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Why do pine stands exist?
I live in the midwestern United States.  I cycle to work, sometimes on heavily wooded roads, and I can't help but notice that in most places within the surrounding deciduous forests Pine and evergreen trees don't seem to be doing so well - the few that exist don't look too happy.
In some places, however, there are majestic stands of pines - often completely free of the "seasonal" variety of trees.
Why is this?  What allows the slow growing pines to out-compete the other arboreal denizens of the forest?  And generally in such particular areas?
Thanks, this is killin' me...

A lot of forest is planted... I've heard that here in Sweden around 95% of forest is planted rather than natural forest, I've not got a source available for that though

Forest Succession 101

Pines are actually fast-growing, shade-intolerant, early-successional species. When land is allowed to lay fallow after being cleared by fire, wind storms, human land use or other major disturbance, the successional sequence will begin.
At first only herbs and grasses grow, but eventually these are shaded out by shrubs and tree seedlings. In this setting, the limiting factor is typically light. Because pines are fast growing in the sun, they usually take over a field and develop a relatively dense even-aged stand.

Because the seedlings grow so well and densely, they usually shade out and prevent most other trees and shade-intolerant plants from growing. The result: a dense stand of mostly pines:

I'll note here that early on in this process (before processes of self-thinning really get to take off), you can end up with what are sometimes called "dog hair" stands. Also, if you see clear rows in the pine stand, that's a good indication the pines were planted.
Eventually (80-120 years), most of these pines will die and fall out of the canopy (both due to "natural" causes and additional wind, ice, pest, or fire disturbance). As large pines fall and clear large enough canopy gaps, shade-tolerant sub-canopy hardwoods can take their place. Because pines are highly shade intolerant, pines do not regenerate again in that stand (without another major canopy-clearing disturbance). The result: a mostly hardwood-dominated forest (with perhaps a few remnant older pines):

So...

The all-pine stands you're seeing are early on in the successional sequence.
The few pines (that "don't look too happy" because of age) mixed with hardwood ("seasonal variety") trees are in a mid-to-late successional stand.

Note: my answer addresses the description of your question -- it is due to succession that you see the forest stands you're observing. This example of secondary succession does not apply to all instances of pine existence (as your actual questions asks). That question would have a very complicated answer involving niche theory, succession, disturbance regimes, interspecific and intraspecific interactions, trait descriptions, etc. and would need to be addressed at numerous scales (biology, population dynamics, community interactions, meta-populations/meta-communities, landscape scales, etc.)

What about non natural forest - most forest these days is managed and has commercial interests. If @user1833028 has an exact location we might be able to rule that out!

@rg255 I've addressed that in my answer. You'll know it was planted if you see a conspicuous rows of trees. If there are no rows, then there's a pretty good chance those seeds arrived on their own (via wind)

In nature, species compete for resources like water, light, nutrients, etc. and need to find 'their place' in this struggle. According to niche theory, every species occupies a certain spot in the multidimensional niche space (the dimensions describe the number of environmental factors) where it performs better than any other species. If there would not be such a place, the species is doomed to extinction in free nature.
Let's look at the pine (Kiefer) and the beech (Buche), a common european deciduous tree:

You see that the beech outcompetes the pine under intermediately moist conditions, although these conditions are theoretically best suited for the pine  (physiological optimum). However, the pine can outcompte the beech at the extremes of the gradient (ecological optimum).
Now imagine many environmental factors and many species. Under the predominant conditions in the midwest USA, deciduous tree species are favored over confifers because they are the better competitors. If conditions change towards the more extreme (very dry/moist, harsh climate,...), the pine gains the upper hand and forms large stands.

So if pines compete better in drier areas, you might find that the soil around pine stands is sandier, and would drain better than the soil where pines don't do as well. If you want to research this, your state probably has a university extension program willing to do soil testing for a small fee, you might find something that distinguishes pine stand soil to non pine soil.

Also, sir, would these be local conditions, temporal conditions (ie, they became established for a period where they had the oppourtunity) or both?

Both is basically possible, especially if you take deliberate alteration of site conditions and competition into account (forestry). However, on the long run and under natural conditions the general site characteristics will dominate temporarily beneficial effects. In general, trees are better adapted to stable conditions, whereas other plants like annuals or biennials are specialized in colonizing very unstable habitats. Trees aren't that good in taking advantage of short-term fluctuations.

But note that in different conditions - for instance the mountains of the US West - evergreens (pine, fir, cedar &c) almost totally dominate the landscape.  The only large deciduous tree is the aspen, and it's restricted to wet area such as meadows and along streams.  The rest are basically shrubs.

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Is the water transpired by plants pure H₂O, or does it contain trace minerals?
I'm considering the idea of drinking water that I trap from what is transpired by trees.
Interestingly, is this water a fairly (or maybe even extraordinarily) pure form of H₂O, a remarkably pure by-product of the respiration / evapotranspiration processes - so does the process give off a fairly distilled form of water into the atmosphere - or is there actually a fairly measurable amount of trace elements that also are transpired in that water through the leaves?
A second complication which would be good to clarify, is that even if minerals / other chemicals are excreted along with the H₂O, would condensing that water in a water trap still only collect the pure H₂O anyway?

My guess is that seeing that the water loss is incidental, other chemicals are incidentally lost as well. Our lungs exhale plenty of things beside CO2 and water: http://en.wikipedia.org/wiki/Breath_gas_analysis

It will depend a bit on the specimen of tree / plant that is doing the transpiration. Minerals will typically stay behind during evaporation, but volatile compounds (think the minty smell of Eucalyptus) would evaporate at the same time as the water, and might condense (in some concentration) at the same time as well; this will depend a bit on the temperature of the leaf, the relative humidity of the air (lower will favor evaporation - higher means there is a lot of moisture already in the air, and you don't necessarily know where it came from) and the temperature of the surface used for condensation (lower condensation temperature will trap things besides water).
Note - this is more a physicist's answer than a biologist's... betraying my background here.

Thanks. That answer helps. Yeah this is one of those questions that straddles more than one scientific area of discipline to know / understand / explain it. Still, I class this sort of topic as 'biological knowledge' with the help of chemical principles, and indeed chemistry does not always explain biological phenomena in and of itself! Now I wonder, wouldn't some minerals themselves be contained in volatile compounds anyway? Unless they tend to just be too heavy- I wonder! I suppose the definitive answer in the end is to just find research that has simply measured all this, in a robust way.

The minerals will stay behind. They are too heavy to be transported via the vacuoles of MOST, and most must be stressed when dealing with plants, plants during transpiration. Though the water-soluble compounds- including the volatile compounds mentioned like terpenes and even flavonoids will and can exit during transpiration. Terpenes are not bad for humans, the term volatile refers only to the reactivity, not whether or not it is bad.

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Alfred Jost's rabbit experiment: how did he actually do it?
I was watching a Crash Course on Biology YouTube video by Hank Green: Great Glands - Your Endocrine System.  Hank humorously describes a sex determination experiment by Alfred Jost as follows (beginning at time 9.17 in the video):

So, he, ah, very carefully... very, very carefully (and this is a little disturbing) removed bunny embryos from their mother, and then, also very carefully, removed the part that would become the ovaries or the testes from the bunny embryos.  And then, also very carefully, he put the embryos back in the momma rabbit.
What Jost found, after the bunnies were born, was that the ones that he performed the surgery on turned out to be girls.  So, in the absence of gonads, and therefore hormones that specifically instructed the development of testes and the growth of a pee-pee and a deep bunny voice, he discovered that the default setting for mammalian embryos is "make it female".

Q: How did Alfred Jost actually perform this experiment?
Essentially I'm after a less superficial description of how Jost implemented this experiment in practice.
I did a bit of Googling; what I found was consistent with Hank's description, but still omits a description of how Jost excised rabbit embryo gonads (instead just asserting that he did it).

I assume the procedure is very similar to castration or spaying practiced on fully developed animals, but done very carefully. The harder part of the operation would be removing the embryo and putting it back without damaging it too much to keep growing.

Check out Fig. 7 in the document at http://ipubli-inserm.inist.fr/bitstream/handle/10608/4343/MS_1991_3_263.pdf . The caption says: "Castration of a 23 day fetus. [Mother's] womb is open, the rear end of the fetus is pulled out, a flank incision is performed, and the testicle, located on the mesonephros, is exposed, then cut. After bilateral testicular removal, the fetus is re-placed in the womb. [..] For ease of explanation, an older fetus is in fact shown."

I don't read French, so I might be missing it, but I can't find any photographs, just some diagrams of the reproductive organs.

sorry, link fixed now

That looks a lot more complicated than when I used to castrate pigs. Thanks for clarifying that.

The picture I indicated shows only the castration of the embryo. Mother's oophorectomy is not described in the above link, and must be trivial. For completion, here's a rat oophorectomy: http://www.nature.com/protocolexchange/protocols/2152

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What triggers the release of gonadotrophin-releasing hormone with the onset of puberty?
I am interested to know the process of development of puberty. During puberty, when boys/girls reache 12-14 (puberty) years of their age, their hypothalamus releases gonadotropin releasing hormone (GnRH) and then this hormone in turn affects the pituitary gland which releases FSH and LH. FSH/LH hormones promote male/female features. For e.g. girls start their first menstruation cycle and males start to produce sperm; their voices become smooth and intense respectively. So all these phenomena are dependent on GnRH.My question is that if those hormones are produced due to the effect of GnRH then how is GnRH production itself regulated. In other words how does our body "know" that we are in the age of puberty and it should secrete GnRH?

