells and it impotent to note that in the study, heparin did not reducing cell growth, antibody secretion, and antigen-binding activity although I'm unsure as to whether heparin would be classified as an anti-clumping agent and whether it interferes with the ability of the cells to get transfected but that can be simple tested by a GFP transfection and looking at the transfection efficiency of the heparin treated and control cells treated with whatever heparin is dissolved in.


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Are mature erythrocytes prokaryotic?
Mature mammalian erythrocytes have all the characteristics of a eukaryotic cell except that they don't have a nucleus, they don't have any cell organelles. Does this mean that erythrocytes are classified as prokaryotic?

I have removed the abbreviation from your title (and also from your content). Titles should not contain other than the most common abbreviations (DNA) so they are immediately comprehensible and index properly. In general you should avoid them, or at least define on first usage.

I don't think any Eukaryotic organism can possibly have prokaryotic cells in their body

@OneFace The ca. 30 trillion cells of your microbiome would like to disagree with you - particularly the 1-2 kg of them in your gut. -- You're right that no eukaryotic organism has genetically identical prokaryotic cells in their body, but that's because the presence/absence of the nucleus is only a diagnostic feature, not a defining feature. Like most taxonomy these days, prokaryotic/eukaryotic is now defined based on cladistics and common decent, rather than a pass/fail checklist of phenotype. If you're descended from eukaryotes, you are a eukaryote, even if you don't have a nucleus.

I meant no eukaryotic organism can possibly have prokaryotic cells as a self tissue. Flora is not considered "you". They are commensals living in you. @R.M.

No.  Nobody considers red blood cells to be prokaryotic, perhaps most importantly because they are part of a eukaryotic organism.  Red blood cells begin life with the full complement of organelles, including a nucleus and mitochondria, but our RBCs shed their organelles during maturation.  In actuality, though, only mammalian RBCs lack nuclei; other animals' RBCs still hold on to their traditional eukaryotic characteristics.
As an analogy, apoptotic or necrotic cells don't have intact organelles, but they are still considered eukaryotic.

How this intellectual deception works
There have been several admirable comprehensive answers to this question, but, having seen it come up again recently, I thought it would be useful to point out why something like this that is clearly wrong can sound plausible. In general there is some sleight of hand involved.

In this case the sleight of hand is the (deliberate?) confusion of
‘cell’ with ‘organism’.

Prokaryotic and eukaryotic are terms that apply to organisms. (see definitions on Wikipedia pages) Prokaryotes are unicellular, so a prokaryotic organism is often loosely referred to as a prokaryotic cell. Some eukaryotes are multicellular, and multicellular eukaryotes such as those containing erythrocytes have a variety of different specialized cells, but these cells are not organisms. The interchangeable terminology for prokaryotes does not apply here, and, as one always knew, it is nonsense to talk about particular cells being prokaryotic or eukaryotic.
The fact that nuclei are a characteristic of eukaryotic organisms does not require every cell of a eukaryotic multicellular organism to have a nucleus (and anyone who tries to define it that way is wrong.)
It should also be emphasized that the term prokaryote has a different meanings from anucleate. Indeed, in anucleate* — “lacking a cell nucleus” — the prefix a- indicates not. In prokaryote — “any of the typically unicellular microorganisms that lack a distinct nucleus and membrane-bound organelles and that are classified as a kingdom — the prefix pro- means before, in a temporal sense. (The karyo portion means kernel or nucleus in Greek.) The idea presumably being that prokaryotes evolved before eukaryotes.
The moral
Don’t look where the conjurer wants you to look.

Note that the reason mature erythrocytes are eukaryotic is the same reason snakes and dolphins are tetrapods. "Eukaryote" and "Tetrapod" are clades, i.e. groups defined by common descent, which leads to pervasive similarities within the group and differences with organisms outside the group which justifies defining that as a group in the first place, even if we didn't know they were descended from a common ancestor.
That is an important fact about life that is obscured with classifications like "mammals are animals that have fur, bear live young and feed them milk". We could imagine a situation where we could list traits ("has fur"/"has feathers"/"has scales", "swims"/"runs"/"flies", "bears live young"/"lays eggs", etc) and we would find creatures with any combination of those traits. If you knew an animal had fur, that wouldn't tell you what any of its other traits were, because the combinations were endless. At that point, "it feeds milk to its young... but it has no fur and swims!" might lead to big questions of "mammals feed milk to their young, but they also have fur, so should we call this a mammal?". But words like "mammal" would also be a lot less useful, because knowing an animal had fur, gave birth to live young it fed with milk wouldn't actually tell you anything more about the animal in question, since its other traits could be anything.
That is NOT how it turns out living things are. Traits are distributed in a very specific way: a nested hierarchy, groups within groups that don't overlap. This was found by Linneaus, the first person to try and classify all of life. He found that when looking at the similarities and differences between animals, they naturally fell into groups within groups; you had mammals and birds and reptiles and fish, and within mammals you had primates and carnivores and whales, and within carnivores you had canines and felines, etc... with no creature that was, say, half like a dog and half like a duck to the point there was a question of whether it fit in "mammals" or "birds".
This classification isn't arbitrary. Linneaus admittedly did have a thing for the nested hierarchy, and tried to classify rocks the same way. That didn't work out; today's biologists have changed Linneaus' classifications a lot, but the nested hierarchy has proved an enduring fact of how the traits in living things are distributed. On the other hand today's geologists classify rocks completely differently, because it turns out the traits of rocks are not distributed according to a nested hierarchy.
Moreover, biologists have since discovered the cause of this nested hierarchy, which is common descent with modification. Organisms reproduce and have offspring that are slightly different from them; over time species differentiate into different groups that are slightly different from the parent species and those groups become species and differentiate in turn. As a result, how similar two organisms are to each other is directly related to how recently they share a common ancestor. Groups emerge within groups because they descend from one another, and don't overlap with far-away groups because there is no mechanism for that to happen (main exception being bacteria, who can swap genes with other bacteria from very different groups, and as a result they don't fall in as clear a nested hierarchy as eurkaryotes do).
This means that there is a difference between modern biology and that of Linneaus's time; Linneaus listed visible traits and classified organisms based on them. It so happened that they fell into a useful nested hierarchy, so "has fur and feeds milk to its young" told you a lot more about the animal, like "has lungs, has a backbone, probably has four legs", etc, but the list of traits was still the main important thing. Nowadays we know of a lot more traits; we know an organism's genes, the structure of its proteins, details of their physiology that biologists of Linneaus's time could only guess at. While in Linneaus' time you might be able to say "dolphins have no fur and swim like fish, but they have lungs like mammals and bear live young; where to classify them? I guess they're kinda more like mammals?", today we know that dolphins are overwhelmingly like mammals down to the molecular level, in literally every way other than "they have no fur and swim". And we also know the reason why: dolphins share a common ancestor with all other mammals dating back to the Triassic or so, while their common ancestor with fish dates back to the Ordovician, hundreds of millions of years earlier.
This means that today's organisms are by and large classified on the basis of common descent. The "Eukaryotes" group certainly is (it's a clade). What makes an Eukaryote an Eukaryote today isn't technically any specific trait, it's whether it descends from the common ancestor of Eukaryotes or not. Red blood cells absolutely meet that criterion. But this isn't just an arbitrary classification choice; it so happens, because of this common descent, that red blood cells are a lot more like other eukaryotes than they are like any prokaryote. "Has/Lacks a nucleus" is one single trait; an important one, important enough to make it the name of the group, but it's not the only one. And in their proteins, ribosomes, metabolic processes,... really everything BUT "does it have a nucleus", red blood cells have more in common with Eukaryotes than with Prokaryotes, so it makes absolute sense that they would be classified that way. Same reason snakes and dolphins are "Tetrapods" even though they don't have four legs; four legs is an important trait, it named the group, but it's still only one trait. "It's almost totally like a lizard, but... it has no legs!" is not actually a riddle or a stumper; "almost totally like a lizard" trumps "number of legs" any day.