GnRH-secreting neurons are not fully independent. To date, their most studied regulators are kisspeptin-secreting neurons. During childhood, kisspeptin-secreting neurons are off, due to GABAergic higher level structures and to lack of free leptin. So both brain and body fat have a word on it.
Caveat: most of the evidence is circumstantial (for example, higher circulating kisspeptin in naturally occurring precocious puberty) and I am oversimplifying, so the picture is more complex and will become even more so.


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How to estimate the DNA density in human sperm head?
I have got an estimate of sperm head volume from internet.Like consider it as a disk of order 4-5µm. Now I wanted to find the DNA density in the sperm head. How to find that?

I don't understand what the value 4-5 microns refers to. If it is supposed to be a volume it should have units of volume.

figure out if 4-5 um refers to the diameter or radius, then calculate the volume of the sperm head, then figure out the volume of a chromosome, assume it as cylindrical and then figure for 23 chromosomes how much space is filled hence you would know the density

@Bez I assume the aim is to get pg per um3 or something similar.

Find, or calculate, a value for the volume of the sperm head.
Find a value for the size of the human genome (haploid or diploid?)
Convert the genome size, which will probably in Giga basepairs, into mass (I suggest picograms).
Divide mass by volume to get a density, pg μm-3
Refinement - does the sperm nucleus take up all of the head volume? Do you need to factor this in?


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Regarding the difference between cDNA library and RNA sequencing (Biochem. technique)
I was wondering why establishment of cDNA library required the step of reverse transcription (i.e. turning the sequence into DNA) why not directly using the extracted RNA for sequencing and converting the U to T base? Why bother to have one more step? super super confusing

because you are stabilising a cDNA library of different expressed products, which you might want to sequence and amplify which is perhaps easier if the product is a DNA?

The construction of a cDNA library involves making a DNA 'copy' of the mRNA because the aim is to synthesise a large set of recombinant plasmid molecules, each containing a different cDNA and each propagated in E. coli.
The heyday of cDNA library construction predates the invention of PCR.
The key difference between the two approaches that you are comparing is that one (cDNA library) involves creation of a physical representation of the expressed genome whereas the other is an informational representation.

oh I see I see thank you so much, but then i have come up with another question...mmm..so sorry i have quite a poor background about this aspect....i was wondering why PCR is only applied to DNA why not RNA?

Oh n also I was wondering what the physical representation means?

I mean that a cDNA library exists as something tangible, not just in a computer.

PCR is carried out with a DNA polymerase, which can only deal with DNA as a template. The exception to this is of course reverse transcriptase, but that can't be used in a PCR because it isn't thermostable and it can't copy the DNA copies that it makes from an RNA template, so exponential amplification cannot take place.


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multiple HIV infection in same T cell
I was wondering can multiple HIV virus infecting same T cell ?
Coz in flu virus they have SA to cleave of those sialic acid residue preventing re-infection of the same cell by other viruses to maximize the amount of cell get infected.
I was wondering is there any mechanism found in HIV virus like what found in flu virus to prevent re-infection of an already HIV-infected T cell.
(little bit more about HIV virus that is irrelevant to the question, coz i was told that there is some HIV possible to hide in our body, but then i don't understand what it is the meaning of this hiding? Q1:Is the "hiding" refer to the genome of HIV that integrated into T cell. some of these infected T cells circulating in the blood Q2: will some of them reside in lymph node? Q3: and what make these infected B cell proliferate so to keep these B cell with the hiv genome long existing? will the virus transform these T cells into self proliferating? but will that be like cancer cell uncontrollably proliferating or well controlled?)
Thank you everybody

HIV doesn't infect B-cell as far as I remember

Oops~ hahahah really thanks for reminding me of that.Omg so embarrassing. Thank you

Yes, HIV does attempt to prevent multiple infection of the same cell. Once a T cell or other cells are infected, HIV downregulates the CD4 receptor which it uses to gain entry. Because of this, there are less receptors so another HIV is less likely to infect that cell. Meanwhile, the infection itself upregulates CD4 receptors on other cells which means the downregulation is even more effective. There are other mechanisms but this is a major one.
Hiding means it is somewhere where we don't know where it is and it isn't that active. When HIV is active it is destructive but also the cell is aware it is there. The cell can then try to alert other cells that it is infected. If HIV isn't active but instead hiding, it can stay where it is without really being detected. Even the drugs we use usually only affect HIV whilst it is replicating. So again if it's in a cell that's long lasting and the HIV is not replicating then it is essentially hiding. Such a cell includes macrophages and memory cells when we are just talking about the immune system.
Will HIV reside in the lymph node? Well yes, this is an exciting place for it. There's loads of exposed CD4 receptors and lot's of it's favourite T cells about. An infected cell will transmit HIV to other cells when they are signalling to each other. Even worse is when a dendritic cell is infected. Instead of instructing the immune system how to detect HIV infected cells, it is infecting them.
HIV is an infection. As soon as the body detects it, it goes into overdrive trying to eradicate it. This means there are more cells for HIV to infect. More foreign material means the immune system is even further stimulated to make even more cells. However it doesn't want CD8 cells to proliferate too much nor too many HIV specific cells so driving too much proliferation is a bad idea. What HIV does do is make lots and lots of useless copies of itself. HIV particles that are so badly made they aren't functional. The body tries to fight these and makes more cells to combat these but there's no point because they aren't the problem. But this immune diversion and a larger target number of cells is exactly what HIV wants. Proliferation of HIV specific cells, particular CD8, is associated with delayed disease progression or control.
Usually the cancers caused by HIV are because of other viruses running unchecked. Kaposi's sarcoma or lymphomas for example.

Though at the same time, i have some questions coming up in my mind. The first one is i was wondering is that T cell the only cell get affected by HIV coz macrophages and dendritic cell are mentioned in the answer. mmmm...i wonder how can the HIV get into these non-T cell by skipping the part that they requires CD4 for entry or actually CD4 is also present in these cell besides T cell as well?? 2nd one is what makes HIV prefer to infect memory cell?

3rd one is about the upregulation of CD4 cell in other yet infected T cell, is there anything to do with the HIV itself, like the hiv bears some genes to selectively upregulate the CD4 receptor on other unifected T cell or it is the feedback system of the immune system while the HIV has no direct role in the upregulation of CD4?

The last question is that really bother me is that cant we activate those provirus and force them into actively proliferating form. Then, large dose of antiviral drug are introduced to the system to prevent the newly produced HIV from infecting those uninfected target cell as to completely eradicate the provirus in our cell. I was wondering is it possible.Oh before that, have the mechanism of those pro-HIV been found out yet?

OH this one is really the last one. I was wondering what is the route for HIV to get into macrophage and other non T cell cell, by recognizing CD4 receptor or other protein?

Make another question. There's so much to write to answer all those. Add a comment here linking me to them and I'll try to answer


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(How) can a pink grasshopper exist?
I saw this foto on Reddit recently:

Is this possible? How can a grasshopper become like this? Is this just natural genetic mutation?

Genetically modified... or naturally mutated... I doubt the natural part though - given the number of genome research out there...

Looks like a Katydid, not a grasshopper, and googling pink+katydid will get you many hits

Pink individuals of the katydid species Amblycorypha oblongifolia are a relatively uncommon but natural phenomenon with a long history of research.
It looks from popular press accounts (Science Friday, Scientific American) that the pink coloration may be caused by a dominant allele, and is only rare because of a high selection pressure against pink individuals (i.e. they're much less good at hiding among leaves, and are eaten before they can reproduce).

Photo by Richard Whitby, via flickr.com/blueboat2 (cc-by-sa 2.0)

I thought I could find a pink praying mantis, but couldn't. Orchid mantis's do come in a variety of colors, and sometimes a pinkish. Since mantids are grasshoppers and katydids are related, it's not farfetched that similar genes could control coloration in all these insects.

Can't edit the comment, mantid's aren't grasshoppers, should read ..."mantids and grasshoppers..."

Any idea, what kind of pigment is involved?

Side-question: if you were to breed with solely pink individuals, what are the odds of the offspring to be pink as well?

@StevenRoose the odds are very good – check the SciAm link where they have results of just such an experiment, looks like it's about 3:1 odds to 7:1 odds that the offpsring will be pink.

In response to Oreotrephes answer I see fit to point that the selective pressure against an insect being pink and a manual being pink is quite different but could also be the same.
Take our species for example: the first humans were dark skinned thought to be as a genetic advantage to our then dark forrest and tree land environment. As we evolved into a plethora of colors each equally evolved but separately specialised (to the same basic tasks) under the pressure of different environments some of us became lighter skinned and lost some of our protection from the sun. Pinkness in caucasians is common but its a genetic disadvantage due to the introduction of an extremely greater probability of Melanoma. Those with darker skin sometimes can develop Melanoma but its rare. It is thought we evolved light skin as a way of knowing we needed greater amounts of D3 in diet due to low UV environments. The same also with blue eyes the eye equivalent of whiteness (melatonin depletion).
If its evolution was simular to ours then I would suspect that your little pink insect needed a key vitamin in its diet but thats just a guess.


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What is the ratio of breathing rate to heart rate?
Breathing rate and heart rate are directly connected. This is because the heart is connected to the lungs via the pulmonary artery.
I first thought that breathing rate would be half of the heart rate since half of the heart cycle occurs in the lungs.
But I know that is not true with a normal 12 BPM(breaths per minute) breathing rate.
So what is the ratio of breathing rate to heart rate?

"This is because the heart is connected to the lungs via the pulmonary artery." It's not like heart rate or breathing rate are regulated by pulmonary arteries. The relation is more sophisticated than that. For example heart rate is controlled by nerves and hormones, and neither comes straight from the lung. But fast breathing leads to changes in blood oxygen and pH, which are picked up by sensors such as the carotid body, which informs the medulla, which then talks to the sinoatrial node. There is also more direct influence, because ample breathing increases pressure in the thorax.
But at each step, there are many other factors interfering, meaning the correlation between the two gets ever looser. There isn't really a "normal" ratio of heart rate to respiration rate. There is a healthy heart rate and a healthy respiratory rate, but they are both wide intervals (60-100 and 12-20, respectively). Dividing one by the other, you get a very wide interval, from 60 beats per minute / 20 breaths per minute = 3, to 100 beats per minute / 12 breaths per minute = 8.
Perhaps in practice the most common values for beats per breath are in a narrower interval. But "normal" values are defined in relationship to abnormal conditions, and there is no disease in which a change in this ratio is a cardinal feature. It makes little sense for clinicians to define a normal range for beats per breath, and therefore it makes little sense for epidemiologists to estimate most common values.

did you mean "breathing rate" in it's not like heart rate or bleeding rate are regulated by pulmonary arteries?

yes, that was a typo

but a disease that changes the HR most likely also changes the BR(breathing rate) and it probably also changes the ratio in lots of people even though the exact ratio varies from individual to individual. One example of something that is beneficial sometimes and changes the HR is ventricular hypertrophy. When caused by excersize it increases stroke volume and thus increases O2 transport which is always a plus. It also lowers the HR in response to the high BP that there is at first so that high BP becomes normal BP so that resting HR is anywhere in the normal range as well as down to 40 BPM.

As I said above, the chances are that when one is high, the other one is high too, and the interval may be narrower than 3-8 beats per breath. But, because it is of limited clinical importance, the ratio was not the focus of high-scale epidemiological studies. To my knowledge, scientists did not look for a "most common", nor for a "healthy" ratio. In the absence of actual data, I was only speculating.

but if breathing rate is clinically important and HR is too than why wouldn't the ratio be important? Cardiovascular disease and Respiratory disease can both change the ratio to where it is out of the normal range of 3-8 beats per breath. And it is important to know whether you have cardiovascular disease, respiratory disease, or both.

like respiratory disease can make it more beats per breath if it is restrictive(In other words problems with getting oxygen into the lungs) and cardiovascular disease can make it less beats per breath if it makes the heart speed up(which it almost always does)

I feel that ideally a healthy adult, under normal static conditions, should breathe 15 times per minute and his pulse rate is should be 60 per minute.

Welcome to SE BIology. I think your answer is plausible but this is a science website so most other uses will like to see data/evidence. Can you update your answer to include some evidence? Thanks.

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Why isn't Bubonic Plague as virulent as it once was?
Although I am admittedly not anywhere near an expert on any topic, I still have a hard time understanding how Black Death and Bubonic plague are one in the same. Since plague still exists, with news stories about it every once in a while, and especially in places like India, why doesn't it spread with anywhere near the rate it did during the Middle Ages?
Obviously global society in general is much more sanitary than it was then, people also tend not to live in close quarters with animals today as they did then, however in places like rural India and China this lifestyle still takes place and plague still exists, so why aren't there large out breaks of plague in these areas if it indeed is Black Death?
Is it possible that Black Death has been miscategorised due to various historical circumstances and scholarly errors?

To answer your first question, just search "plague" in Google News: "Just last month the Chinese government sealed off a city of more than 100,000 people, fearing the spread of a plague outbreak.", and even "Struggling Liberia creates 'plague villages' in Ebola epicentre". The way poor people deal with plague changed from the times they thought the miasma is to blame, to the point that it is a model for fighting other epidemics. Also, the antibiotics are only 70 years old: old enough to be patent free and easily manufactured. China and India are in fact top manufacturers for such drugs.

@simontemplar I think you have answered your own question. sanitary practices, quarantine techniques and improved diagnosis and fast communication of such events prevents their rapid spread.

The identification of the Black Death with plague is now fairly well-established - see this paper (open access) in which PCR and protein detection were used to detect the presence of Yersina pestis in human skeletons from plague-related mass graves across Europe.
Outbreaks of plague do occur in rural environments, see this WHO page for some details. The WHO plays a role in responding to these outbreaks, as long as they are notified by the relevant countries. Plague infections respond well to antibiotic treatment.
There has also been a recent outbreak in Madagascar. According to the epidemiologists we are still in the midst of the 3rd plague pandemic, which started in China in the mid 19th century.

Thank you for all of that. It's still unclear to me, though, how it managed to spread so incredibly fast during the time of Black Death, but subsequent outbreaks didn't spread as far and wide even in the Middle Age Europe, or rather that seems to be what I've inferred. I realise the population was much smaller, but even after it bounced back a lot, it still didn't seem to be as dangerous. Did people learn something or change something about their lives?

An addition to Alan's answer:
Some sort of selection for more resistant genotypes inevitably did take place and left distinct footprints in the human populations1.
Specifically, the paper linked above presents evidence that Toll-like receptors, which are immune system proteins that recognize molecular patterns of pathogens, likely adapted to better recognize the plague bacterium Yersinia pestis:

Reconstruction of evolutionary history of European populations has identified Toll-like receptor 1 (TLR1)/TLR6/TLR10 as a pattern recognition pathway shaped by convergent evolution by infections, among which plague is a likely cause...

Reference:

Laayouni, H., Oosting, M., Luisi, P., Ioana, M., Alonso, S., Ricaño-Ponce, I., ... & Netea, M. G. (2014). Convergent evolution in European and Rroma populations reveals pressure exerted by plague on Toll-like receptors. Proceedings of the National Academy of Sciences, 111(7), 2668-2673.


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Why has grey hair evolved?
A vast majority of humans get at least some grey hair as they age. As far as I know this applies to both genders and all races. Presumably this means that at least some grey haired humans have noticeable reproductive advantage, or maybe they had it in the recent past.
Theoretically, because this feature is so prevalent, there must be a strong evolutionary pressure to keep it. Am I right? If so, what is it?

gray hair happens after the optimal reproductive window period so after that window there is no selection pressure to eliminate it.

i would think that showing age will prevent less viable offspring, so it might be adaptive.  not everyone believes in such social adaptations though

There was a discussion on Reddit a while ago, and the general opinion was that other primates and even dogs show gray hair if they live long enough. That puts your question on the wrong premises.

@NickSandor can you share a link to that reddit discussion?

http://www.reddit.com/r/askscience/comments/hm3k2/what_is_the_evolutionary_reason_for_grey_hair/ I wasn't sure I am allowed to link to competition.

New development: http://www.bbc.com/news/health-35687287

@Bez Men are usually still fertile after they grey, and so are many women. I agree that this is a lack of selection pressure to avoid it, but I don't buy specifically that argument without citation.

Thus, the question is not "what makes hair grey"?

Presumably this means that at least some grey haired humans have
  noticeable reproductive advantage, or maybe they had it in the recent
  past.

No it doesn't.  Natural selection is not that strong, it doesn't optimize every single possible physical trait towards maximum reproducing.
And as others have mentioned, having lots of grey hair usually happens after reproduction is over.  Historically, lots of women did a lot of reproducing before they had any grey hair.

This seems to be almost completely correct, but some grey-haired men could still be reproducing.

"it doesn't optimize every single possible physical trait" emphasizing this in the study of evolution would eliminate much of the confusion.

Grey hair is one of many age related traits. Other traits showing a positive correlation with age include Parkinson's, cancer, and Alzheimer's. There are two key theories as to why age-related disease & decline occurs. But the key message is just because something evolves, it doesn't mean it's advantageous.
First of all is mutation accumulation (MA) theory. This theory basically suggests that as we age there is less likelihood that selection can remove the alleles that cause genetically determined aging. If we consider something like cancer, which is clearly deleterious it becomes clearer, though grey hair may be deleterious (reduces fitness) it is at least less obvious. If a cancer has early onset, affects people aged 10, then it is highly unlikely to spread through a population because those carrying the allele are unlikely to reproduce. If a cancer has late onset, causing cancer at 60 years old, then there is a much lesser chance it will affect reproductive success - most 60 year olds don't have more children in the future. In the case of MA the effect of selection is weak if a trait reduces survival post-reproduction. The same could be true of grey hair, even if it is costly it's arrival late in life is not that surprising.
The other theory is antagonistic pleiotropy (AP) which suggests that genes which improve fitness might reduce survival. For example, the genes that cause cancer at age 60 might also make you better at attracting mates, fertilising, and raising offspring. In this case it would be beneficial to carry the cancer gene (from an evolutionary perspective). I think there is some evidence (but can't find it right now) that grey hair is associated with higher fitness, in that case it could be that grey hair has evolved directly because of sexual selection (people might prefer silver haired partners) or because of AP - grey haired people are better at other fitness related things because of pleiotropy.
So to answer your question: direct selection is not necessarily the reason that grey hair has evolved, it could be because of mutation accumulation or pleiotropic gains associated with the genes affecting grey hair.
You can read more about these theories of aging in this answer and for references.

I do not think there is a reproductive advantage in gray hair - it's the other way around:
Normal colored hair has a reproductive advantage.
But it also has a cost in terms of substances needed to build it.
I make the assumption here that grey hair - which is often also more sparse - has a lower cost in terms of material.
I think we are investing the cost for the part of the live that is exposed to direct evolutionary reproductive pressure.
Later, we do not longer invest the cost.
That makes sense if we assume that hair becoming gray is a process of degradation.
It is not supported by an investment, but by the absence of an investment, following from absence of evolutionary pressure.

Can you elaborate how grey hair of same thickness "has a lower cost in terms of material"?