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Accuracy of a particular genetics test
Consider the question - Are genetic tests accurate?
I don't believe they are as the genes may not provide the complete information or maybe there are other genes responsible for a particular trait but they may not be known at the point when the test is conducted. This may not be the right answer though — I simply wish to understand from people here as to what they can say about the accuracy of these tests. If they are not accurate, can you explain why that is the case?

There are a lot of "genetics tests" you can do. Please describe more detailed, what kind of testing you mean, otherwise this question is too broad. (Accurate as in "Now we know 100% sure that...?" Of course not. Like all other tests you do on organisms. They are just too complex to be understood 100%)

Like the comment said this question is very broad but Im going to try and clear some things up for you. A "genetic test" is just simply a test that tells you whether or not you have a certain genotype. Yes, it is often times used to tell if a person has a disease or not, but that doesnt always have to be the case. I may just want to know, for example, if a mouse I have carriers a certain transgene. The reason why genetic tests are good at determining if someone has a disease is because many diseases are simple, or at least have a well-defined genotype. Sure, you can make a genetic test for a complex disease like obesity if you want, but no one does this because as you pointed out in your question there are sometimes more than one gene involved, so a genetic test for that would not be very good.
But for genetic tests of diseases of a known genotype, they are very accurate. Of course you have some false positives and false negatives. Look up the terms selectivity and sensitivity. If you have a sensitive test you will catch a lot of people with the disease but also many false positives. If you have a selective test you will not have many false positives but you may miss people who actually have the disease. Its a trade-off. Testing someone twice will clear things up usually.
And then there are cases where you have a disease with a known genotype but still have an inaccurate genetic test on rare occasions. Heres a paper about a disease known as Spinal Muscular Atrophy. There is a genetic test that works 95% of the time but sometimes it does not match up with the phenotype. In the paper they find a mutation that explains why the genetic test does not match the phenotype. Two things are interesting about the paper. One, the genetic test is not wrong, its just that the phenotype is not what you'd expect. And two, not all people who have a discordant genetic test have this mutation. So whats going on in these patients and why their test doesnt match their phenotype is anyone's guess.
The first point is especially important so I will repeat it. The genetic test was not wrong, the phenotype just did not match it as expected. Genotype and phenotype are not always correlated, and mistakes can happen when you assume they are.

@von-mises summed it up nicely enough, but you'll want to read the Wikipedia articles on heredity and heritability, in particular the latter.
Our genetic information can be informative, but it's not complete.  As you mention, there are lots of other factors that could and usually do come into play.  Often times there isn't just one gene, but rather many genes playing a role (these are called polygenic traits).  For example, see my answer to a question on hair color; there are dozens of simple changes that can affect the color of hair and eyes.  These complex traits are really hard to tease out!
Additionally, not everything is 100% from genes; the environment can also play a huge role. Often we talk about how heritable a gene or a trait is by giving a percent, meaning how much of is due to genes you inherit from your parents.  The heritability of IQ is an interesting read for an introduction to the concept. But this quantity is itself misleading, as it sometimes includes environmental variation, and it is only as good as the data you use to compute it.
So, what is the use of the genetic tests?  Well, for starters, ancestry is really interesting and useful for people.  Not just paternity or maternity (which is obviously accurate and widespread) but knowing where you are from.  23andMe can be informative, but you should know that their business model depends on getting genetic information for free from you.
There are, additionally, a number of traits that we've studied, or that do have strong genetic factors.  Sickle-cell disease is a classic example of something just from your genotype, whereas other things are less determinate; for example, the heritability of baldness is around 81%, and I know from my genome that I have a slightly lower chance of becoming bald.  There are other, more serious health risks that people would want to be tested for (BRCA for breast cancer, LRRK2 for Parkinson's, APOE for Alzheimer's) as well as inherited traits that are very genetically determined (like sickle-cell or Tay-Sachs).
In short, the genetic tests are very good at determining what the genotype is, which can be very useful for certain traits but completely useless for others.  The more we learn about what our genes do the more we learn how complicated the whole system is.  We are more than just our genes.

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histamine inter-cellular and cytoplasmic binding site
I noticed that HRH (histamine receptor) has an inter-cellular and cytoplasmic binding site of anti-histamines which are equal in binding energy. Does anyone know what is the function of the well formed cytoplasmic ligand binding site?