Oh yes, I notice I did not say that, I was thinking not of general mass, but of substances/elements that are scarce in the body, (and may be neede elsewhere). But as I wrote that is an assumption, not validated.

I think grey hair does have an evolutionary advantage related to Vit D. Vit D is crucial to life and severe deficiency may lead to death. The main source of this vitamin is the production in skin cells through exposure to UV light.
As you might know, humans who live in colder climates with limited sun exposure lost the pigmentation in their skin. This is to allow more UV rays to reach the deeper layers of skin to produce Vit D. Humans living in sunny areas had the opposite need as their skin pigmentation is protective against skin cancer, and it still allows enough UV rays to produce Vit D in sunny areas. This is why people with pigmented skin living in cold climates are recommended to take Vit D oral supplements, and why people with less pigmentation in hot climates are more vulnerable to skin cancer.
Grey hair allows more UV rays to reach the skin due to the lack of pigmentation in the hair. Humans in general need more Vit D as they age and start becoming vulnerable to osteoporosis and fractures. This explains why grey hair commonly starts at age 40-50 when the bones start to become increasingly weaker.

Welcome to Biology.SE. Could you add some references or additional evidence to your answer? I do not think this answer is correct; people at age 40-50 do not substantially (at least before recent times) contribute to the next generation and selection will thus have a hard time on such a phenotype (as has been mentioned in the comments) ...

Although I agree with the idea that a useful trait at old age has a weaker effect on natural selection, this weaker effect can't be entirely disregarded. Older people do contribute to improve the next generation's survival chances in many ways other than directly passing their genes. A parent who manages to survive till age 60 can support their offspring longer than a parent who dies at 40. The offspring of a parent who had them at age 38 and died age 50 have less chances of survival than if the same parent died at 70.

Please give (cp. AlexDelarge's comment) some reference: how does black, brown, red hair relate to the colour of white in respect of uvc or uva radiation.

My theroy is that gray hair allowed a predator to pick out the weak one in the group and focus on it as a possible food source allowing the younger ones to escape and survive.
Gray hair is also a signal to a potential mate that you might not be providing young healthy genes.
Both of these could have allowed our species of human to succeed over others.


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Do alternative start codons code for methionine after transcription?
There is some literature which shows that all start codons code for methionine. However, in the standard genetic code, the alternative start codons clearly code for leucine. Does that mean these codons will code for leucine when they are encountered during translation (after start codon has been initialised and translated).

Duplicate http://biology.stackexchange.com/questions/604/the-effect-of-the-start-codon-gtg-on-translation-in-e-coli also http://biology.stackexchange.com/questions/1629/how-are-there-alternative-initiation-codons?rq=1 It seems to be the case these codons are still recognised by fMet-tRNA in the context of a translational start. See also WP http://en.wikipedia.org/wiki/Start_codon

@AlanBoyd.. I always thought that it would be possible to map the translation start site only if the nascent polypeptide is captured. In many proteins the N-terminal is chopped off. Or otherwise stall the ribosome at translation initiation (by using lets say an analogue of $tRNA^{fMet}$ or $tRNA^{Met}_i$). Are you aware of any such studies?

Translation from the IRES can start from amino-acids other than methionine [Ref].

I commented that this was a duplicate, but reading the question more carefully you seem to be asking something slightly different.
In the context of a 'start' these codons will be recognised by fMet-tRNA and a formyl-methionine will be inserted as the first amino acid. Subsequent occurrences of the same codon within the open reading frame will be translated normally (e.g. GUG > valine).
The use of GTG as an initiation codon in the E. coli lacI gene
In this paper

Frottini et al. (2006) The Proteomics of N-terminal Methionine Cleavage. Molec. & Cell. Proteomics 5: 2336-2349

the authors report assays of E. coli methionine aminopeptidase with model peptides showing that when Lys is the 2nd residue, Met removal is very inefficient. They also show that when Pro is the 3rd residue, Met removal is very inefficient.
This explains the fact that when the lacI repressor protein was sequenced:

Beyreuther et al. (1973) The amino-acid sequence of lac repressor. PNAS 70: 3576-3580

it was found to have a Met residue at its N terminus (sequence Met-Lys-Pro-).
However, when the lacI gene was sequenced:

Farabaugh (1978) Sequence of the lacI gene. Nature 274: 765-769

the corresponding DNA sequence was GTG AAA CCA, demonstrating that the N-terminal residue is encoded by a GTG(Val) codon. LacI residue Val23 is encoded by a GTG codon, demonstrating the normal use of that codon in the body of the mRNA.

Thanks! Do you have any literature that explains this?


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Sansevieria species specification needed
What are the botanical differences between the species S. parva and S. senegambica? Please highlight the main ones.
I have 2 groups of plants. One with label "Sansevieria dooneri" (a synonym of S. parva) and one with label "Sansevieria senegambica" and sadly both groups look awfully the same at first sight.

You could use this key to the genus. The differences between both species should become obvious when tracing back the decision tree. It seems that they can be distinguished mainly by the leaf size/shape of adult plants.

Thank you! I've searched in BHL, but didn't found this key. It would be useful. :)

authors: Атанас Танев


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How do I interpret this graph regarding introduced genes and virus-infected cells?

This graph appeared in a practice test for the MCAT. I am trying to interpret it, but it confuses me a bit. On the x-axis we have some introduced genes, and on the y-axis we have % of cells infected. What I don't get is what the top part represents. How do the "Culture cell genotypes" relate to the rest of the graph. I would also like to know what -/- and +/+ mean. By the way, information in the passage lists CatB and CatL as mammalian proteases, and their inhibitors reduce the infectivity of viruses with the EGP glycoprotein (found in Ebola virus).
Here are some questions based on the graph:
Based on the passage, does optimal VSV-EGP infection in vitro require CatB, CatL, or both?
Based on the passage, is CatL expression sufficient for VSV-EGP infection of the mouse cell lines presented in Figure 1?

For -/- and +/+ see this recent answer: http://biology.stackexchange.com/questions/20593/what-is-an-ihh-mouse/20594#20594

Plus and minus describe what is happening in a specific locus in the genome. When a + sign is shown, the locus contains the natural, fully working gene (wild type). When a - is shown, it means that by natural mutation or lab manipulation, cells lack that natural gene, or make a negligible amount of it, or make a broken variant etc.
These cells are diplod, meaning they have two homologous chromosomes. If +/+ is shown, both chromosomes carry, in that locus, a working gene. If -/- is shown, both copies are not working. If a cell is CatL -/-, both its natural copies of CatL are missing or defective, and the cell is unable to make the corresponding protein. The manipulation through which a naturally occurring +/+ is turned into a defective -/- is called a knock out.
The top part of your chart shows what is happening in the nucleus, on the chromosomes, at the actual places where normal cells store their CatL genes. You don't give much detail, but the bottom of the chart appears to show some manipulation away from the normal locus. There are ways to introduce more copies, to stick them into the nucleus, or even in chromosomes etc, but the main point about introducing DNA is that often it will not work as well as the natural thing.
Optimal infection means something close to the first column, about 25%. By skimming through the chart we are definitely seeing good infection in column 3. Also by comparison with the low levels, we could call acceptable the infection in column 8. The other columns are all clear failures to infect.
The second column is the simplest to interpret: knock out CatB alone, and the infection is gone. Thus, CatB is required for infection. The third column reinforces the same point: restore CatB and infection is back to normal.
The sixth column shows cells where CatL and CatB were knocked out, but then CatB was reintroduced. We know from column 3 that knocking out and restoring CatB should keep infectivity, but in column 6 infection is gone. The only difference between columns 3 and 6 is the knockout of CatL, and its consequence is lack of infection. Thus, CatL is also required for infection. You may say both CatL and CatB are required.
The other columns are control conditions which show that the experiment was well designed and yielded expected results, rather than gibberish. For example, column 5 show that if you knock out both, infection is gone. It would have been very concerning if it weren't gone. Etc.
Your second question is really one of logic: is CatL sufficient? We established that CatB is required, and so there is little CatL could do to supplant its absence. Therefore, logically, CatL should not be sufficient.
But we have a better proof, from the experiments. In column 4, those cells have their natural (endogenous) CatL, topped by some more CatL. But they are still not infected, beause they lack CatB. So CatL, even in larger-than-life amounts, cannot compensate the absence of CatB. CatL is not sufficient.


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Applying drugs to brain via scalp (transdermal)
Many medications are intended only for the brain, but are taken orally. Hence <10% finds its intended target, while the remaining >90% is at best wasted, and at worst causes unwanted side-effects.
Valproate is a classic example; it is medicated as an antiepileptic, but only a small fraction crosses the brain blood barrier to make it into the brain. Because of this, a large dose is required, and unwanted side-effects are common.
However, certain (small molecule?) drugs (e.g. Ibuprofen) can be applied transdermally.
For a drug intended for brain tissue that allows transdermal application, is there any sense in applying on the (preferably shaved) scalp?
Is this a known mechanism of administration? If so, does it have a name?
Is there any way of correctly scaling the dosage? For example, if experiment shows that 50% of substance X taken transdermally reaches the bloodstream, if it is administered to the scalp is there any way of figuring out how much ends up in the brain and how much ends up in the rest of the body?
Since this is a tricky and obscure question, may I also ask this: how to go about finding an answer to this? Where else can I ask?

If you wanted to deliver a drug directly to the brain, it might be doable with microdialysis, where a tube is inserted into the brain and chemicals can be added or removed for analysis. It's done fairly often for research in mice, but I've never heard of it being used for drug delivery. Here's a review article: http://www.ncbi.nlm.nih.gov/pubmed/19340812

The short answer is no, it will take forever for a drug to pass through skull bones.
The usual reason to apply drugs on skin is if you want them to act right there, on the skin. Acne creams fit here. You need less drugs, you get where it is needed sooner, and you have fewer off-target effects, when compared to taking them by mouth. The brain is not "right there", so this scenario does not apply.
The second reason is convenience. Some drugs cannot by taken by mouth, because they would be degraded by the stomach or guts. In most cases, the drug has to be given through painful, expensive injections. But if such a drug does pass through skin (usually when it is a fat-loving small molecule), you may get away with applying it on skin. Testosterone is one such drug. However, it usually doesn't matter whether the skin you are applying on is close of far from the target organ. The drug will be taken from the skin by blood, get to the heart through veins, and then spread to the whole body, eventually reaching the target. There is no reason to shave your head, since it will go through the same detour before reaching the desired destination.


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Why was disease transfer to the Americas one-way?
It is well known that the European colonists brought many infectious diseases to the Americas, and that these had a deadly effect on the native populations, because they had no immunity to them. Were there any local infectious diseases to which the colonists were not immune? I’ve never heard of such. I’m not aware that the colonists suffered any epidemics, or that they brought any new and unusual diseases back to Europe.
Why not? Is this merely an accident of history, that there were no infectious diseases in the Americas which did not already exist in Eurasia? Or is there some explanation?

I assume because if a disease is contracted and mutated at a certain rate, then the chances of it developing further into new strains in a large number of population is faster than lets say the few native colonies, hence if you stretch this through time you can see that even the simplest of viruses that people have build immunity to over say 100 years can be deadly to a few that might have never encountered the virus before. but thats just my guess.

http://history.stackexchange.com/questions/15036/did-syphilis-polio-hepatitis-and-encephalitis-come-to-general-world-from-the

Malaria killed a large number of English colonists, e.g., at Jamestown. That wasn't west-to-east transmission, but it was transmission from Native Americans to Europeans. Malaria is a tropical disease, so it wasn't going to be transmitted to England. More generally, the people who came across the Bering Land Bridge went through a kind of quarantine, so you'd expect a certain number of infectious organisms to die out.

@BenCrowell That malaria may have been carried by the slaves instead of being indigenous in the natives. http://en.wikipedia.org/wiki/History_of_malaria#Spread_to_the_Americas

In "Guns, Germs, and Steel" Jared Diamond includes quite a bit on this topic. His conclusion is that Europeans, and old world humans in general were much more exposed to their farm animals, often living in the same buildings. This allowed a much greater number of diseases to jump from animal to human, forcing us to development immunity against these pathogens.
The native americans never domesticated as many animals, and weren't exposed to as many pathogens. As a result the foreign pathogens could freely move through their populations.
So why did it only go one way? A lot more Europeans came to American than vice-versa, so there just wasn't as much opportunity for American pathogens to move to Europe. Additionally, the Europeans brought a lot of animals here, including cattle, horses, and pigs. These would have carried pathogens as well, again, very few American animals were taken to Europe.

I find this very hard to believe (though I know absolutely nothing about it so I am likely wrong). Surely at least the parasites were a problem for the colonists! We know there are all sorts of parasitic pathogens endemic to the Americas, none of which would be familiar to the European immune systems. Weren't they an issue?

I'm not an expert on parasitic diseases, but off the top of my head parasites just don't seem as contagious or as deadly as the viral or bacterial diseases of the time. Some parasitic diseases did slow European colonization of Africa, particularly malaria and sleeping sickness, but these weren't present in the Americas at the time. And the same conditions that exposed Europeans to more viruses and bacteria would have probably exposed them to many common parasites, possibly conferring at least some resistance to the parasites they encountered here.

@user137 - As a small extension of what you've written, I'd suggest pointing out that most Europeans who came over here and got sick probably died here rather than take the disease back to Europe.

Yeah, we don't remember how many people were killed by disease. Cities were so bad that deaths outpaced births until the 19th century, they relied on immigration to sustain themselves.

@Bobson I agree... but at some point in the next centuries, many americans DID visit Europe. Didn't they carry the American diseases?

There is at least one important exception - it is generally thought that syphilis came to Europe from the Americas.

But as far as we know it's the only exception. And the percent of Europeans killed by it was much smaller than the percent of Americans killed by European pathogens. And the 2011 paper that supports an American origin for syphilis analyzed skeletal evidence. I'd like to see PCR evidence for the bacteria in skeletons dating prior to 1492 on either side of the Atlantic, but 600 year old skeletons probably aren't the easiest to get treponema DNA from.

@user137: There's also direct genetic evidence from the bacteria itself the  that modern syphilis descends from a related South American disease.

@slebetman, thanks, that sounds like better evidence.

http://history.stackexchange.com/questions/15036/did-syphilis-polio-hepatitis-and-encephalitis-come-to-general-world-from-the @user137

@caseyr547 I read the article that question refers to, and tried to follow the sources for evidence of those diseases originating in the Americas, and couldn't find anything beyond those assertions. However, wikipedia claims that polio probably occurred in ancient Egypt and Rome, even if not in widespread epidemics. Viral hepatitis is caused by several different viruses, from different families of virus. Encephelitis is similar. Some of these may have originated in America, but probably not all. Part of the problem is that tracking old disease requires those diseases to have symptoms obvious

Comment too long... Obvious and unique enough for ancient physicians to recognize them, and for historians to recognize the description. Polio is kind of like that, with its paralysis. However, syphilis had symptoms similar to other diseases often described as leprosy before 1492. Hepatitis and encephelitis would be very difficult to distinguish from other illnesses, so it would be hard to rule out their presence in Europe before 1492.

@user137 : this paper presents interesting phylogenetics for Treponematoses which suggests the most recent ancestor of venereal syphilis was a central American variety of Yaws (caused by a very similar organism). http://www.plosntds.org/article/info:doi/10.1371/journal.pntd.0000148

I want to point something important out and that's why I make it a answer. It is not sufficient explanation (maybe I'm misunderstanding) user137's answer. Let me explain why. He says that not many Americans visited Europe, it was the other way around for a long time, and it's 100% true... but they DID visit Europe after the primary colonization, in the centuries after 1492, a lot of times. Traveling from America to Europe has obviously occurred.
So, at some point there should have been a similar effect to the one occurred in the colonization of Americas with the continents reversed.


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Subtypes of Acute myeloid leukemia
I am a computer scientist with no biological background and working on analyzing lab  results of patients with Acute myeloid leukemia. They have been tagged with following subtypes of AML:

AML with No maturation
AML with granulocytic differentiation
AML with monocytic  differentitaion.

I know there are two classifications for AML subtypes: FAB(M0-M7) and WHO. I think these patients have been classified using FAB, but their corresponding subtypes' names do not match in any of the names associated with M0-M7:  http://www.cancer.org/cancer/leukemia-acutemyeloidaml/detailedguide/leukemia-acute-myeloid-myelogenous-classified.
I checked a lot of literature but still not sure about the class of the last two tags in FAB classification. Could someone please help me with that?

"AML with No maturation"  is M1?
"AML with granulocytic differentiation" is M2 (or M4, M5) ?
"AML with monocytic  differentiation" is M4 or M5 or both ?


text:
How to measure the total number of cells in an average human body?
I have got one assignment to calculate the approximate sum total of all cells in the human body. How to tackle this problem? I know that the current statistics is $10^{13}$ cells. I wanted some hints.

@kmm Actually I don't know where to start.

yes I calculated it by dividing the volumes. Volume of average human body / avg. volume of a mammalian cell. Around 10^14 cells.

So that's larger by only one order of magnitude. Not that bad for a rough approximation.

This is a classic Fermi estimation problem. The usual approach is to estimate the volume of a body, estimate the volume of a cell, and divide one by the other, remembering of course to have both volumes in the same units.
My quick attempt gave 1013 to the nearest order of magnitude.


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How much are phase-contrast and dark-field microscopy used in biological research?
How much are phase-contrast and dark-field microscopy used in biological research today? It seems these were invented a long time ago, so I am thinking would it be a good idea to learn these techniques. (I will start an undergraduate program in biology next spring.. but I am still mostly interest how much the researchers use these technologies: if little, I should use my time better)

both are primarily used in cell culture work such as cell assessment and imaging. I have posted an answer to a similar question here (http://biology.stackexchange.com/questions/5470/what-to-look-for-when-buying-a-light-microscope/17313#17313)

I use phase contrast very often, as it is only a matter of switching a lens group from bright field. Instead of spending hours with staining, or, worse, immunostaining, I get the big picture (cell diameter) in a few seconds. I can even go back to the same cells next day. Switching to dark-field is also a matter of turning a dial or pushing a switch.
If you already use brightfield, there is not much to learn about them in terms of actually useful physics, or sample preparation. The things you could learn - say, that colors are altered in darkfield - will rarely be needed in practice. These methods are the sort of things you don't really need to know in depth unless your experiments require them. Even then, practice and elbow grease would be more helpful than advanced optics. Remember that in most cases, the scientific hypothesis is more important than the tools you can use to solve it.

If you're planning on doing any kind of cell biology work (and if you're going into biology, it is almost certain you will at some point), learning how to use a microscope is a must. You will use a scope frequently when growing cells to analyze their morphology, count them, look for signs of contamination, visualize differentiation, etc. Microscopes are also used when performing immunofluorescence and immunohistochemistry staining protocols.
So, even though the instruments and some of the techniques have been around for quite a while, they are still very relevant today.