What is HRH ? Tried googling...didn't get anything.

HRH is histamine receptor


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How essential is vitamin B3 to the diet?
I know this might seem contradictory since by definition a vitamin is an essential part of the diet but I have read that nicotinamide, a form of vitamin B3, can be synthesised from L-tryptophan. Is it possible for a person to synthesise all their vitamin B3 requirements from one's dietary intake of L-tryptophan?

According to one study:

It was calculated that if the excretory percentage of niacin metabolites in the urine were 60%, of the tryptophan ingested, the conversion factor would be a value of 67, meaning that is 67 mg of tryptophan is equal to 1 mg of niacin.

However, the study has a pretty low power with only 10 participants and an indirect measure of niacin.
Is it possible that a person could get all of their niacin from tryptophan? Probably - you just need to eat enough tryptophan, which is also an Essential Amino Acid. The body may preferentially keep Tryptophan (which it does not store) until Niacin runs out (which also cannot be stored).


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Expression of plasmid genes
Are plasmid genes always expressed? If so, then isn't a bacterium wasting it's resources in expressing genes (like antibiotic resistance) which are not required in "normal" conditions?
If not, then what triggers bacteria to express genes of recombinant plasmids? Can a bacterium survive in "normal" conditions if it is deprived of all the plasmids?

What makes you think that genes on plasmids are not required in "normal" conditions?

@terdon Because (as far as I know) mostly plasmids contains genes like antibiotic resistance which are useful under some conditions.

Not really, those are simply the ones we tend to add when cloning.

It would depend of the plasmid, the genes it contains and the promotors those genes have. Basically, regulation of extrachromosomal genes follow the same patterns of the rest. Bacteria, Archaea and some other organisms that can have plasmids will express the genes if the promotors of those genes are constitutive, or if they trigger by conditions that are present in a given moment. The degree of expression would be a function of the characteristics of the promoter and the number of copies of the plasmid. Finally, the number of copies of the plasmid would depend of its size and the characteristics of its replication origin.
Organisms can loss the plasmids if doing so don't suposse a negative effect (this is a big problem in industrial microbiology, since the recombinant strains may be unstable and reduce its productivity). In laboratory, a plasmid containing resistance genes towards an specific antibiotic would remain stable as long as this antibiotic is present in the media. The characteristics of its replication origin also play a big role determining the stabilty of plasmids. You can even select for the loss of plasmids, take the example of URA3 in Saccaromyces (not a bacteria, but the mechanisms are the same), wich can be used as a negative selection factor if the media contains 5-fluoroorotic acid.
So there's no particular advantage in expressing plasmidic genes all the time. When that happens, actually there exist an evolutionary pressure against the presence of the plasmid, and thus it trends to dissapear. Bacteria can survive without plasmids (with the exception of some that carry megaplasmids that acts more than little chromosomes. In some of this cases, the plasmid may contain genes for important methabolic pathways and other key elements of the cell, thought if the genes they carry are very importants, like polymerases or ribosomal RNAs, the term minichromosome is prefered). However, plasmids may contain genes that confer an important advantage to the population (like in presence of an antibiotic), and if so the plasmid spread. If at some point the ecological pressure cease, the plasmid would turn unstable again. Note that it's not impossible to have horizontal genes transfer between plasmid and chromosomes, and plasmids (alongside viruses and foreign transformed DNA) are important sources of new genetic material.

So to reduce the loss of recombinant plasmids, are bacteria kept under a selective pressure in which the plasmids would give advantage?( In Industries)

Yes. For instance, you can use auxotrophic strains that packs the enzymes required for prototrophy in the plasmid.

Could you simplify what you said in the previous comment ? I don't understand the terms. Thanks!

You can use a strain than cannot sintetize a certain compound and needs it to be present in the medium. If, alongside what genes you want to insert in your microbe, you include genes that allow them to produce that compound, the bacteria won't lose its plasmid as long as that compound isn't present in the media.


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Number of MHCs in neurons
I have read that neurons have proportionately less MHC molecules than other cells of the body. What is the advantage of this?

Antigen presentation by MHC will induce a cytotoxic response by the immune system, which is usually a good thing in the body since most cells can just divide and replicate again.  Neurons, however, are particularly ineffective at regenerating from such an attack, and are not easy to come by; they are also rather important!  Better not to risk it, eh?
That being said, neuronal expression of MHC is actually a pretty complex case, and this open-access article is a good start down the rabbit hole (see also here, here, and here if you have access).

What happens if a neuron is infected by bacterium, let's say which is definitely gonna kill it ? If it presents an antigen then also it will be lysed and if it doesn't then the bacteria will kill it.

Are the few MHC molecules there just so that the immune system is warned of the presence of bacteria ? Does that make any difference if few MHC presents the antigen or thousands present it ? Is there a threshold over which a cytotoxic response takes place ?

@biogirl Listeria monocytogenes does just that and can cause bacterial meningitis, which is highly lethal.  Neurons can respond to interferons and can upregulate MHC expression during infection; there's even some evidence that impairment of neuron function itself spurs that process (here and here).  T-cells can respond if presented with as few as 3 MHC-peptide complexes.

The brain also has resident immune cells, in particular microglia.

I might be wrong but I don't see any advantage of having lesser MHC. As you say T cells respond with as few as 3 MHC complexes. So then what is the point of having fewer MHC to protect it from cytotoxic response ; as you say in your answer ?

Just because they can doesn't mean doing so is particularly efficient.  Besides, T-cells aren't floating around through the brain like elsewhere.  Usually, it seems, MHC is not readily expressed unless induced by infection.


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How do processes of one osteocyte establish contact with processes of the adjacent cells within the mineralized matrix?
Are the processes and canaliculi formed and contacts established after the osteocytes are embeded in the matrix or are they formed during the embedding process itself. Is there any evidence to suggest either?

Osteocytes attach to each other by cytoplasmic extensions through gap junctions [1]. The connections between these cells are formed since they were osteoblasts and osteoid-osteocytes (type II preosteocyte) [1]. Osteoblasts have a greater volume than osteocytes and the lack of extracellular matrix favors their adhesion. As they begin to synthesize extracellular matrix, their volume is reduced and this matrix takes space between cells, but with respect to the existent intercellular junctions around which matrix forms canaliculi.
"Osteoblast Organization" by Physio Muse - I drew this figure in drawperfect, printed to .pdf, and converted to .jpg
Previously published: Not published in any form, including not used on any website. Via Wikipedia.
Osteoblasts are connected via gap junctions mediated by connexin43 protein [2]. Mature osteocytes attach to the bone matrix by integrins (alphavbeta3) [3].

References:

Wikipedia contributors, "Osteocyte," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Osteocyte&oldid=618657480 (accessed July 27, 2014).
Civitelli R. Cell-cell communication in the osteoblast/osteocyte lineage. Arch. Biochem. Biophys. 2008 May 15;473(2):188-92. doi: 10.1016/j.abb.2008.04.005. PubMed PMID: 18424255.
McNamara LM, Majeska RJ, Weinbaum S, Friedrich V, Schaffler MB. Attachment of osteocyte cell processes to the bone matrix. Anat Rec (Hoboken). 2009 Mar;292(3):355-63. doi: 10.1002/ar.20869. PubMed PMID: 19248169.


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Female preference for males who are already in a relationship
A common saying is that women are generally more attracted towards men who are already in a relationship, and this phenomena does seem to have its own place in popular culture that is not matched by a corresponding male preference for women who are already in a relationship.
From an intuitive viewpoint I think it would make sense from the woman's viewpoint in an system of information economics where the fact that a male is engaged in a successful relationship with another female, or several other females, might provide extra and positive information about the evolutionary value of the male.
But how about the possibility for a male to use the same trick?
Is there any empirical evidence for this behaviour at all either in humans or in other species, or is this just a cultural artefact in some human societies? If there is empirical support, is there a consensus on the plausible evolutionary pathways involved here?

Im not sure this is true. How does one measure 'attraction' anyways? And maybe the relationship has nothing to do with it. Maybe a guys who are desirable tend to be in more relationships, simply because they are desirable

@vonMises i agree with you girls look to be more attracted after a boy is in relationship,even though they were in touch with the person(boy).

This question appears to be off-topic because it is about social interactions.

There's tons of evidence and it's all anecdotal.  People in relationships tend to be people who it would be good to be in a relationship with, go figure.

This is a widely researched topic in the overlap between social sciences and evolutionary biology.  Evolution has become very influential in understanding human interaction and preferences.
This chapter from "The Adapted Mind : Evolutionary Psychology and the Generation of Culture" will give you an idea of how all this plays out in the big picture - its a fairly comprehensive review of many factors considered in human mate choice.  The study may be psychological, but the logic is derived from biology these days.  (stackexchange won't let me link to google books - you can search for the title and look at chapter 6).
Evolutionary tendencies will favor more successful offspring.  But for people it includes not only the genetic qualities of the mate (appearance, height, disease resistance, health) but also social qualities (how reliable or willing a mate is to support offspring).
First off you can see that there are many many factors which women take into consideration in their preferences.  Its commonly said they are more complex than men, but that's another question.  You have to take a range of factors holistically including the social environment.
I can't find this particular issue addressed in the literature, but I think that it might be attractive to women in some social settings.  If there is a lot competition for 'quality' mates or resources for instance - if you have very few secure males or pessimistic females might create pressure which would cause females to prefer males which were successful.
Its pretty easy to feel good about hypotheses like this.  I couldn't find a specific study, but perhaps someone else will.  There's a lot of such papers out there.
I should say that men are as easily led to do things by 'mate choice' psychology that aren't totally healthy or socially acceptable.  That's biology.


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How did viruses learn to utilize the workings of a cell?
This is my first post here, so excuse me for its simplicity.
Viruses can infiltrate a cell, overtake it and multiply. It has projecting fibers whose ends are shaped as kind of a "key" to a mobile sentry on the cells membrane so it can be permitted access into the cell. When it enters the endosome of a cell, a protein pump blows an acidic gas onto the virus to break it down, thinking it's a special nutrient. But the virus expects this of course, and when the protecting fibers break off (and so too the body of the virus) proteins are released that rips apart the skin of the endosome so the virus can escape.
These are just two of many things the virus does to compromise a cell. Its entire existence is for the sole purpose for infecting a cell, and it seems to know how to do that perfectly. How did the virus evolve to know how to do things like this?

Do you have a specific virus in mind?  This is incredibly broad, and we'll honestly never know; we weren't there to study most evolution.  The short answer is "over many years."

@Amory Lets just say the common cold.

It's a numbers game.  Viruses can produce thousands, millions, even billions of copies every day, and only one of them needs to be slightly better to get ahead.  Rhinoviruses make roughly one error every time the genome is replicated; over many, many replications a single change can arise giving an advantageous effect.  As another example, it's been said that HIV mutates every single spot on its genome every single day.  Evolution is simply a waiting game.
This article is a pretty cool write up detailing the process.  It says exactly what I said: large numbers, high mutation rate.  Besides, the virus only has to take advantage of cellular processes, not make new ones every time.  That's much more efficient.  It also details some specific changes that explain some differences between similar viruses.  It's amazing, but a single base change can mean a single protein is different which can mean a different receptor is used for binding, which can make all the difference.
And there's this cool quote:

[T]here may well be more viruses in a single common cold infection than there have been primates in the entire history of life on Earth.

Scientists are unsure, but it seems that viruses have been around a very long time, and have been specific to every domain of life and possibly even may have infected the last common ancestor. It isn't impossible to imagine a co-evolving arms race that makes both viruses and cells as complex as they are today.


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Does evolution take place universally?
Why does evolution (namely the evolution of primates into humans) take place both uniformly and universally on the earth? Why aren't there any creatures who have not taken the same evolutionary steps as their same species elsewhere on earth? For example, why aren't there any humans on other parts of the world who look the same as our evolutionary descendants?