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How much does a typical biologist know about signal processing, machine learning, and (theoretical) computer science?
How much does a typical biologist know about signal processing, machine learning, and (theoretical) computer science?
Coming from a neuroscience background where knowing about algorithms and computer science is a must, it seems to me that in biology there is much less cross disciplinary work. Though, yes, there are bioinformatics (but you only do sequence alignment and clustering?).
Anyway, given a typical PhD student in biology, how much does he/she need to know about programming, signal processing, etc?

I think this question could improve if you added the reason why you're asking this (depending on which it may or may not have an actual answer). As it is, you're just requesting comments and the StackExchange Q&A format isn't really useful for that. Feel free to take this to chat of course: http://chat.stackexchange.com/

I don't know what a "typical" biologist is, but I'd guess they don't know much about computers, because the population in general is computer illiterate. In my department, we do have a lab that does a lot of computational work on proteins. And of course bioinformatics relies on computers.
I can see where programming would come in handy for an ecologist, and maybe hardware and electronics too. Lets say you want to track animals in the woods. Traditionally, you'd give them a radio collar, then you'd have to triangulate their position in the woods, and at the end of the day all you'd have is location data. You could use something like a Raspberry Pi or Arduino to create a device that has GPS, a camera, and cell phone antenna, which could record much more information about the animal's location and activity and send it back you without as much effort.
In our modern computerized age, knowing some programming is always a plus, no matter what field you're in. Finding ways to apply that skill aren't always easy. I know both Java and C++, but I've really only written a few programs that I've used in research, 1 to calculate number of possible peptides given a size and some amino acids that won't change, and one to calculate how much DNA to use in ligation reactions.

First I want to say that studying the dynamic of enzymatic reactions, studying the movement of the arm, studying the structure of the DNA, Using mathematical modeling (and individual-based simulation) in population genetics, studying the turnover of soil nutrients, and others, ... require cross-disciplinary. Cross.disciplinary knowledge in biology is not restricted to the intersection between computer science and Biology.

Then I guess/hope that if I give you an overview of my knowledge in computer science and how I acquired it, it may help you (in addition to other answers) to estimate the level in computer science of an average biologist.
From my Bachelor and Master
During my Bachelor and Master degrees I have learned about statistics (and statistics applied to genetic data) and learned to program in R for data analysis purposes. I have been involved in a project during my Master where I had to use Approximate Bayesian Computation.
Self-learning
I have learned by myself the basis of theoretical computer science (NP-hard, genetic algorithm, running time function (the Big O notation), …) but I still know very little. I also learned Python (and a bit of Java) and Object-oriented programming. I also learned HTML and CSS in order to construct my website. All I know about information theory and signal processing comes from a bunch of Khan academy lectures on the subject that I watched.

I agree that a "typical" biologist (if such thing really exists) is generally not skilled in CS nor, very scaringly, in statistics.
My experience is that most biologists think of these things as burdens that do not really interest them and only get to do some basic statistics (most biologists would sort of know what a t-test or an ANOVA is, although they most probably won't master the statistical theory behind it) before writing a paper, so that they can put the little stars on their graphs.
However, if you go into fields like neuroscience (which I count as biology, I am not sure why you seem to imply it is not) then you start meeting people who know quite a bit of CS. Generally you either have these hybrid mathematician/statistician/programmer/math-y guy/biologist or you have biologists working together with more CS people.
In my last lab, for instance, we used to have a physicist and a programmer to help out with biological data analysis.
Furthermore, if you're into imaging, then there may be a lot of programming needed  for 3D reconstruction, image segmentation, particle tracking, etc. etc. Although there is some fairly impressive off-the-shelf software out there for the most common tasks, as soon as you want something a bit more specific you're better off programming it yourself, or finding a collaboration with some computer scientists.
I would say that as a biologist it is important to understand these things, but not necessarily to be able to actually perform them, as you can rely on CS specialists/bioinformaticians to do that for you. However, it is very important for the biologist to understand what the bioinformatician does, and vice versa, as communication is obviously of great importance in these situations.

Without addressing the "typical biologist" aspect of your answer, I have some computer science background but mostly programming and little "theoretical."  In my initial Ph.D. program in the late '80s and early '90s, I took several programming classes in Pascal and C.  I wrote a fairly involved dBase program for a systematic research fish collection.  I haven't messed with these for a number of years but I've retained enough knowledge to write programs in R and dabble in Python. I've used these for various professional reasons, from research to teaching. I teach very basic R in my biogeography class so my students even get some exposure. I'm teaching myself Postgresql as time permits. I use LaTeX regularly, which isn't always programming but its draws from a similar mindset. Plus, I can read the LaTeX code when I want to learn how something works.
I have a colleague in my department who is very fluent in SAS programming but I don't know what other programming skills he might have. Yet another colleague took lots of computer science courses during his Ph.D. program. And yet another colleague, now departed to the administrative dark side, was very proficient in Perl and probably a few other scripting languages.  On the other hand, many of my colleagues use word processing and spreadsheet programs and that's about it.
Scientists are no different from other people. They go where their natural interests take them. For some of us "typical" biologists, that includes computers.

As much as they need to know, but rarely more.
I would say that the 'typical' biology undergrad is not so much of a tech freak and thus has not so much knowledge about programming and computer science in general. One might speculate that young people that feel attracted to these things tend to study math or physics rather than biology. Machine learning just isn't such a fundamental part of basic biology as it is to other scientific disciplines. This is by no means a as there are lots of other things to learn and understand before you can even apply computer-based solutions to biological problems. Many biologists will hardly need any programming skills ever.
However, as a PhD student you will need programming skills at least to some degree, let it be some R to do statistical analyses or some Python to automate workflows. And of course you will find really skilled programmers among biologists as well. As an ecologist, the first thing that comes to my mind are complex ecological models mostly written in C++.
To summarize, the pressure to be familiar with concepts of CS increases with the academical degree, and so does the proportion of proficient biologists.


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Does bioluminescence communcation occur on macroscopic level?
Some bacteria are known to communicate using bioluminescence (quorum sensing). Do we observe the same phenomena in any macroscopic species?

don't know about bacterial light speech, but fireflies find their mates that way; or is your question specifically about quorum sensing?

Almost certainly. In the deep-sea, some species of laternfishes (Myctophidae) show sexual dimorphism in their light organs. Males have large light organs. The females are much smaller. Here is a brief summary, based on an interview with Dr. John Sparks at the American Museum of Natural History.
Sparks is discussing his recent publication with colleagues (Davis et al. 2014) that suggests that bioluminescent communication may actually facilitate speciation in some deep-sea fishes.
There are probably more instances of communication using bioluminscence in deep-sea organims but, to my knowledge, the Davis et al. paper provides the best evidence so far.

Davis, M.P. et al. 2014. Species-specific bioluminescence facilitates speciation in the deep sea. Marine Biology 161: 1139-1148. (open access)

On land, Stoltz et al. 2003 has demonstrated that positive selection has acted on bioluminescent color in Jamaican click beetles. The male beetles use the flashing to attract females for mating. Some males emit yellow light while males in a separated area have orange light.

Stoltz, U. et al. 2003. Darwinian natural selection for orange bioluminescent color in a Jamaican click beetle. Proceedings of the National Academy of Sciences USA 100: 14955-14959.

Some species of fireflies (Lampyridae, Coleoptera) synchronize their light patterns during the mating procedure. link


text:
Rhizosphere vs. Endorhiza?
In relation to microbiology and the naming of the various areas of the plant as it relates to microbial inhabitance, I am confused as to the difference between the terms endorhiza and rhizosphere.
In this case I see rhizosphere referred simply to as the 'roots', but in this case I also see endorhiza explained simply as 'roots' also.
However in this case, I see a further explanation for endorhiza (which does make sense etymologically): 'internal root tissues'.
Does this mean endorhiza is be a sub-term for the area inside the roots, and the larger area of the rhizome in general represented by rhizosphere, and that is the difference?

Healthy plant growth depends on a microbial community that lives around and inside the roots of plants (Bais et al. 2001). Roots secrete from the roots a number of chemical compounds that influences the microbial community around but outside of the roots. The microbial community can include bacteria, fungi, and single-celled parasites, as well as larger organisms like insect larvae and even roots from other plants. Some chemicals attract certain organisms while other chemicals repel organisms. This community of organisms around the roots is called the rhizosphere (Walker et al. 2003). The paper by Walker (open access) describes some of the many types of symbiotic relationships that occur in the rhizosphere.
Endorhiza refers to the internal environment of the root system. The endorhiza contains another microbial community of bacteria and fungi (Backman and Sikora 2008). The organisms of this endorhizal community are collectively called endophytes. Like the rhizosphere, the organisms in the endorhiza are important symbiotic species that benefit the health of the plant.
Similar communities have been identified for other regions of the plant, such as the phyllosphere, the organisms that live on the leaves, stems and other plant parts above the ground (Backman and Sikora 2008).

Citations
Backman, P.A. and R.A. Sikora. 2008. Endophytes: An emerging tool for biological control. Biological Control 46: 1-3.
Bais, H.P. et al. 2001. Root specific metabolism: The biology and biochemistry of underground organs. In Vitro Cellular & Developmental Biology - Plant 37: 730-741.
Walker, T.S. et al. 2003. Root exudation and rhizosphere biology. Plant Physiology 132: 44-51.

The endorhiza is not the same as Endomycorrhiza. It's the space that AM (endomycorrhiza aka arbuscular mycorrhiza) occupies within the root cell.

Many thanks for the answer. Please add some references to complement your response.