Could you clarify what you're asking a bit?  As it stands, it's a little unclear; it sounds like you're asking why there are primates if humans evolved from them.  I think you're a little mistaken on evolutionary history.  Humans did not evolve from chimpanzees, for example, but rather both species evolved from a common ancestor.  See the chimpanzee-human last common ancestor article.  So yes, this process is happening, has happened, and will happen again.

@Amory I realize humans evolved from a common ancestor. My question was why does evolution take place at the same rate with the same results to every member of the species all around the world? Why doesn't it vary even dramatically?

The evolution path a population takes depends on many factors. Environment, random genetic drift, random mutations, population size, population structure, ... If you think of a population that has been splited into two, the two descending population might differ in their initial alleles frequency just after the split or differ by their initial population size. Then environment might differ, the mutation they get might differ, etc... It can drives two initially similar population into very different species.

@0x499... Another thing to consider is that in the modern world, there's no longer the same severity of selection pressures required to cause dramatic shifts in evolution of our species.  There are minor evolutionary shifts, like slightly increased rates of sickle cell or g6pd deficiency in malaria-endemic areas of the globe, but not the kind of thing you seem to be referring to.

"Uniformly and universally"? WTF are you talking about? Primates do not, on a daily basis, "evolve" into humans. Monkeys stay monkeys, chimps stay chimps, and humans - well, humans, in general behave like a bunch of bone-headed jackasses, and yet they remain humans. Evolution acts on populations of organisms, typically over long time spans in response to a variety of stressors. Global warming should prove interesting, evolutionarily-speaking... :-)

My question was why does evolution take place at the same rate with the same results to every member of the species all around the world?

It doesn't.  Evolution acts on populations, not individuals.  I will never evolve, you will never evolve, but humans are evolving, and sure, certain pockets evolve at different rates.  Here's a long but straight-forward write up that deals with perhaps the best example, beak size in Darwin's finches.  A select population of birds on an island may be evolving rapidly and differently than that same species elsewhere, perhaps eventually resulting in a divergent species.  There is no need for natural selection to operate equally everywhere; in fact, the pressures must be different otherwise we would never see the diverse set of species we do observe.

Why does evolution (namely the evolution of primates into humans) take place both uniformly and universally on the earth?

Short answer: it doesn't. All human beings descended from the same group of Homo sapiens. There has been some genetic deviation since, but not enough to call it a "species". Evolution happens, but at very long time scales and not at any sort of defined pace.
Read this first.
Long answer: As the link above shows, evolution is dependent on several key factors. Heritable variation and change to selective pressures.

Why aren't there any creatures who have not taken the same evolutionary steps as their same species elsewhere on earth?

Think of humans! Different races, especially ones that have not intermixed, are significantly different. indigenous Africans, indigenous Europeans, and indigenous Japanese, for example. All of these races has genetically diverged into distinct populations with different traits, but the isolation between them hasn't been that long. That's why all humans can still reproduce.

Why aren't there any humans on other parts of the world who look the same as our evolutionary descendants?

Over a very long period of time, Homo sapiens had evolved to become a more advanced, competitively dominant species. although Neanderthals and Homo sapiens did intermix for a while, we're not completely sure how they went extinct. One of the reasons stated is that it's hard for a worse species to exist when a better species comes along.

If I got your question correctly,
you were aware that humans in some way, shape or form have descended from a common ancestor shared with other primates;
You then realized the relative 'distance' of modern Homo Sapiens from these other primates;
You concluded (or know) that there have been various morphological stages in between, none of which has survived until today;
You were basically puzzled by the question why no intermittent evolutionary stages exist of say the human species. Actually, this is not a bad question.
I think it can be explained with population growth. The modern species has just multiplied so dramatically, continuously selecting for certain features, that there was ultimately less and less room for older forms which have not been able to survive into today.
Monkeys also exist today, which means they have 'survived', but their populations are relatively smaller, and in their case, selection has not emphasized too many new features (correct me if I'm totally wrong).
I think especially when selection is fueled by intelligent awareness, its evolutionary momentum increases dramatically. Our older ancestors (early hominid stages) have then simply been outnumbered by the newer ones, dwindled in numbers and simply become extinct whereas the entire monkey-, or for that matter alligator population has selected relatively more traditionally and remained more homogenous (over-simplification!) - so they're still around, too.
On the other hand, today there are in fact many different types of homo sapiens around with somewhat distinct features, but they're all able to reproduce interracially without much of a problem. In the last few hundred thousand years I'd say there was not enough change to reproductively cut off any (isolated?) group from the main gene pool. Just our common, older ancestors were unable to catch up. This could theoretically happen again in the future, maybe not on this interconnected world, but with different human space colonies.

This is another one of those question where the premise is so crazy wrong, it's hard to answer well without writing a thousand words to explain why every sentence is wrong, wrong wrong.

Why does evolution (namely the evolution of primates into humans) take
  place both uniformly and universally on the earth?

That's ridiculous.  Most of the earth doesn't have primates, and 2 million years ago, most of the ones that did exist weren't evolving into humans.  The ancestors of today's New World monkeys didn't evolve into humans.  The ancestors of today's lemurs didn't evolve into humans.

Why aren't there any creatures who have not taken the same
  evolutionary steps as their same species elsewhere on earth?

I don't think this makes any sense as written.  We do observe different species sometimes evolving the same response to pretty similar environments, like cacti on different continents evolving in to similar-looking forms, despite being far apart evolutionary.  But we don't expect every population to evolve the same way, because evolution builds on the random changes that came before in that population.  That's the basic premise of evolution, that's the premise that explains what we see very well, and if you think some other wildly different premise is in effect, and insist on forcing explanations and data to fit something that is just wrong, nothing in biology will make sense to you.

I'd like to remind you of our policy on civility: http://biology.stackexchange.com/help/behavior

authors: Bob Jarvis - Слава Україні


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Calcium for Humans: Supplements vs Fortified Sources
I'm trying to be vegan, and purely natural foods lack sufficient calcium for the Recommended Daily Intake. Links 2 to 4 (but not 1) assert a correlation between calcium supplements and disease.