The rhizosphere is the narrow region of soil that is directly influenced by root secretions and associated soil microorganisms (wiki)
And endorrhiza (also termed Endomycorrhiza, AMS or AM) is a special case of the mycorrhiza, a mutualistic relationship between fungi and plant roots, where the fungus cells are stored within the root and not on its surface.

authors: Алексей Незачем


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what is the modern, molecular explanation of independent assortment of alleles?
in case it isn't obvious i'll begin by stating that i'm a layman, trying to understand something about this subject from reading books. the books i've looked at so far give murky and confusing accounts of meiosis (example: a schaum's outline refers to chromosomes that are "identical, but not the same"), and they always seem to duck the questions i most want answered. what i'm reaching for right now is a coherent, schematic understanding of meiosis. i'm aware that the real world is messier than that, but there clearly is a simple schema that accounts for the most typical cases of meiosis in an approximative fashion. in particular, there must be some way of deriving the approximate correctness of mendelian independent assortment of alleles from the molecular process of recombination.
here's what i think i can make out so far: if two chromosomes x1...xn and y1...yn get paired together then some number of interstices (spaces between successive loci) get picked and each chromosome gets broken at each interstice. after crossover each of the two resulting chromosomes have x-segments alternating with y-segments. for example if only one interstice is picked, and it's between the k-th and (k+1)-th loci, then the chromosomes that are there after crossover are x[1]...x[k] y[k+1]...y[n] and y[1]...y[k] x[k+1]...x[n]. it also seems clear that all interstices are equally likely to get picked. have i got at least this much right? and if so, how many interstices get picked?
also, if anyone knows a book that might suit my needs i would obviously be glad to hear about it. thanks if you can help
peace
stm

Homologous recombination does not occur randomly at every locus and thus independent assortment really only holds for genes that are far apart or on different chromosomes.

Parts of your general idea are correct, others need some refinement. To skip ahead to the conclusion: I'm going to recommend that you read up about linkage disequilibrium. Everything else is background information that will hopefully help you understand why linkage disequilibrium is what I think you're looking for.
Background: Meiosis Basics
Firstly, in the bare principle, meiosis is quite simple. Let's consider meiosis in a human cell, i.e. the division of a primary spermatocyte (the only other example is division of primary oocytes). That's this one we're talking about: http://en.wikipedia.org/wiki/File:Figure_28_01_04.jpg In simple terms, the ready-to-develop primary spermatocyte contains 46 chromosomes, two (2n) each of chromosomes 1-22, an X and a Y chromosome. Two chromosomes of the same type (e.g. "chromosome 4") are called homologues. Homologues contain different versions (= alleles) of the same genes. During Meiosis I, homologues align in pairs, recombine, and then separate into two new cells (which are now 1n). The following Meiosis II is basically a mitosis, meaning that the two (identical apart from previous recombinations) chromatids of the chromosomes are separated and packaged into separate cells.
Recombination and Interstices
During the alignment of homologues in Meiosis I, the attraction between the two chromosomes depends on their homology - i.e. similarities in DNA sequences that end up being close to each other in this setting. This attraction is on the molecular level, so the tightly-condensed neighbouring DNA double-helices actually physically stick to each other because the polarities/charges across relatively large stretches of the molecules complement each other. I don't think how this exactly works is well understood yet, but what is clear is that homologues attract each other at this point because they contain mostly the same DNA sequence, apart from small differences (which make the different alleles).
How exactly recombination occurs at this point isn't entirely clear either on the molecular level (http://en.wikipedia.org/wiki/Homologous_recombination#In_eukaryotes). Just to get an idea of how it could work: while the two chromosomes are aligned, it's not difficult for them to actually tangle up and break, leaving the repair machinery with the potential to fuse the wrong chromosome ends together. The breaking and exchange might also be a programmed process with dedicated cell machinery (quite probably so I think personally).
In any case, not all locations are equally likely to recombine. It depends on levels of homology (i.e. "stickiness") between individual stretches of DNA and other unknown factors. Just in the same way, the number of break points in each chromosome isn't pre-determined.
Mendelian Inheritance
First of all, the concept of loci is arbitrary and has no molecular basis. A locus is simply "a place on a chromosome" and could refer to an individual base(-pair) or a whole stretch of DNA. The concept is however useful when talking about inheritance, as it illustrates the principle of linkage, or rather linkage disequlibrium.
As far as I am aware, it comes from a time before we began thinking in chromosomes. One could study whether there was linkage between two traits (or more generally loci), i.e. a higher-than-random chance to inherit the two together. We now know that linkage simply means that the two loci are on the same chromosome (for example, chromosome 6). Thus, if no linkage exists, the chance to inherit both loci together is no larger than expected by random Mendelian inheritance (which makes sense as there is no molecular mechanism that makes offspring e.g. more likely than 50/50 to inherit chromosome 6 and 19 together from the same parent). If linkage exists , the loci are on the same chromosome, and any case where the two are not inherited together must be caused by recombination.
The idea of linkage disequlibrium is that loci that are close to each other on a chromosome are more likely to remain together (and be inherited together) than far-apart loci. This is obviously due to the increased chance of a recombination event occurring between them with increased distance. This actually seems to be what you are looking for as a pointer for where to go next, so I recommend using your preferred internet search engine to learn more about that :)

some number of interstices (spaces between successive loci) get picked
  and each chromosome gets broken at each interstice.

That number is usually around 1.  It's not common to have a lot more than that per chromosome.

It also seems clear that all interstices are equally likely to get
  picked.

No, there certainly are "hot spots" that are more likely to be cross-over junctions than other sequences.


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Western Blot: Fischer ECL substrate 2:1 instead of 1:1?
i recently developed a b-actin-ab-incubated PVDF-WB-Membrane with the Thermo Scientific Pierce ECL Kit. According to the manufacterers orders i mixed Reagent 1 and Reagent 2 1:1. But unfortunately i got kind of "unbalanced" bands (on the right side of the picture). Then someone gave me the tip to try to mix the reagents 2:1. For this substrate i got the result on the left side which actually looks much better.
Has anyone of you had the same experience and can anyone explain to me why this is so?
Is it "legal" to do so, or does it alter somehow the results of my experiment?
Yours,
p1ssn3lk3

I have put some potential reasons for your observations, however it would be great if you expanded your question in terms of the the exact steps you followed.

Yeah you're right, i should add some more details :)!
So it's a beta-actin-antibody which is already coupled with HRP, i didn't use a second antibody. I incubated on a roller board overnight in the fridge. I washed 3 times with TBS-T afterwards and also after the first ECL reaction i washed 3 times (10mins each) with TBS-T.

when you did your second ECL, was it without any new Ab staining?

Thats it.. no new staining..

I think the problem is unequal ECL distribution and if you done immediate ECL second staining without washing the membrane thoroughly and waiting a while before second ECL. There is a chance that when you overlaid your film on the membrane, you didn't get a good contact. what is your exposure time? This can also be a one of results! to make sire of the difference, redo the experiment as I have discussed in the first paragraph of my response. p.s why do you use a single step staining? is that part of your project?

Well usually in an ECL kit, one of the reagents is the substrate and the other one is hydrogen peroxide, which activates the substrate for breakdown using the HRP on your secondary antibody (Ab) so I genuinely doubt what you are seeing is the result of ratio difference. In order to make that conclusion you need to run your samples twice (on two separate membranes) and do a 1:1 and 2:1 ECL and if you observed such a difference then you are on firmer grounds.
I suspect what has happened in the above experiment is that you have done a 1:1 (with 1Ab and 2Ab not distributed equally on the membrane) then after perhaps not a very thorough wash, you have done another 1Ab and 2Ab incubation using the a 2:1 mix. I suspect what has happened is that in your 1:1 the left hand side has not received the Ab mixtures very well and when you did the 2:1 since the right hand still Ab attached to it (if you didn't strip the membrane) so the left hand side was "forced" to get the Abs hence again the Ab mixture and ECL not equally bound. It is obvious since one image is opposite the other so its the Ab incubation step that has gone wrong. Otherwise if you have done the second ECL incubation mixture straight after the first and didn't do a wash step, the same can result if the membrane did not receive the initial ECL mixture equally since you can get a blocking effect by the old ECL mixture and perhaps what has happened is that the H2O2 or the substrate was present in excess in the second incubation step hence amplifying the signal in the sections of the membrane that did not receive the ECL mixture very well in the first place, relative to the rest of the membrane, which still has ECL liquid on it from the last experiment (again if you haven't washed the membrane well as ECL can be active for up to 24 hours in some kits but after a few hours the activity usually reduces but can still be observed)
What you need to do is after ECL, wash the membrane with TBST for a few minutes followed by TBS, leave the membrane in the sun to dry so that the Ab slowly denature (although that doesn't always happen specially with high affinity Abs such as anti-tubulin and actin). After at least 24 hours, strip the membrane from Ab and redo the Ab incubation. The best thing to do is to do all the incubation steps in a sealed bag then make sure the membrane receives the ECL mixture equally and do the visualisation. I would say however since the membrane is unequally "contaminated" with the Abs then the best thing to do is to redo the experimental run and re-run the gel. Its a pain but you need to get to the button of this!

U sun dry your blots? Really?

indeed! it helps reducing the signal from any previous Ab staining which uses the same secondary or even a different 2Ab sometimes, specially for anti-Tubulin!

Interesting stuff, I've always used BME but may try this sometime.

@buzrw after ECL wash with TBST first, then TBS and then just leave it on a filter paper to dry but then you need to go through methanol socking step etc once you need to re-use the membrane. If you found the response helpful would appreciate a vote. If you needed any further detail just leave a comment.

I had a similar problem. In my case, I realized that it is absolutely essential to wash the membrane in TBS without Tween (TBS, not TBST) before you use ECL. If you have any amount of soap (Tween) on your membrane it reacts in some way with ECL and each time you should be getting a different pattern of these stains. Washing the membrane in TBS and then incubating with ECL made a difference for me and fixed the problem.

Pierce (or Thermo Fisher now) recommends washing the blots with a buffer containing Tween. It also doesn'z list Tween as a problem in the trouble-shooting section of the manual. And I haven't seen problems with detergents in my blots with ECL. It was rather a problem of incomplete mixing or distribution.

Try rinsing the blot in TBS or PBS before treating. Shake it try and place on level dry surface. When I pour the a chemo reagent on there I just pour enough so the surface tension keeps the fluid on the paper not allowing it to run off.
Other possibilities I see could be in your transfer. The temp could not be uniform in the buffer


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Is mammalian vision processed as a sequence of frames?
I often read that people believe that human vision has an inherent frames-per-second rate (FPS) that causes stroboscopic effects - such as seeing the spokes of a rotating wheel apparently rotating at a different speed or appearing stationary when moving.
For example: in a Physics.SE answer to Can a “superhuman” move so fast that an average person cannot see them?

The human eye-brain visual refresh rate has an "effective frame rate" of around 30fps.
Have you never watched the rims of the wheel in a car next to yours? I can clearly recall many times watching as the wheels sped up how it appears to stand still then move backwards.

This surprises me as I would expect there is no synchronisation of neuron firing in the retina, that neuron firing rates would vary widely depending on light levels and that the brain has no need to process the continuous signals in fixed cycles or in cycles whose length is invariant.
I believe this question, or a good answer to it, would differ from What is the equivalent of shutter-speed in Human eye?
Is human vision in any way subject to a fixed frame rate of 30 FPS?

Short answer: no, there is no fixed frame rate or frame-based processing in mammalian vision.
Photons arriving at the photoreceptors at the back of the human retina interact with photo-sensitive pigments called opsins, and modulate their release of the neurotransmitter glutamate . The level of glutamate released from a photoreceptor then changes the membrane potential of the other neurons in the retina connected to the photoreceptor (bipolar cells, for instance). Signals are processed within the retina, then passed through retinal ganglion cells (RGCs), along the optic nerve, through sub-cortical structures and in to visual cortex.
This process occurs continuously, but all of the elements along the way have intrinsic time constants and other temporal constraints (number of photons required for opsin activation; recovery rate of the opsins in the photoreceptors; membrane time constants and refractory periods of neurons; synaptic delays; etc.). Persistence of vision (the effect underlying the perception of a movie as a continuous stream rather than a series of distinct frames) probably relies on the conjunction of many of these time constants.
Concretely, a flashed visual stimulus produces a response in (primate) visual cortex after around 30–50 ms (Maunsell and Gibson 1992). You can recognise and subsequently recall a lot of detail from a sequence of images flashed at around 100–150 ms per image [citation needed]. These are still not hard and fast definitions of the "speed" of vision.
Since we only learnt to produce movies as sequences of distinct frames, it's tempting to guesstimate the speed of human vision in those terms. Biology, as always, is more complicated.
As far as the "spinning rims" issue goes, there are many aspects of cortical and subcortical activity that tend towards oscillatory activity. In a system with an intrinsic frequency (for example, the neurons in the thalamocortical loop between LGN and primary visual cortex), providing an oscillatory stimulus can synchronise the system to the stimulus.
Many of the intrinsic time-constants I described above could result in a tendency to oscillate at some intrinsic frequency, and then be subject to phase locking due to a periodic stimulus close to that frequency.

While in human made cameras light sensor and any image processor are separate devices, in the living eye the first steps of image analysis begin in retina already as light sensing cells are part of the nervous system. The optic nerve carries pre-processed information and not the encoded original image to the brain. This pre-processed information is not segmented into frames.
The "image processing system" of the human vision would generalize a presented sequence of frames into logical continuous movement, even if the frame rate is as low as few FPS only. This does not mean the eye cannot see that is going on. Frame rates as high as 120 FPS are required to reach the inertia limits so that the flickering really cannot be seen.


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Deduce length order of 4 decapeptides based on the Ramachandran plot
I have stumbled upon the following past exam question:

4 decapeptides A, B, C, D, made only of glycine residues, have
  different conformations, and the phi and psi angles of individual
  peptides are indicated on the Ramachandran plot (unfortunately I
  cannot provide a specific plot). Order these peptides by decreasing
  length.

How should I solve this, what information useful in solving this problem can I deduce from the Ramachandran plot?

When φ = ψ = 180° the peptide is in the fully extended conformation i.e. it is the 'longest' it can be.
If it isn't possible to deduce a length order based on this information then I guess you will have to do some geometry to calculate the sums of the distances between the α C atoms using the known values for all of the bond angles - sounds laborious to me!
This site tabulates values of φ/ψ for typical structures (helix, sheet, turn) so it may be possible to decide if some of peptides are adopting these.

The Ramachandran plot describes secondary structure. If you see a lot of beta sheets in your plot you will have a more compact molecule than one which is wholly alpha helix. Gly can be almost anywhere in any quadrant. Look for residues with secondary structure to determine tertiary structure.


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Calories burn rate calculation — scientific studies
There are many online calculators for measuring walking/running/bicycling calories burn rate. They differ in input parameters like some might need my weight as well as height and some don't. Almost none take into account duration of the exercise (and this is crucial in my opinion).
So my question here is: Where are these formulas (used in these calculators) coming from? Any scientific studies perhaps? Are they reliable?
Also I would like to know what is the most accurate method available for measuring the burn rate (I'm only interested in the scientific part, not going to do this myself).

This might be off-topic on this hub, also asked here http://fitness.stackexchange.com/questions/18730/calories-burn-rate-calculation-scientific-studies

If you are measuring a rate (calories burnt per until time) why would the time matter - are you suggesting that  the rate varies over the period of exercise?

Small note: burning calories is a wrong terminology because (a) Calorie is a unit of energy (basically heat); burning calorie is like saying lifting kilograms (doesn't make sense unless you say how many kilograms) and (b) Nothing is burnt in the body.
As per the second law of thermodynamics amount of storage energy consumed $\geq$ amount of work done. Whether or not fat is used up is a different question altogether.

Disclaimer: Not my field but I'm doing my best.
We often measure the calories consumed indirectly by measuring the quantity of oxygen consumed. As we have a reserve of ATP(ATP is a molecule, a stock of ATP is some kind of battery of our body) in our body, at very short term the oxygen consumption is not necessarily perfectly correlated with energy use but at a longer term it works perfectly fine. Seek for further information on the Citric Acid Cycle to understand why the oxygen consumption is directly related to the energy created (which is itself at a long enough term directly related to energy use). If I am not mistaken a bunch of seconds should probably be a long enough term (time to consume all ATP at the start of an important effort) but I would appreciate if someone could give a reference for that.
For small animals we often put the animal in a chamber and calculate the energy consumption by measuring the volume of CO2 that they expire. For this purpose we have to measure the volume of CO2 at the entrance and at the exit (of the chamber) to measure the difference. For humans, we often put a mask on the face of the "cobaye". We allow him to breath normally without doing any effort for a while and then we ask him to run/bike/whatever on a home trainer.
I don't know much about such studies but it is important to 1) know the variance in energy consumption in the population for a typical exercice 2) understand that lab condition probably differ in various ways from person-to-person real life condition (no wind, no dust, stress of the experimentator, discomfort of the mask, ...).
As I have no idea concerning the variance in the population I cannot tell how representative are the summary values that we can find on many popular websites but I would tend to think that given the experimentation, these numbers has probably been fairly accurately measured.


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Main mechanism of the evolution of sexual dimorphism
Sexual dimorphism is very common and (normally) requires the evolution of sex-specific genetic variation/regulation so the genetic correlation between the sexes can be <1. Is there consensus as to how this type of variation predominantly spreads?
I can see it could evolve by drift and selection and I expect it is predominantly via selection (sexually antagonistic selection for different optimal genotypes)- We typically associate sex differences in traits with sex differences in selection (ecological, sexual selection...).

Sexual dimorphism evolves, as you suspect, via natural selection, specifically sexual selection (which I view as a form of natural selection).  Genetic drift, by definition, is random. Random changes of allele frequencies are extremely unlikely to lead to the consistent evolution of phenotypic differences between males and females.
Sexual selection on the other hand can lead to rapid evolution of secondary sexual characteristics (sexual dimorphism). If you consider natural selection in the broad sense, an organism's traits affect survivorship but do not guarantee reproduction. Individuals that live longer have an increased chance of reproducing more frequently but this does not mean the organism actually will reproduce more often than any other individual. In contrast, sexual selection acts directly on mating success. If a female chooses a male based on his secondary sexual characters, then that male will mate. His fitness (offspring produced) will be increased relative to males that are not chosen and do not mate. This can lead to runaway sexual selection for male traits and even speciation.
You are correct that sexual selection results from sexual conflict. Such conflict can arise because females invest considerable energy into relatively few eggs. Thus, it benefits her to be selective for her mates. If she chooses poorly, her fitness can be decreased quite a bit. On the other hand, males can produce copious quantities of sperm rapidly and with little energy cost. If a male wastes sperm on a genetically-poor female, his fitness is not really reduced. He can quickly mate with other females at little cost.
References
Any evolutionary text. They cover the basics of sexual selection in some detail.
Gavrilets, S. 2000. Rapid evolution of reproductive barriers driven by sexual conflict. Nature 403: 886-889.
Hosken, D.J. and P. Stockley. 2005. Sexual conflict. Current Biology 15: R535-R536.
Lande, R. 1981. Models of speciation by sexual selection on polygenic traits. Proceeedings of the National Academy of Sciences USA 78: 3721-3725.