[1. WebMD :] "Keep in mind that there's really not that much difference between getting calcium in a supplement and calcium in food."
  "Calcium-fortified foods -- such as cereals, some juices, and soy milk -- are excellent sources of the mineral, experts tell WebMD."
[2. health.harvard.edu :] An 8-ounce portion of off-the-shelf orange juice contains about 300 mg of calcium. The calcium in fortified soy milk also compares favorably to whole milk.
  Breakfast cereals (which are also fortified) contain substantial amounts of calcium, especially when combined with low-fat milk.
  A portion of oatmeal on its own contains just 100 mg of calcium. “But if you cut up some dried figs and add it to a bowl of oatmeal with milk, you easily get about half of what you need without having any supplements,” Dr. Hauser says.
[3. NY Times Blog :] All the researchers agree that, given the widespread use of supplemental calcium, better studies are needed to clarify possible risks and benefits, and to whom they may apply.
Until such information is available, consumers seeking to preserve their bones would be wise to rely primarily on dietary sources of the mineral and to pursue regular weight-bearing or strength-building exercises, or both. Walking, running, weight lifting and working out on resistance machines is unquestionably effective and safe for most adults, if done properly.
[4. NY Times :]  The institute’s expert committee, which included bone specialists, concluded that most people don’t need supplements of these critical nutrients and warned of serious health risks from the high doses some now take — including kidney stones and heart disease linked to calcium supplements, and the very falls and fractures that vitamin D is meant to protect against.

5. How and why would the calcium carbonate from calcium supplements be asserted as worse than that in the fortified foods?
6. Isn't solid calcium carbonate (e.g. in supplements) chemically the same as aqueous calcium carbonate (e.g. in fortified drinks)?
7. Are calcium supplements really worse than fortified foods with calcium?

This is close to a personal medical question, so I'll try and be vague and avoid advice.
There's nothing inherently bad about calcium supplements, and those links and thousands of others that are easy to find tend to all say that same thing.  Basically, for typical people on a typical diet, enough calcium is supplied through food that supplements are unnecessary.  The problem arises when people take too many supplements, such that their intake is significantly higher than the daily recommended intake.  These people can experience a number of symptoms, including kidney and heart failure.  Fortified food and supplements are, as best as I can tell, no different, except that food is simpler route for intake with built-in limit-setting.  That is, you can easily pop five calcium pills (BAD IDEA) but nobody is ever going to drink five containers of fortified soy "milk" on a whim.
My go-to example is that of astronauts.  Astronauts who are in space for extended periods of time must take calcium supplements, in addition to a strict exercise regimen to help stem the tide of bone loss.  Bone loss still occurs, however, because they can only take so much calcium before it starts to cause serious heart problems.  There's nothing inherently wrong with calcium supplements but for most people they are completely unnecessary.  You should talk to your primary care physician and perhaps a dietician.

1 - probably because of regulation in the U.S. (and maybe other nations??). Nutrients added via fortification are regulated by the F.D.A essentially as foods.  Nutrients in supplements are regulated essentially as manufactured goods.  The difference -- despite both being ingested by us -- is a major source of concern. See http://www.fda.gov/Food/DietarySupplements/
3 - as a patient, that question is best answered by your doctor via blood sampling. My doctor found VitD deficiency in me, which can cause calcium uptake problems; but like the previous answer, people who aren't monitoring their serum levels and medicating themselves could overdose on any fortified or supplement nutrients.


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Why does radiation sickness cause hair to fall out?
As I understand it, radiation poisoning (acute radiation syndrome) is fatal because the radiation kills cells. However, why do victims experience hair loss at such an early stage in the process?

Any link at hair loss? I doubt it. Hair loss may be due to chemoterapy if the affected persons contracted cancer or leukemia.

Radiation levels used for treatment of cancer does kill nearly all hair in the target zone.

Radiation poisoning causes mutations in DNA that affect normal cell function, often causing them to die.  Cells normally have a number of repair mechanisms but if the damage is too great they won't be able to do so.  In particular, cells that are dividing quickly will not have time to repair their DNA before division and so die far quicker than other cells.  Chemotherapy is built on this concept.  By selectively introducing drugs or radiation that target fast-dividing cells, the cancer cells, which are very dividing rapidly and unchecked, are killed off before most normal cells.
However, there are some cells in the body that are very rapidly dividing.  Hair cells are one such type, hence hair will often fall out during chemotherapy or radiation sickness.  Another big cell type are those in the gut, which are constantly dividing.  That's why you often see people in movies who have been exposed to radiation vomiting.  The radiation targets those cells first, hence those are the first symptoms.

I suppose that in any radiation exposure, the skin is what is damaged first. So radiation burn on your scalp, may be the primary cause for acute hair loss. Possibly because of the lower penetration depth of α-radiation, which is more damaging.


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Variation in MHC in humans
What evolutionary process lead to so much variation in MHC? What is the advantage of having such variation?

Here are two free articles that go into the subject very nicely, I think:

Major Histocompatibility Complex (MHC)
How pathogens drive genetic diversity: MHC, mechanisms and misunderstandings

The MHC loci are the single most important determinant of our immune system's response to foreign invaders and are absolutely necessary for discrimination between self and non-self.  Because of the massive diversity amongst those pathogens, no one single MHC allele will allow the best response.  For example, the delta-32 deletion that bears resistance to HIV also increases susceptibility to West Nile; if you're more likely to suffer from the latter, that is a fitness reduction that could be selected against.  Thus, more alleles will survive in the population as all can be advantageous.  This is called balancing selection.
Additionally, the microbial invaders mutate and evolve much, much faster than our genome does, so you want to have the greatest breadth of MHC present in the population and in an individual in order to maximize resistance to whatever may arise.  At a population level, it is also advantageous because it means that the entire populace won't succumb to a certain infection.  If everyone has similar alleles one virus could wipe everyone out; we observe something similar happen with our crops, for example, when grown in massive monocultures.  There is also a fair amount of evidence, mainly in humans and mice I believe, supporting a role for MHC in mate selection.  Individuals seem to find potential mates with different MHC alleles more attractive, presumably to maximize the fitness of their offspring.
MHC is an absolutely fascinating subject (I'm researching it at the moment!).


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What did we learn with Nazi human experimentation?
Was there actually any useful knowledge gained from the Nazi experiments on human test subjects? Wikipedia cites freezing and phosphine gas reactions, but I would like to know other potential results from the Nazis.
At a first glance, it looks like the problem is that, in addition to the obvious ethical issues, there was also a lack if scientific rigor. Is this true or can some results actually be of some use?

Can you add links to the relevant wikipedia articles, or other references you have looked at. This makes it easier for others to fill in.

Basically nothing.  The Nazis did unfathomably terrible things of little value, and they did it poorly.
This* is a fascinating, albeit long, read.  It goes through some of the ethics of the data, but first lists some more of the "experiments" the Nazis performed.  To add to your list: high-altitude, sea water potability, tuberculosis, poisoning, artificial insemination, and numerous woundings.  They also did terrible things to twins.  Aside from being torturous and cruel, the "experiments" rarely if ever used anesthetics and were usually designed to kill the prisoner.
The article goes on to list a few case studies where some of the Nazi works came up and could have been considered, but were repeatedly shot down.  It then details a number of reasons why the "experiments" were worthless.  In particular,

"[I]t is doubtful that physiological responses of the tortured and maimed victims represented the responses of the people for whom the experiments were meant to benefit."
Nazi "researchers" were racists who were looking to validate their own beliefs.  No good science comes from that.
The results weren't ever actually published.
The "data" are inconsistent.

The article moves into ethical arguments and hypotheticals, but ends up saying theoretically some of it could be considered, or that "Absolute censorship of the Nazi data does not seem proper, especially when the secrets of saving lives may lie solely in its contents."  It's a complicated scenario where that would arise.

Editing a few years later to add this discussion from the NY Review of Books.  It's a little removed in tone, and is over-generous as regards the intent of the Nazi torturers, but makes the interesting point that one good thing to come out of the experience was the first codified guidelines for human experimentation:

As part of the judgment, the court issued the celebrated Nuremberg Code in 1947—the first, shortest, and in many ways most uncompromising of the major ethical codes and regulations for the conduct of medical research on humans. Although the code had no legal authority in any country, it had great influence on ideas about human experimentation, and subsequent international codes and legislation.

In particular, the concept of "informed consent" is directly traceable to the Nuremberg Code:

The first provision of the Nuremberg Code is unqualified: “The voluntary consent of the human subject is absolutely essential.” No exceptions are permitted... Furthermore, the code is clear that consent must be given by subjects who are fully informed.

*I should note that the article is from a Jewish law website, so some may discount that as not a perfectly neutral source.  Which is silly.

This is an interesting question and one that really has two parts: the factual and the ethical. I remember discussing this topic in my 'ethics training' classes in graduate school (where I admit that I may have acted as an ass simply to demonstrate that our ethics training was unfailable).
The factual: "Are there any valuable findings published by the Nazis?" Actually, yes. There is a classic anatomical atlas by Eduard Pernkopf, 'Pernkopf Anatomy,' that was quite probably put together using the bodies of political prisoners as subjects. However, it may be that this is the only text that has real value, but it's enough to get us to the second question.
The ethical: "Should we persist in using information assembled under unethical conditions? Doesn't this provide an incentive to these practices - or at least not condemn them sufficiently?" Here my assly behavior was meant to send a message of, 'all morals/ethics are relative. And why should we not benefit from all sources possible? I would deny funding for unethical methods, but I would still read the paper. (obviously this part of my answer is just opinion and really shouldn't be printed here, but I think the question demands that it be considered)


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Why don't raisins lose water when in air?
It is common that we soak raisins in water, and they acquire water by endosmosis. That means that the cells are permeable to water, right? Then why don't they lose water when kept in air? Or kept in sugar without any water?
EDIT: Also, take the example of peeled potatoes. Put them in a hypertonic solution, and they lose water, but when kept there, in air, they don't. How come?

That means that the cells are permeable to water, right?

Correct.

Then why don't they lose water when kept in air?

They do, but it occurs very, very slowly. It might take a few months (or years in some areas), but if you leave raisins exposed to air they will eventually become harder until the water reaches equilibrium with the surrounding air.
This slow process is why there are tips on how to reconstitute raisins that are too hard to make them more moist and plump after getting a bad batch or finding old ones in your kitchen.

They already have!  Raisins are dried-out grapes, and according to a brief search are less than 20% water by weight but over 50% sugar by weight.  They've lost plenty of water already.  Your average grape is probably hypertonic to most solutions and thus will not readily lose more water.  Additionally, for water to be lost to air, it must be vaporized via evaporation, which is slow, inefficient from something as dry as raisins, and miniscule in effect.  Sun-dried raisins already went through that process.


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Variations in Genome Sizes
Why is there wide variation in genome size amongst groups of protists, insects, amphibians and plants, but less variation within groups of mammals and reptiles?

You're asking about the C-value enigma, in particular this kind of diagram:1

The quick answer is that there is no "why" in evolution; things happen and if they're beneficial they tend to stick around more than the deleterious things.  The longer, (slightly) more satisfying answer is non-coding DNA.  Thanks to non-coding DNA the size of a genome doesn't even correlate to the number of genes.  The human genome, for example, has over 20,000 genes but is less than two percent protein-coding; the flower Utricularia gibba, however, has over 28,000 genes with about two orders of magnitude smaller of a genome, due to the fact that its genome is 97% protein-coding.  In short, there is no real meaning to be found in genome size variation due to non-coding portions, which while they are sometimes important regulators can often be just transposons (40% of our genome).  I will also point out that all of those groups you mention have species with significant polyploidy.

The are a number of other interesting ideas.  In the process of researching this, I stumbled upon the Animal Genome Size Database, which is an absolute gem of a treasure trove.  It's an unbelievable mine where I've spent a good half-hour just reading.  In particular, the statistics pages list interesting correlations for certain groups.  Mammalian genome size, for example, correlates:

Positively with red blood cell size, despite lack of nuclei
Negatively with metabolic rate
Not at all with developmental rate or longevity

For amphibians, however, there is:

Positive correlation with red blood cell and nucleus sizes in both frogs and salamanders
Negative correlation with developmental rate in many groups
Negative correlation with brain complexity in both frogs and salamanders
No strong relationship with metabolic rate in either frogs or salamanders
Some association with intensity and frequency of metamorphosis

If you have time, I highly recommend reading through T. Ryan Gregory's PhD thesis entitled The C-Value Enigma.  It's around 350 pages, but each chapter is in separate pdfs and is the most in-depth treatment I've seen, despite being about a decade old.  It's been moderately life-changing for me to read, some of the interpretations he presents challenged my thinking on the subject of genome evolution entirely.  Should genomes be treated as individuals, and what would that mean?  I digress.  Chapters 3, 4, 6, and 7 are what you'll want, in particular the last twenty or so pages of chapter 7.
Dr. Gregory now has a faculty position and his lab's research page is a little easier to read.  I love this image:

As genome size increases in eukaryotes, the percentage of the genome composed of genes (white circles) becomes smaller. Conversely, the percentage of the genome made up of transposable elements (black circles) increases with genome size.

It seems like the best way to look at genome size and find some meaning is within a specific group.  There are correlations, for example, that are present in frogs and salamanders, but not in either group alone.  Some of the groups are very unbalanced; in insects, only Orthoptera tend to have very large genomes.  Interestingly, a number of those groups also undergo some form of metamorphosis, but the correlations aren't what you might have expected:  insects that develop quickly and metamorphose have smaller genomes, but "[i]n a more general sense, small genome size seems linked to rapid diversification... Conversely, insects without metamorphosis may possess very large genomes..."


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3 fates of this matter
When an animal eats something, it obtains matter and energy right? But, what are the 3 possible fates of the matter and 3 possible fates energy. I don't understand what they are even asking. What would be the 3 possible fates of each.

Please tag this as homework question.

I think the poster wants only a simple answer, so I am going to answer in simple terms. The fates can be -
1 Used in cellular respiration as fuel and some amount can be converted to useful energy which can be used to build other substances and some energy can be lost as heat.
2.The animal can become prey for other animal.
3.The animal throws away some matter as feces.

I understand the matter portion but, the energy can be lost as heat? I get that it can be used to create substances in the body. And that is only 2 fates of the energy.

@John it can be passed on from the animal to the prey.

Maybe this video might help you:
Matter and Energy in Organisms


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Number of introns in a genome
Humans have approximately 21000 genes but they probably make more proteins than that. This has been explained by many mechanisms like alternative RNA splicing.
My question is - If what we call as "introns" and "exons" vary so much, then how is the  number of introns present in a genome determined ?

What do you mean? What we call "introns" and "exons" is actually quite well defined. It is the concept of "genes" that causes problems. Counting introns is relatively straightforward (as long as you have an accurate count of genes). It is not a very useful exercise but it is not hard.

@terdon I didn't mean to say that our concept of what we say as intron and exon vary. I meant that for each different protein from the same pre m-RNA , what sequences we call as introns and exons would vary.

Ah I see, well anything that can make it into a mature mRNA is an exon by definition. Anything that does not is an intron. So yes, the same stretch of genomic nucleotides can actually be both in different mRNAs.

Yes, the individual number of exons/introns will vary in a transcript, but what you can do is just count all possible exons of a gene
For example, lets say you have an alternative exon in these two isoforms. The XX's are exons
XX---XX---XX---XX
XX--------XX---XX
We would say this gene has 4 exons and 3 introns, even though one isoform only has 3 exons. Its the transcript that varies in number of exons, the gene remains constant.
Heres a slightly more complex example. Mutually exclusive exons
XX---XX--------XX
XX--------XX---XX
We would still say it has four exons. Pretend that every exon of every isoform is included and thats how you get the number of exons in gene. So for the above example, just pretend both mutually exclusive exons are included
XX---XX---XX---XX
According to this old paper there are 8.8 exons per gene (7.8 introns). Their gene number count is high because its older, but they estimate that there are 207,344 introns in the human genome.

Introns is not always "exons - 1", you can have spliced UTRs with a leading intron for example, or a trailing one in the 3' UTR.


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Which hormones can cross the blood brain barrier?
Can hormones such as testosterone, aldosterone and estrogen cross the blood brain barrier?
I looked on Wikipedia and there no mention of it in the testosterone article. Through Googling around I also didn't find a list of which hormones can cross the barrier.

Yes, both steroid and peptidic hormones can enter the brain, the obvious proof being that the brain responds to changing blood concentration of hormones.
The situation is different for steroid hormones (such as estrogen, testosterone, cortisol etc) which are small and lipophilic, and peptidic hormones (such as insulin, ghrelin, prolactin etc) which are big and hydrophilic.
The blood-brain barrier (BBB) is selectively permeable to steroid hormones: some of them (such as the gonadal steroids) can readily pass the BBB, while others (such as corticosteroids) pass only in small concentrations. This may however be modulated by hormone carrier proteins in the plasma.
See: Transport of Steroid Hormones through the Rat Blood-Brain Barrier - Pardridge et al., JCI, 1979

When speaking of peptidic hormones, the classic hypothesis is that hormones pass through the areas where the BBB is "leaky", i.e. where capillaries are fenestrated.
These include circumventricular organs such as the median eminence (where the terminals of many neuroendocrine neurons are located), or the organum vasculosum of the lamina terminalis (OVLT), important for reproduction and osmoregulation. The chorioid plexus is also often mentioned as a site for hormone entrance and/or sensing.
However, how exactly hormones enter the brain is still very unclear.
Our lab published a paper on this topic recently:
Rapid sensing of circulating ghrelin by hypothalamic appetite-modifying neurons - Schaeffer et al., PNAS, 2013

Yeah indeed they can.  The obvious proof is puberty and development, but a more involved look into how that is achieved can be found in this free article from last year.  In particular,

Nearly every mechanism by which a substance can cross or interact with the BBB is used by one hormone or the other. In general, steroid hormones cross the BBB by transmembrane diffusion whereas thyroid hormones, peptide hormones, and regulatory proteins cross by saturable systems.

In particular, I like figure 1: