text:
Is there a Lyme disease vaccine?
Each Spring, our local health unit begins its campaign of Lyme disease and tick-bite awareness. I was wondering if there has ever been a vaccine available, and if so, what antigen does it target?

According to Wikipedia in 1998 a vaccine was approved by the FDA. It was directed against the outer surface protein A (OspA) of B. burgdorferi, but was taken from the market in 2002 after a large number of recipients reported the development of autoimmune diseases. An investigation of the FDA and the CDC found no connection to these claims, but afterwards the sales went to the bottom until the vaccine was withdrawn from the market. An interesting article on this story (with a number of references) can be found here.
There are two new approaches to develop vaccine candidates. One is directed against the outer surface protein C ("An octavalent lyme disease vaccine induces antibodies that recognize all incorporated OspC type-specific sequences.", another against glycolipoproteins on the bacterias surface ("Synthesis of an experimental glycolipoprotein vaccine against Lyme disease."). As far as I see, none of these vaccine candidates is already licensed.
Another approach is to vaccinate the animal reservoir hosts, as this has been done successfully for rabies. Here either vaccinated baits ("Reservoir Targeted Vaccine for Lyme Borreliosis Induces a Yearlong, Neutralizing Antibody Response to OspA in White-Footed Mice") or recombinant vaccines ("An ecological approach to preventing human infection: Vaccinating wild mouse reservoirs intervenes in the Lyme disease cycle") were used with good results. Neither of these methods is already been used, as far as I see.


text:
Does the genetic material the sperm carries affect its physical properties
Basically, what I'm asking is, is the actual sperm cell built from the blueprint in the DNA of the man or is it itself also a consequence of the DNA it carries?
I'd like to know a few more things related to this. For example, which DNA is in the nucleus of a sperm? Is it the same as the DNA of other bodily cells in the man's body, or is it just the DNA it's delivering? Can the sperm's performance be affected by any specific genetic traits that can be observed in a potential human the sperm could make? For example, a sperm swims faster if it's carrying the genetic material that would result in a tall person (probably a silly question).
The original question I had is if the statement that female sperm live longer is true. If it turns out that the man's body makes all the sperm more or less the same and they're just boxes that can swim, then I would guess the answer is no.

Does not answer your question but is related: (inter-males) Sperm competition

Sperm Biology: An evolutionary perspective might help here - I'll take a look this week at work. There is also a group in my department looking at selection in the haploid/gametic phase so I'll chat to them.

I think there is a strong driving force for sperm to be free living haploid versions of human beings.  Since they are a product of meiosis sperm are the product of recombination of both the male chromosome sets.
While I'm sure that if we look closely enough, the germline cells that produce the sperm are contributing some protein and structure to the sperm, the life cycle of the sperm is mostly the result of the genome that it contains within itself.  Sperm are prone to defects.  On the average in human beings about half of sperm are non-motile: simply unable to form the flagellum or power its motion adequately for motility. That's a pretty strong selective force in the life of our other, 'half genome' selves.
Sperm selection - the sorting of which sperm from a single male achieves fertilization is pretty rigorous.  It can take 30 minutes to days.  Once in contact with the ovum, the sperm executes a critical set of transformations and biochemical activations to get past the various layers of the cell.
Sperm are from the man, but they are each living creatures on their own which we hope will deliver themselves up to the ovum to create another human being.  They vary in their genetic quality and effectiveness and this is highly related to their genetic make up.
Because each sperm is the product of two stages of Meiosis, they can be full of genetic defects, most of which would be fatal in a diploid human being.  The functions of the sperm as it goes through its short but competitive life weed out genetic abberations and help assure that the next generation of diploid human beings is as healthy as they can.
So they are not DNA boxes that swim.  I'd be hard pressed to think of a passive role for a cell in biology - they are all working pretty hard... I'd be interested in a comment with suggestions of something that is not under selective pressure in biology.
It sort of reminds me of the old argument about passive mating in females. Behavioral biologists used to think that female animals had little or no active role in mating.   That myth was retired about 30 years ago now.  That link points to an introduction to an entire volume reviewing that whole discussion of active female roles in reproduction in case anyone reading is interested.
BTW I'm not an expert on gametes, but I'd be surprised if the ova also didn't have a complimentary but quite different selective process they had to get through to become a fully presented candidate for fertilization.
Just to add a note about how the functioning sperm genes affect the diploid organism: This is one of the most important things that sperm does.  The genes that function in the living spermatazoan are the same genes the diploid organism uses, or at least a substantial number of them.  Further, these genes are scattered across all the chromosomes and so major chromosomal defects and important genes are functional if fertilization is completed.  As an example here's a cool blog post about how mosquito sperm have been shown to use odorant receptors to orient themselves in the fertilziation process. Those same receptors and the signalling genes that link that signal to the sperm behavior are probably quite useful to the adult mosquito.  I'd be surprised if human sperm also did not use similar pathways to function.
Not to beat a dead horse, but the recent nature has a report of small RNAs in mouse sperm as being an epigenetic carrier for stress.

Thanks for the answer. What's still confusing to me is the connection between a sperm not functioning properly and a potential human not functioning properly. For example, humans with mental retardation often have above average strength. Does that mean the sperm they used to be was defected or above average? It seems to me that there would have to be some defined standard of a normal DNA that the sperm would check against to determine how "broken" it is, and I doubt there's something like that.

Hey Darwin - I've added a note above.  you have to remember that a substantial of human genes are found in yeast.  Those core functions are absolutely necessary for viability. Our lives as single celled organisms use most of the same genes.  neat, eh?

Meiotic drive would be a cool example of a sperm cell's genotype affecting it's phenotype

@GriffinEvo are you thinking of selfishness, sometimes referred to as Drive?  If so you have brought up one of the most famous examples of sperm activity - a locus which causes a sperm that contains it to actually inhibit other sperm even if they come from the same male.  A classic example of sperm genes in action and evolutionary biology.

yes, SD in Drosophila and T-haplotype in mice are the two main examples if i remember correctly

That is indeed the classic example of active sperm selection isn't it? There are books about it now. @Darwin if you want you can search at bn.com/amazon for 'sperm competition'.  its a big world out there. As an equal opporunity presentation, here's a picture of a team of sperm using hooks on their heads to cooperate and swim together.  http://www.nature.com/news/2010/100120/full/news.2010.22.html

Apropos of nothing... giant fossil sperm longer than the male animal itself. http://www.nature.com/nature/journal/v509/n7501/full/509402c.html

Shigeta, you have some good points there.  I wanted to clarify some things.
Sperm and ova are considered tissues, not individual living creatures.  They are not individually capable of cell division nor production of offspring.  They are specialized cells with specific functions that are created by a multicellular organism as a means of transferring DNA.
The sperm carries 1/2 of a chromosome set from the male's own DNA, after cross-overs during meiosis (meaning that the DNA in a sperm has some different combinations than the parent DNA).
Metabolism primarily occurs at the mitochondria.  Protein synthesis does occur in the sperm, using nucleus-encoded mRNA.  What I was unable to find an answer to was whether this mRNA was transcribed from the nucleus of that same sperm, or whether it was from the primary spermatocyte DNA (diploid) or from the sperm nucleus (haploid).  The chromatin in the sperm nucleus is several times more tightly wound than in a somatic cell, so I am not sure how it would be accessible to transcription, nor am I sure that the full set of enzymes required for transcription, modification, and translation is present in the spermatozoa.  I'll be very interested in hearing if anyone is able to find this information!

what does a sperm do besides reproduce?  The haploid phase of some animals like coral can be weeks long.  Yeast haploid genetics are a big topic in research and the halpoid phase can be maintained for quite a while.  Here's a reference for sperm mitochrodrial transcription. Sperm are not the main system for research of hapoid life cycle though http://humrep.oxfordjournals.org/content/22/6/1585.short

I really don't know who makes these decisions, but I'm not sure this is an unanimous opinion nor one that is necessary to hold in all circumstances.  you are of course free to have whatever opinion you like.

For example, a sperm swims faster if it's carrying the genetic
  material that would result in a tall person

and in the comments

It seems to me that there would have to be some defined standard of a
  normal DNA that the sperm would check against to determine how
  "broken" it is, and I doubt there's something like that

If some aspects of sperm cells indirectly connected with some parts of phenotype, so we can expect that result, but not because of sperm cell carries that noble phenotype gene.
DNA in sperm cell is packed and not expressing (not transcribed).
Because DNA is packed and because test checks consuming energy, which sperm needs for another tasks - pretty wise to shut down checks, repairs.
Also DNA is not like ZIP archive, where cell can check the check sum, to make shure it works witch good DNA. Cell have difficulties working with information, if it needs to connect information results from distance sources. (Let say as example: if gene A have mutation A* and gene B have mutation B* then do X).
Also there is big big difficulties with that mater: some defined standard of a normal DNA - all DNA that leads to organism which is able to procreate, to survive - is good enough for nature. Thats Evolution spirit). And who can, who not - will be sorted out, later and with 100% accuracy.

For example, humans with mental retardation often have above average strength.

Our DNA actually consists from imperfections, which showed up long ago and became standard de facto, some are compensated at the moment and are RFC(Request for Comments). This or another set of genes is a balanced system. Balance can be shifted and that will have some consequences, actually thats how another system is prepared for testing by Evolution factors. By shifting balance far enough, for making some things at extreme, we may expect that another things have to break. But strength is not because of mental retardation, or vice verse. (It may be connected, may be not; also I would not trow away, some ontogenesis matter in that case) They both are results, not cause. But there are some reasons to be connected, if you take look on apes behavior as example.

just boxes that can swim

Man it's a Rocket

source: Stack Exchange

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

sort: votes


text:
Where does the fate map of a human embryo end?
I'm confused about the fate map of a human embryo. Is it just a particular part of the embryo development or does it include everything, from the conception (germinal stage) to the day the baby is born?

Are you talking about projects like this: http://embryo.asu.edu/pages/fate-map?

@Chris Yes, but it doesn't give any information about the fate map of a human

Ok, I will answer this later today.

In the developing embryo you have the three germ layers: Endoderm, mesoderm and ectoderm. From these layers all cell lineages of the body develop and can be traced back through their differentiation and migration to this three layers.
Have a look on the image below, which illustrates this pretty nicely:

The figure is part of this PhD thesis, which also seems worth reading when you are interested in this topic.

Great figure!  The thesis (p20) cites the image as "adapted from Gilberts Developmental Biology, Fourth edition, Figure 9.1."

That is right. I don't have access to the Gilbert, so this should be ok.

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


text:
Most human-like teratoma ever recorded?
I'm curious to learn about the 'most human' teratoma ever recorded. By that I mean a teratoma which most resembles the form of a human being.
I suppose there are several factors which would contribute to this criteria:
-Most organs, and components found in a human (e.g. brain, teeth, organs, etc.)
-Most closely organized structurally like a developing human.
Also I was wondering. Given the right conditions could a teratoma grow into a living being? Could they theoretically develop the necessary organs to be excised from their host and sustain the functions necessary for survival.
Basically I am curious to learn about the possibility of teratoma maturing into a bonafide organism.

There's a 2003 paper published in the Journal of Korean Medical Science describing a case of a 'homunculus' within a teratoma: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3055135/
It contained some hair, brain tissues, cranial and other bones, but no internal organs.

Way cool. This is the best example I've seen thus far. Thanks for bringing it up.


text:
Roles of creatine and bilirubin in foetus circulation
I think they are not inputs from maternal placenta.
I think they are the results of foetus metabolism.
However, I do not understand it how and where exactly.
What are the roles of creatine and bilirubin in foetus circulation?

Creatine is an important energy source for body, especially for the muscles, so it is no wonder you can finde it there. I don't think it has a special role besides that. See the Wikipedia article for more information.
For bilirubin this is different, this substance is a breakdown product of the heme metabolism (basically hemoglobine). It is not water soluble and needs to be conjugated to a carrier protein (albumin). In this way it is transported to the liver, where the glucuronyltransferase conjugates it to glucuronic acid. This step makes the bilirubin water soluble and it can be excreted from the body.
Newborns have a higher bilirubin level, since their glucuronyltransferase activity is at about 0.1% of that of adults. This can lead to the typical newborn jaundice. For more details about bilirubin, see here.

Thank you for your clear answer! Creatine for energy, while bilirubin fro hemoglobin, in short.

Yep, thats the short form.


text:
Coalescent Theory - Probability for $k$ alleles that of one coalescence event occured $t+1$ generations ago
From this textbook
Under the wright-Fisher model of genetic drift and under the assumption that all alleles are neutral, the probability that $k$ alleles had $k$ distinct parent alleles the previous generation is
$$Pr(k) = \prod_{i=1}^{k-1}1-\frac{i}{2N} ≈ 1-\frac{{k \choose 2}}{2N} $$
The chance of two alleles not coalescing for $t$ generations is $\left(1-\frac{1}{2N}\right)^t$ , and the chance that they coalesce in the next generation is $\frac{1}{2N}$. Therefore, the probability that 2 alleles had a common ancestor t+1 generations ago is
$$\frac{1}{2N}\left(  1-\frac{1}{2N} \right)^t ≈ \frac{1}{2N}e^{\frac{-t}{2N}}$$
I understand up to this point!
The probability that the $k$ alleles do not coalesce for $t$ generations, and then one pair coalesce to give $k-1$ alleles at $t+1$ generations ago is as follows:
$$Pr(k)^t \left[ 1-Pr(k) \right] ≈ \frac{{k \choose 2}}{2N}exp\left[ -\frac{{k \choose 2}}{2N}t \right] $$
Can you help me to understand this last part? (both the left and right part of the equation)

Is this the exact text from the book? The left side seems to represent the probability for

"No coalescence in $k$ lines in $t$ generations (i.e. the $Pr(k)^t$ term), and at least one coalescence among those lines in generation $t+1$ (the $1-Pr(k)$ term)"

which is the same event as

"First coalescence event in $k$ lines is exactly in generation $t+1$".

The right hand side is derived analogous to the second equation, with $1-\frac{1}{2N}$ ("no coalescence in two lines") replaced by $1-\frac{k\choose2}{2N}$ (approximation for "no coalescence in $k$ lines):
$$
\begin{align}
Pr(k)^t \left[ 1-Pr(k) \right] &≈ \left( 1-\frac{k\choose2}{2N} \right)^t \left [1 - 1 +  \frac{k\choose2}{2N} \right] \\
&\approx \exp\left( - \frac{k\choose2}{2N} t \right) \frac{k\choose2}{2N}
\end{align}
$$
were is first approximation is due to your first calculation. The second one seems to use a first order Tailor approximation of $\exp(x)$:
$$
\exp(-xt) = exp(-x)^t \approx (1-x)^t
$$

+1 Ok, I got the idea. No, that is not exactly the same text than in the book. I summarized it. Thanks a lot for you answer. The answer would be perfect if you could just show that $$\frac{1}{2N}\left(  \prod_{i=1}^{k-1}1-\frac{i}{2N} \right)^t ≈ \frac{{k \choose 2}}{2N}exp\left[ -\frac{{k \choose 2}}{2N}t \right]$$

I extended my answer to show the equation. I have never seen this approximation of $\exp$ before...


text:
TCGA gene expression data are missing matched normal
I'm trying to use the TCGA data portal to get gene expression data for cancer tissues, but I'm not sure what "Tumor matched normal" means.
It is unclear to me if the values are already compared to a control (non cancerous) tissue or there is another sample which gives the healthy tissue values. Assuming it is the latter, I don't see these samples anywhere.
This is a screenshot of my filter
http://www.clipular.com/c/5452873408184320.png?k=rlA9jy3Kb2U47JT7GrXBTzdsln4
And here is a picture of the result (only TNs appear).

These values are not already normalised to normal tissue controls. That a tumour is marked as tumour with matched normal doesn't mean that all of the platforms used by the TCGA (Expression, CNV, protein and methylation) have normal tissues available - in most cases Tumours with Matched Normals are annotated thusly because mutation calling was performed using tumour vs normal comparisons.
If you are looking for normal tissue controls for your given platform type (RPPA in your screenshot) you will find them labelled NT or N. If you don't see any that are labelled with those descriptions it means normal tissue samples have not been processed using that platform.
The TCGA doesn't do loads of normal tissue analysis for anything other than mutation calling because the project is focused on classifying tumours into subgroups using unsupervised approaches, primarily, and therefore all comparisons that get heavily used are tumour vs tumour after allocation to subtypes.

The TCGA Project has been collecting primary tumors and matched normals per patient per cancer indication and has been exome (WXS) profiling those samples, and genome (WGS) profiling a subset of them. In those cases, the primary tumor is tissue collected from the primary tumor and the matched normal is usually a blood samples, but could be derived from a buccal swab or some other source. As you can imagine, it would make less sense in terms of expression to assay matched control that derives from another tissue type such as blood.
For the expression data, the majority of the data comes from RNA-Seq and array-based profiling of the primary tumor data, and in some cases where adjacent normal tissue was collected and submitted, the TCGA has also profiled those samples. These are probably what you are seeing with your TN filter, and generally why you are having trouble finding equivalent amounts of matched normals as compared to primary tumor samples for the expression projects.
Incidentally, the company I work for has recently launched a free genomics data portal for the research community called GeenPool Reference. As part of it, we have deposited all of the publicly available TCGA RNA-Seq. The data along with all the associated clinical metadata is readily available for navigating and data mining. You'll easily be able to figure out the quantity of samples, and their matched pairs. If you're interested, you can take a look at the data projects available in GenePool Reference here: http://www.stationxinc.com/reference-library
~Sandeep


text:
Development of vitreous humor
I have tried reading about development of vitreous humor but it is all very confusing. When does it first developed ? Does it renew itself ? Please provide reliable sources..

Look at this scheme -

As I stated before, vitreous is 99% water and is not an organ itself, thus the "replacement of vitreous" is actually = 99% water re-production and the only organ inside the eye which can perform this - ciliary body.
Consequently, if the vitreous was removed and replaced by gas or saline it will be replaced by aqueous which produced by ciliary body - this process takes 8 weeks to completely replace foreign substance as a gas by aqueous.


text:
Average face shape
I am doing face detection application where every face detected is inside a rectangle. The rectangle always contains some background behind the face and now I need to extract as much of the face as possible.
Also the method should be fast so I've decided to extract just some basic shape from the rectangle, like an inscribed circle. This circle unfortunately also doesn't fit so well. The best shape I've tried right now is ellipse:  (2*width of the rectangle)/3 x height.
So right now I am looking for some better ratio between the width and height of the face maybe the best would be if you could point me to some research papers.
Thank you.

According to an article in Vision Research Volume 50 issue 2 :

"The face’s vertical distance between the eyes and the mouth is approximately 36% of its length, and the horizontal distance between the eyes is approximately 46% of the face’s width."

The article can be found at:
http://www.sciencedirect.com/science/article/pii/S0042698909005045


text:
Can I force evolution in a group of cells by removing all the smaller cells?
I actually have algae growing in water in a container. I was thinking if it was possible to filter the water so that all the small cells will be filtered out and only the bigger ones will remain to reproduce cells that tend to be bigger.
Is that possible?
What type of filter should I use?

A formal showing of your 'selection pressure' might also require proof that your initial algae population consists of only 1 type of algae.

Wouldn't this actually be artificial selection?

@evamvid which is a form of evolution.

Short answer
Yes that would work in the condition that the trait you select for (size) is heritable.
Long answer
The kind of selection you would apply is called truncated selection because you fix a limit in size (depends on your filter) under which individuals do not survive and above which individuals survive and reproduce equally.
The response to selection ($R$) is given by the breeder's equation:
$R = h_N S$
, where $S$ is the selection you apply. In your case, $S$ is the difference between the mean size of the parent generations and the mean size of those you allow to reproduce in the parent generations. $h_N$ is the heritability (more info in additional info).
So, if you measure the mean size of your cells, filter them, measure their size again (or infer their size based on previous measurement and the size of you filter) and calculate the difference between the two measurements you get $S$. Then you let your filtered individuals to reproduce and you measure the size of their offspring which is $R$. By dividing $R$ by $S$ you get the heritability $h_N$. If you do not observe any difference in size between your two generations it means that the heritability is 0 ($\space h_N = 0\space$). Of course, you'll need a population that is composed of enough cells in order to have a good estimate.
Additional info
To be a bit more accurate $h_N$ is the heritability in the narrow sense. It represents the part of variance in the population that has to be accounted to additive genetic variance. The word additive genetic variance might seem obscure. In other words
$$h_N = \frac{V_{Ga}}{V_{P}} = \frac{V_{Ga}}{V_{G}+V_{E}} =  \frac{V_{Ga}}{V_{Ga} + V_{Gd}+V_{E}}$$
, where $V_{GA}$ is the additive genetic variance, $V_{GD}$ is the dominance genetic variance, $V_E$ is the variance due to environmental variance and $V_P$ is the total variance (phenotypic variance)
Hope that helps. Do not hesitate to ask further question if something is unclear or if I missed one of your point.
Edit
Filter
The filter you need should allow you to discriminate the cells based on their size. Therefore, it should be relatively accurate. It is common to classify the phytoplankton based on their size, see this. You should try different filters and see what filter allows a good discrimination.
EDIT
I assumed your cells were all of the same species. Is it the case? If you just sampled them from a lake and let them grow in a container then you very probably have various species. Therefore, you would select (based on their size) for species with your filter rather than selecting individuals within a species (based on their size again). It is kind of the same process anyway and the breeder's equation still holds.

thanks for the very helpful answer. can you tell me what filter i can use?

@SumitSingh See my updated answer.

I just saw your edit re single species after I had commented the question.  OP sounds like a fun science project, if it can be performed accurately!

I think one would not have a lot of success using a filter to do this, rather using a centrifugal gradient and comparing the fractions to a standard I think would be preferable. Nitrocellulose filters are made with precision but not very astounding accuracy which is the main reason they are commonly used at set sizes (like 0.2 and 0.4 microns) and not often in between. Good question though


text:
Book recommendations for evolutionary models
I was recently working on getting a statistical model of a DNA sequence. To do this I found that understanding evolution quantitatively seems to be quite important. I would really appreciate any book recommendations on the basics of evolution.
I come from an Electrical Engineering background and have a limited knowledge of evolution and biology.

You're looking for a introductory textbook that explain the principles of evolution, explain what is speciation and how it occurs, what is a gene, an allele, a locus, etc… explain stuff about phylogeny and so on. Or you want a book of population genetics (mathematical formulations of how an allele change in frequency in response to selection, to genetic drift. How does the population structure influence the probability of fixation of one allele etc..). Or something else more specific to bioinformatics.It's probably wiser to start with a book that gives an general introduction of evolution.

I was looking for something more quantitative. I did read Dawkins'  'The Selfish Gene', which was quite brilliant in my opinion.

Ok, so I think you might want to try one of the book given in the second paragraph of the answer of this other post

I actually wouldn't have recommended Dawkins as a first book on evolution. He has some interesting ideas, but he is also has very radical views away from what the mainstream science agrees on. You cannot undo it now, of course, but for future reference for other people who see this question, it's probably better to start with a more basic and conservative text. And if you later read Dawkins or a similar author, you then have the basis to recognize what part of his arguments is consistent with the widely recognized knowledge, and what part makes large philosophical leaps.

I agree that Dawkins has an idiosyncratic perspective, and I think he's very wrong about a lot of things, but for an entertaining book oriented to the general public, The Selfish Gene does a pretty good job of introducing a lot of real biological thought, some of it based on serious and still-influential work by George Williams, William Hamilton, John Maynard-Smith etc.  So I personally would not necessarily steer people away from TSG, but would recommend reading something else later and not taking Dawkins' view to be the last word.

You either want a introductory book in evolutionary biology or a book that offers mathematical models of evolutionary processes.
In my first class of evolutionary biology I had this textbook: Futuyama, Evolution I think it gives a good start to the field and offers a good overview of the difference subfields.
If you think you already know enough about the concepts selection, genetic drift, molecular evolution, etc… and you want a book that provides mathematical formulations of evolution, then you might want to have a look into the field of population genetics. On this post you'll find some book-recommendations
If you are particularly interested into molecular evolution, I'd suggest: Yang, Computational molecular evolution
Maybe you are particularly interested into the statistical methodology used in DNA annotation or in phylogeny. Then…. I don't know! It's not quite my field!

Thanks a lot. By evolutionary models, I meant mathematical formulations.

I really good intro to evolution book is The Evolution of Vertebrate Design by Leonard Radinski.
Also, for a more math based approach you could look into Narrow Roads of Gene Land. These are collected papers of W.D Hamilton.

I'd like to add a few books to to the above suggestions. The book by Sean Rice "Evolutionary Theory: Mathematical and Conceptual Foundations" covers a lot of ground, including allele-based models, quantitative genetics, Price's formalism, and MLS. If you're interested in social evolutionary models, I found R. McElreath and R. Boyd "Mathematical Models for Social Evolution" to be extremely accessible for those that don't have a solid math background. Another great book on social evolution is S. Frank's "Foundations of Social Evolution" but it is not as easy to follow as McElreath and Boyd's book.


text:
Why doesn't the avocado turn brown when it is kept with its seed?
Why doesn't the avocado turn brown when its kept with its seed?
What does the seed release that slows down the oxidation process?

This is actually only partly true: When you cut the avocado in half, only the part where the seed really sits stays green, while the surrounding cut area gets brown over time.
Avocados turn brown because of an enzyme called polyphenol oxidase, which oxidizes the green contents of the avocado upon contact with oxygen. The seed blocks the access to oxygen, thats why it helps here (but only where it makes close contact). See this and this links.
There are two ways of preventing the browning of cut avocados (besides avoiding oxygen contact): Use either lemon juice, which inhibits the enzyme (by chelating the metal ion from its active center) or keep it cooled to slow down the procession rate of the enzyme (which will only work for some time).

For some reason I was under the impression that lemon juice worked by lowering the pH to a sub-optimal level. What is it in lemon juice that is the chelating agent, I wonder?

It is the citric acid which has this property, see here.


text:
List of heritability estimates in humans?
Many people on this site ask questions that directly or indirectly have to do with heritability in human.
Do you know a list of estimates of heritability of various traits in humans? Or could you try to create such list?
That might be great to have various kind of traits, personality traits, life-history traits, morphological traits, …
I am not necessarily asking for GWA studies that inform about what genes explain the observed variance (although that would be really great) but just some estimates of heritability and eventually information about the method used (parent-offspring regression, twins, ...) and which population was studied.

Do you think about a list of traits (for example hair color) and genes associated to it?

@Chris I did not expect something as accurate as the results of a GWAs. I was just thinking about a list of values of heritability for a list of traits. If one wants to add the way it's been measure, on which population and if it is a GWAs, give more info about what genes and how many genes explain the variance then it is really really cool but I will accept the answer even if it is not that perfect!

You may consider consulting the H2DB database. The database is quite new, so the number of heritability estimates is not very high at the moment (currently 225 estimates for human, 838 estimates in total), but it's a start. The database is described in a paper by Kaminuma et al.(2)


text:
What is the main challenge in creating a chemical male contraceptive?
More than 50 years after hormonal contraception for women was invented, a contraceptive pill for males is still not available. With the obvious major biological differences in mind, why does it appear more difficult to create a chemical contraceptive for males? What are the main challenges that must be overcome to create a viable, reliable and marketable contraceptive pill for men?

You could try to target the production of semen. The problem here is that this needs to be reversible, otherwise you couldn't reproduce afterwards any more. In that way it is easier with women since you can trick the body into "believing" that it is already pregnant. This is something that obviously doesn't work in men :-)

see: http://www.newmalecontraception.org/nonhormonal-pills/  As a market, I think men have a tendency not to want to take chemicals contraceptives...

I'm not so sure about that. A study in Australia found that 75 % of the men asked would consider trying a hormonal contraceptive. https://www.mja.com.au/journal/2002/176/5/will-australian-men-use-male-hormonal-contraception-survey-postpartum-population

See also http://www.medscape.com/viewarticle/775627_7

@shigeta neither men nor women have any desire to take chemical contraceptives. I don't see why that would be truer for men than for women. The only difference is that women are expected to while men aren't.

While you may be right after some period of adjustment that male contraception may be adopted, there is the fact that men are not left carrying the baby, a fact of which some biology does take note of.  Men often complain about condoms for instance. If you look at the link I sent above there are reversable (nonchemical) male contraception available. If you ask 20 of your male friends how many of them have adopted?  Attitude reports like the ones you all link are not absolutely proof of your point, btw.

@chris some antipsychotic medications have shown significant attenuation of seamen volume

Well a nice hot bath really reduces sperm count... A couple of reasons you don't see male chemical contraceptives is that the female ones are very effective and fairly safe. Condoms are effective and protect against disease. Because of all this the drug companies probably think there would not be much demand. No demand, no recuperation of the high cost of R&D, clinical trials, licensing, marketing and production.

I recall some touring academics claiming that injected testosterone works as a male contraceptive. That has a few drawbacks, the major one being: are you seriously expecting men to do something? Also, related to your question, one can't take yet testosterone by mouth.

I am going to summarize a few reasons for both why contraception is "easier" for women, and for why it is "harder" for men. They are both biological and sociological.
Easier for women
The female cycle is more complicated
The female cycle leading to ovulation is regulated by several hormones that interact. As such, it is easier to disturb.

The system is so sensitive that even the slightest alteration in any of these factors can disrupt its fluidity and lead to anovulation

(Anovulation = a cycle where no ovulation occurs) Source: Anovulation: Background, Pathophysiology, Epidemiology
Even in young women, this occurs naturally.

Estimates of chronic anovulation rates range from 6-15% of women during the reproductive years

Female bodies l already have a "built-in mechanism for contraception
As ovulation needs to be suppressed during pregnancy, there is already a mechanism in place by which this can happen.
Women are more affected by pregnancy
Since women are more affected by pregnancy and childbirth, the risk they feel they have when they don't use contraception or use it incorrectly is larger.
Contraceptives for women have more than one use

More than half of pill users, 58%, rely on the method at least in part for purposes other than pregnancy prevention. Thirty-one percent use it for cramps or menstrual pain, 28% for menstrual regulation, 14% for acne, 4% for endometriosis, and 11% for other unspecified reasons.

Beyond Birth Control: The Overlooked Benefits of Oral Contraceptive Pills
Harder in men
It only takes one
While the saying "it only takes one sperm"  is probably an exaggeration, it carries a certain truth - you really need to shut down the production of sperm or the risk of a pregnancy is too high. Both the pill and the various IUD options have set a high bar for what's considered an acceptable risk.
Side effects and effectiveness
While hormonal contraception for women already has a multitude of side effects, often unrelated to the reproductive system, this is certainly not easier in men. The most prohibiting side effect encountered so far is impotence - not much use in taking birth control to have sex without risk of pregnancy when doing so leads to no sex at all.

Progestins have been used in multiple small studies of men for suppression of spermatogenesis and testosterone production. Progestins used alone result in significant side effects such as loss of libido and erectile dysfunction.

Update on Male Hormonal Contraception: Is the Vasectomy in Jeopardy?
(Decreased libido is also a side effect in female hormonal contraception, though. The reasons why it's seen as more acceptable there are probably sociological)
That review is a good overview on what has been tried until 2010. Many solutions failed because of side effects or because they didn't work well enough.
On testosterone:

Of note, this international study revealed that 91% of Asian and 60% of Caucasian patients became azoospermic, suggesting an ethnic difference in endocrine response

Testosterone proved to be rather good in other doses and combinations, but is not that easy to handle because it requires injections and can't be taken orally.

Testosterone alone has side effects, including acne and oily skin, mood changes, increased hemoglobin and hematocrit, weight gain, decrease in testicular volume, sleep apnea, gynecomastia and possible effects on cholesterol. There are no long-term data with testosterone use and normal men regarding prostate symptoms, growth or cancer. In an era of fear of using medications on relatively healthy individuals, acceptability of routine use may be a major concern, given recent data on medical treatment of menopause with estrogen/progestin therapy. In addition, anabolic steroids are a controlled substance and regulation of this industry is very strict at this time. Abuse of these drugs could easily become prevalent with its widespread use and availability for contraception.

On cryproterone acetate:

Doses ranging from 25 to 100 mg per day have suppressed spermatogenesis, but side effects have precluded subsequent studies.

And so on...
The market factor
A side effect of the contraceptive options for women being so well-accepted, women often feeling responsible for contraception and also using hormonal contraception anyway, for reasons unrelated to pregnancy, is that the market for male contraception is not that easy and pharmaceutical companies have been pulling away from it. Especially in light of the research difficulties.

Although Bayer, Wyeth and Organon were once active in research and development of a male method, all three discontinued their programs between 2005 and 2008 although the industry continues to actively pursue programs for hormonal contraception and hormonal-replacement therapy for women. In withdrawing support, company representatives cited corporate changes in direction and the perception that safety standards demanded by regulatory bodies would require such extensive evidence as to make further research financially infeasible

Current challenges in male contraceptive research
This is not to say that there really is no market. As you mentioned in the comments, at least in questionnaires, many men say they would use male hormonal contraception and many women say they would like their partners to use it. See, for example, Market size for male contraception (plus the following pages of that paper)
But you asked about the challenges ;-)
I think it's also interesting to note that the search for hormonal contraception started for both men and women. It's just that the "solution" was found for women first and then got popular really fast.


text:
Why does methylation not occur in viral DNA?
Why does methylation not occur in viral DNA? Can viral DNA undergo the process of methylation? If not then why does this process does not occur in viruses?

Are you mostly interested in bacteriophages ?

Contrary to the question title, viral DNA can be methylated.  See for example Bonvicini et al. 2012. (1) and Hoelzer et al. 2008 (2).
Hoelzer et al. give a review of the presence and role of cytosine methylation in DNA viruses of animals:

To understand the impact of cytosine methylation on the viral life
  cycle and the evolution of base composition, the particularities of
  each virus will need to be considered. Differences will inevitably
  exist between actively replicating viral DNA and that which is
  integrated into the host genome. The type of viral persistence will
  also be of importance. The integration of adeno- or polyomavirus DNA
  into the host genome is usually a terminal process since the viruses
  cannot liberate their genomes and are therefore no longer infectious.
  The evolutionary roles of methylation in these cases will likely
  differ from those seen in other viruses, such as Herpesviruses, which
  can liberate their genome after periods of latency. But differences
  may also exist between large and small viruses—with many larger
  viruses encoding their own replication machinery and additional
  proteins which modify host cell processes and immune responses. The
  susceptibility of the viral genome to methylation and immune
  recognition will also be affected by other factors, such as the
  location of replication within the cell and the specific intracellular
  trafficking route.

Viral DNA methylation has mostly been studied in large DNA virii, and the extent of methylation may be related to repression of viral replication. Bonvicini et al. writes that

Epigenetic mechanisms, and in particular the impact of cytosine
  methylation at CpG dinucleotides on the viral life cycle have been
  mainly studied for viruses that can establish latency and undergo
  reactivation, such as viruses in the Herpesviridae family, or for
  viruses that can integrate their genome into the host genome such as
  Retroviridae or Papillomaviridae. In general, a correlation has been
  found between the extent of CpG dinucleotides methylation of viral
  genomes and viral quiescence [24]. Scarce information is on the
  contrary available on the possible occurrence and role of methylation
  for actively replicating viruses

Methylation played different roles for different types of organisms throughout evolution. For bacteria, methylation protects against self-digestion of DNA by restriction enzymes. In eukaryotes, methylation assumes many different roles (e.g., mutation-rate regulator, gene expression regulator, chromatin structure regulator, etc.). Insects have very little methylation and it is not entirely clear what they use it for. Viruses don't encode for methyltransferases that modify DNA. However, when a virus integrates into a host genome that is methylated, the viral DNA usually assumes the methylation pattern of the integration locus.


text:
How is bacterial plasma membrane made?
Eukaryotes have ER which manufactures plasma membrane of cells. How is prokaryotic plasma membrane made ? What is the pathway and which enzymes are involved ?

The processes that occur at the ER membrane in eukaryotic cells take place directly at the bacterial plasma membrane. Phospholipids are synthesised and inserted at the plasma membrane, and there is a protein translocation apparatus for translocation of proteins into the periplasmic space and insertion of transmembrane proteins into the plasma membrane.

Thank you Alan. It would be nice if you could add some more detail.


text:
Do any nonhuman species have effective ebola immunity?
I've read that ebola is an effective killer in humans because it has the ability to interrupt dendritic cells from manufacturing proteins that cause the immune system to destroy the dendritic cells when they're infected. Do any other animal species have different kinds of dendritic cells that don't get thus interrupted by ebola?

Recently some cases have sprang up in some African countries.

While at least some other primates are suspectible to Ebola, pigs appear to be immune. From the WHO factsheet on Ebola (1):

Although non-human primates have been a source of infection for
  humans, they are not thought to be the reservoir but rather an
  accidental host like human beings. Since 1994, Ebola outbreaks from
  the EBOV and TAFV species have been observed in chimpanzees and
  gorillas.
RESTV has caused severe EVD outbreaks in macaque monkeys (Macaca
  fascicularis) farmed in Philippines and detected in monkeys imported
  into the USA in 1989, 1990 and 1996, and in monkeys imported to Italy
  from Philippines in 1992.
Since 2008, RESTV viruses have been detected during several outbreaks
  of a deadly disease in pigs in People’s Republic of China and
  Philippines. Asymptomatic infection in pigs has been reported and
  experimental inoculations have shown that RESTV cannot cause disease
  in pigs.


text:
Speed of effective lymphatic drainage?
Lymphatic drainage occurs from many portions of the body:
To venous angle:

head
axillary lymph nodes

hands
abdomen

legs (I think legs' drainage goes through abdomen)

The speed of the lymph drainage is different in each part of the body depending on the situation at hand.
Assume you have tense muscles in the hand (biceps and trieps).
The lymphatic drainage there can be lowered and be the limiting factor in the system.
I think lowered lymphatic drainage in one part of the body causes more lymph goes to other parts of the body.
What are the negative results of too high lymphatic drainage in an organ?
My intuition

edema
hypertrophy in some cases (excess of nutrients)
hypertension

Negative results of too slow lymphatic drainage are the prolonged intoxication times of

biological,
chemical and
physical factors.

I am trying to find any studies about the effective speed of lymphatic drainage.
I have an intuition that the lowest drainage of one section is the limiting factor in the whole system.
Is there any studies about how to quantify the speed of lymphatic drainage from one part of the body?
Heart pumps (blood) and sucks (lymph).
So probably some cardiovascular study relates the pumping to the lymphatic drainage.

I vaguely recall an old study looking at lymphatic flow in sheep, and the range being very heterogeneous (virtually no flow at the lower bound). I would agree that, in general, this is a very heterogeneous effect subject to many chemical (hydration, osmotic balance, blood pressure modifying drugs) and physical (cardiovascular tone, posture, activity level) factors.

Probably, this one: http://www.ncbi.nlm.nih.gov/pubmed/3444363 ?

Looks correct, Masi.

Do you know any research about the normal lymphatic drainage in different organs? What is too high level and what is too low? For instance.

I'm sorry I really don't remember.

Oh Masi, you and I share the same interests (pharmacology and  lymphatics) and I do enjoy your questions... very old school... I wondered the same question your asking leonardo myself and I ended up buying this book: http://www.sciencedirect.com/science/book/9780120425204... the cheapest way to buy it is on google play... I've only had the time to read certain parts, usually focusing on lymphatics, but I haven't even finished that... it's an old book from the mid 80s, and the information on lymphatics is often incomplete... but it's the best I know of...

@JasandPruski We need technical tools to evaluate the speed of lymphatic drainage that is to investigate the flows of liquid phases and energy transfers. This is a part of Soft Matter Physics where the leading books are 1) Hamley - Introduction to Soft Matter, 2) Intermolecular Surface Forces by Israelachvili, 3) Giant molecules - here, there and everywhere. Still, these books do not cover the topic fully only provide some tools. You have to do the computation and visualisation yourself. I am actually doing a course about this topic called "Soft Matter Physics" in Aalto University right now.

wow, I'm jealous! I'm looking at the programs in alto and it seems they're not too focused on biology more engineering, but in a way thats great, new methods for studying things hard to study. I appreciate the book recommendations on soft matter, I'll look into them and perhaps when I have the funds I'll purchase one. It seems like theres some overlap on soft matter and rheology (not that I know anything about that either)... the word "liquid crystal is great. Also it seems like it's a meeting point for studying physical properties of cell membranes and ECM/interstitium...very interesting. :)

Leonardo's answer:

Animal study on sheep - here.

where

[L]ymphatic flow in sheep, and
  the range being very heterogeneous (virtually no flow at the lower
  bound). I would agree that, in general, this is a very heterogeneous
  effect subject to many chemical (hydration, osmotic balance, blood
  pressure modifying drugs) and physical (cardiovascular tone, posture,
  activity level) factors.


text:
Effect of nerve pills and relationship to Shingles
Do nerve pills actually suppress the nervous system and how would that effect the Shingles virus which is known to activate under large amounts of stress?

Please be a bit more specific. What type/brand of "nerve pills" are you referring to?

Aren't all nerve pills made to calm your nerves but say Xanax to throw one out there.

I gather you are talking about anti-axiety drugs (anxiolytics). Benzodiazepines is one of the major groups of anxiolytics, and includes Xanax. Benzodiazepines are central nervous depressants, meaning that they reduce the activity of neurotransmitters in the brain. They do this by binding to the GABA-A receptor and enhancing the effect of the inhibitory neurotransmitter GABA when it binds to the same receptor. The binding of GABA to a GABA receptor on a neuron causes hyperpolarization of the neuron by ion flow through the cellular membrane and decreases the chance of an action potential. So yes, nerve pills act by supressing the nervous system.
As for your question about interaction with Shingles, I think that's considered off-topic under the personal medical questions policy.

What makes you decide that that is a personal medical question?  If suppression of the nervous system would affect shingles, its a valid question.  As shingles affects the nervous system, its a valid question.  Saying that its under the "personal" medical questions policy is a cop out. But good answer on the first part.

I'm not deciding that it is, just giving my opinion. Others may disagree, but in any case I'm not capable of answering that question.

@jody it's borderline, it's not strictly a medical question but if we answer it someone could use it as "medical advice" and end up doing something stupid. And saying someone is using it as a cop out is not a very good way of showing gratitude.


text:
Percentage of understood human DNA
I want to know what's the approximate percentage of understood human DNA, as in, which part does what. I'm not asking for details, just the amount.
Thank you.

I am not sure if this can be said. Understanding the human genome is a process still going on today. Additionally this field is moving rather fast.

You would need to define "understanding". This is not a book where we simply have to read the words. Each "word" can have multiple different functions and we can't say with complete certainty that we understand any of them 100%. We have a pretty good idea about a relatively large part of it but understand is a loaded word.

Thank you. So if I understand this, DNA is being deciphered. But, we still can't say for certain that we know what each part exactly mean. Is that correct?

The devil is in the details, and therefore we cannot just state that we have understood X% of the DNA. We know e.g. that 2% of the human DNA encode proteins. And for a good number of proteins we know what they do. So you might know that a particular codon AGT encodes a serine residue in a protein, which could have a catalytic activity. Or it has a structural activity. Or we are not sure what it does. Sometimes protein-coding and regulatory sequences overlap. So even if we first understood the protein-coding function, there was still the regulatory function to be discovered.
The upshot is that there are multiple levels of understanding, and big controversies of what they actually imply (see e.g. the ENCODE saga).

Okay, I didn't understand your example but I got what you meant by it. Your answer was satisfactory. Thank you. You also gave me something interesting to read about.


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

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

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

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


text:
How can CI repressor both activate and repress $P_{RM}$ promoter found in $\lambda$ phage?
I'm reading a paper where the authors constructed a toggle switch that uses bidirectional $P_R/P_{RM}$ promoter found in the $\lambda$ phage. There are 3 binding sites - $O_{R1}$, $O_{R2}$, $O_{R3}$ - located between the two promoters. CI is expressed by $P_{RM}$ and CI dimers bind to these binding sites:

What I don't get is that CI seems to function as both an activator and a repressor of $P_{RM}$.
First, my understanding was that $P_{RM}$ is an inducible promoter activated by CI which also represses a constitutive promoter $P_R$:

CI is a transcriptional activator of $P_{RM}$, thus producing positive feedback.
CI preferentially binds to $O_{R1}$ and $O_{R2}$, repressing the constitutive promoter, $P_R$.

However, it is also stated:

In high concentrations, CI binds to $O_{R3}$ and acts as a repressor to $P_{RM}$.

This seems to suggest that the CI can function either as an activator or as a repressor depending on the binding site bound; specifically, CI dimer binding to $O_{R1}$ and $O_{R2}$ will repress $P_R$ and at the same time activate $P_{RM}$, while CI dimer binding to $O_{R3}$ will repress $P_{RM}$. Is this correct?
I (a computer scientist by training) was always given the impression that a transcription factor is either inherently a repressor or an activator of a promoter, but this doesn't seem to be the case here. I would expect that e.g. CI would act as a repressor to $P_R$ and an activator to $P_{RM}$ regardless of the binding site. So why does CI binding to $O_{R2}$ (and $O_{R1}$ as well?) activate $P_{RM}$, while binding to $O_{R3}$ represses it - why the inconsistency? Note that I'm primarily interested in this from the modeling perspective.
What I also don't understand is whether or not $P_{RM}$ promoter is inducible or constitutive (e.g. in the absence of bound transcription factors, how leaky is it)?

many DNA binding proteins have more than one role... ;)

There's no rule that says a transcription factor must be either a repressor or an activator. The lambda repressor (CI) is in fact a repressor and activator of transcription, depending on where it is bound and to what promoter you are referring to. I know your question isn't directly about lambda phage, but I think this mechanism may be best explained in the context of where it was first invented: nature. So, I will try to briefly explain how the lambda repressor's dual role allows regulation of its own expression and controls lysogenic induction.
The cI gene is under the control of the PRM promoter. The PRM promoter is weak because the sigma factor of RNA polymerase (RNAP) holoenzyme has low affinity for it. Binding of RNAP to PRM, and thus transcription from there, at a reasonable level requires an activator. There is another protein involved in this process as well, called Cro, that can also bind the OR operators. The cro gene is under the control of the PR promoter. PRM is not a constitutive promoter because it requires an activator. I have heard PR called constitutive because it is a strong promoter and can bind RNAP without an activator. But, at the same time, it is under the control of the lambda repressor. I suppose it depends on which definition of 'constitutive promoter' you use.
The OR operators are not identical and thus CI and Cro bind them with different affinities: CI has the highest affinity for OR1, followed distantly by OR2 and OR3, while Cro binds OR3 with highest affinity. Binding (of any two molecules) is dependent on both their affinity to each other as well as their effective concentration. At lower concentrations, CI can only bind OR1 and OR2 cooperatively. That is, each lambda repressor dimer binds to another, forming a tetramer, with one half binding OR1 and the other binding OR2. Binding both operators as tetramer allows for a stronger interaction. At higher concentrations, CI can bind OR3. Furthermore, OR1 and OR2 are located in the PR promoter, while OR3 is located in the PRM promoter.*
Most lambda genes are under the control, directly or indirectly, of the PR and PL promoters (PL is similar to PR, but the promoter itself is not directly involved in cI regulation). When lambda exists as a prophage, its DNA is integrated into the host genome and most of its gene expression is repressed. This requires CI repression of PL and PR. When the viral DNA is first integrated, there is no CI in the cell (because it is a phage gene). Expression of cI is initially dependent on a different promoter (PRE), but I won't get into this here. Once CI concentration is high enough, it can bind to OR1 and OR2 as a tetramer. Binding here physically blocks the PR promoter and prevents expression of cro (CI acts as a repressor of PR here). It also interacts with RNAP (actually the sigma factor) and facilitates is binding to the PRM promoter, which leads to further cI expression. This process is commonly called recruitment: since CI is bound tightly to the DNA and has some affinity for RNAP, it can create a stronger interaction between the DNA and the RNAP-CI complex. Simply put, it induces the PRM promoter and is thus functioning as an activator of cI transcription. As CI concentration increases, it will bind OR3 more (which is located in the PRM promoter) and repress the PRM promoter by physically blocking RNAP from binding. In these ways, cI can autoregulate its expression level, both positively and negatively.
When the lysogen is in some kind of stressful condition, normal host processes will result in proteolysis of CI and its DNA/sigma binding domain is cleaved from the dimer- and tetramerization domains. This means that CI can no longer oligomerize and is no longer able to bind cooperatively to OR1 and OR2. The result is loss of PRM activation (leading to vastly reduced cI expression) and also a loss of PR repression (leading to cro expression). Cro can then bind OR3 and represses PRM. Lack of PR repression also allows expression of early phage genes (which are under the control of PR).
Note that a similar situation occurs at the PL promoter region, and binding of CI to both OR and OL as well as CI octomerization is important in prophage regulation, but that seems even further out of the scope of your question. Hopefully you can see how he lambda "repressor" actually functions as both a repressor and activator of transcription. If this kind of stuff interests you, I highly recommend a textbook called Molecular Biology of the Gene by Watson et al.
*See comments. Upon further research, the PRM and PR promoters both overlap OR2 (Autoregulation and Function of a Repressor in Bacteriophage Lambda, Ptashne et al.), as the diagram in the OP shows. It appears that the -35 region of both PRM and PR overlap OR2 by 2 and 3 base pairs, respectively. That led me to wonder that if CI binds to OR2, which is in PRM, wouldn't it physically inhibit RNAP binding and thus repress transcription? Well it appears that CI interacts with the same region of sigma that is responsible for binding the -35 region of PRM (Amino acid substitutions in the -35 recognition motif of sigma 70 that result in defects in phage lambda repressor-stimulated transcription, Kuldell and Hochschild). So instead of blocking sigma binding here, it enhances it.

I wish I could accept both answers, and upvote answers like this more than once. I'm accepting this one for its very clear description of the process, particularly the physical blocking of PR and CI interacting with the sigma factor. The only thing I'm confused about is that the paper I linked shows OR2 as located (?) or - rather - shared by both the PR and the PRM promoter (judging by the picture), while you wrote "OR1 and OR2 are located in the PR promoter, while OR3 is located in the PRM promoter".

The schematic I was looking at showed it that way, but perhaps I shouldn't have said it so definitively given the contradiction. Upon further research, you were right and I have updated the answer to reflect this. Thanks for pointing it out!

I'm tempted to say, "It's complicated."
CI does indeed act as both a repressor and activator. Transcription regulation in the lambda bacteriophage is quite complex for such a small system, so some confusion is understandable. Lewis et al. gives a rough description in a relatively recent paper (1):

The CI protein autoregulates its synthesis. At low cellular CI concentration, CI enhances its own synthesis from PRM; when high, CI
  represses PRM (1, 8, 9). It was originally believed that both positive
  and negative autoregulations are achieved exclusively by the action of
  CI dimers at the PRM-OR-PR sequence of the phage genome (1, 10) (Fig.
  1A), based on the following observations. (i) There is a hierarchy of
  intrinsic binding affinities of a CI dimer to individual operators
  sites: OR1 > OR2 > OR3 (11–17); (ii) CI bound to the intrinsically
  weak OR2 site is strengthened by cooperative interactions with CI
  bound to the stronger adjacent OR1 site, and the ensemble of two CI
  dimers at the OR1 ∼ OR2 sites represses PR and activates PRM (13, 16)
  (Fig. 1A); (iii) at high CI concentrations, a CI dimer can bind to the
  weakest operator site, OR3, repressing PRM (1, 2) (Fig. 1C).
  Incidentally, a second pair of CI dimers binds cooperatively to OL1 ∼
  OL2, and represses PL (7).

CI binding affects transcription of Lambda phage DNA through several mechanisms, including DNA looping between the OR operator sites at the Prm/Pr promoters and OL operator sites at the Pl promoter. The behaviour of an engineered transcription system derived from Lambda phage thus depends on whether the possibility of DNA looping between these sites are retained.
The discussion section gives addditional exposition:

Our study confirmed several predictions of previous investigators
  discussed above about the mechanism of autoactivation and
  autorepression of PRM by measuring in vitro transcription on
  supercoiled DNA templates containing different combinations of
  operator mutations. Our transcription data support the model that
  autoactivation requires CI binding to OR2, and that activation is
  stimulated by cooperative dimer–dimer and tetramer– tetramer
  interactions between CI molecules at OR2 and those bound to other
  operator subsites. First, cooperative interactions of CI not only
  occur between OR1 and OR2 in cis, as reported previously, but also
  between OR1 ∼ OR2 and OL1 ∼ OL2 in trans, resulting in individual site
  occupancies at lower CI concentrations as judged by their effects on
  PRM activation. The trans-cooperativity by octamer formation requires
  adjacent CI binding sites between OR1 ∼ OR2∕OL1 ∼ OL2 or OR1 ∼ OR2∕OL2
  ∼ OL3 and not OR1 ∼ OR2 and OL1 ∼ OL3 (Fig. S3 F and J). Similar
  trans-cooperativity between OR3 and OL3 is inferred from PRM
  repression at lower CI concentrations. Cooperative interactions lead
  to DNA looping when they occur between CI at OL and OR sites. PRM is
  autorepressed by the binding of CI to OR3 as reported previously
  (1–3), and this is stimulated by dimer–dimer and tetramer–tetramer
  interactions that occur through DNA looping. Our results are in
  agreement with Revet et al. (18) that looping per se strengthens the
  binding of CI to the suboperators (Fig. 5). Our work provided
  quantitative evaluation of the contribution of each operator to
  autoregulation.

Phew!
If you wish to accurately model the system described by Huang et al., I would look very closely at the circuit sequence and determine which parts of the lambda phage system are actually present. They may not have taken into account the latest knowledge about regulation of the Pr and Prm promoters when discussing their system.
On to the second question: When isolated and with no CI present, the Prm promoter may be used as a constitutive promoter (2). Under such conditions, the Prm promoter showed similar rates of transcription as the constitutive promoter ptet.

Great answer! Just one more thing: if the Prm promoter can be used as a constitutive promoter, why would it require CI for activation in the first place? Is the constitutive expression level too low without activation?

CI is just one component in the "gene circuit" that determines the lifecycle transitions in the Lamba phage. Expression from the different promoters need to be regulated for the circuit to operate properly, and if the promoter was "always on", it couldn't perform its function in that circuit. Consider an analogy to a computer: Transistors work by turning electrical current on and off, corresponding to 1s and 0s. You can't do any computing with constant current, and likewise a constitutive promoter is not very useful for creating a "genetic circuit".


text:
In an open circulatory system, how is blood moved?
In the mollusks section, the powerpoint mentioned that gastropods and bivalves have an open circulatory system. According to the note, this means that the blood does not travel in vessels. How, then, does blood move? Does that mean that these organisms are simple enough to be able to survive by just pumping blood straight out into the body?
How does this type of circulatory system work?
Thanks!
evamvid

In a closed circulatory system, all of the blood stays within blood vessels or the heart itself.
Organisms that have open circulatory systems, such as arthropods, have hemolymph (a fluid that is essentially a mixture of blood and interstitial fluid). The hemolymph actually does travel in vessels for a very short amount of time, as it is leaving the heart. After this, it goes to the body cavities of the animal and directly bathes the tissues in the fluid in order to deliver oxygen, nutrients, etc.
Hemolymph moves throughout the body when the animal moves. Also, when the heart relaxes, hemolymph is drawn back toward the heart through ostia, or open-ended pores.
So to answer your question, yes, these animals can survive just by pumping hemolymph straight into the body. This is only effective because their body cavities are very small. In humans, an open circulatory system would never work because it would require an enormous amount of work to pump and circulate blood throughout our entire body cavity.


text:
Could someone Identify this Insect Hive on my Balcony Grill
A smallish insect hive has been forming on the grill of my balcony in the last month or two, and I wanted to know should I be worried or can I just let it be. Its 13th floor in Singapore, if the height helps in ID. So far they have not been very aggressive, and have not bothered us even if we get within few feet of it, but want to know if that can change in horror movie style..
You can find the pictures below, both are pretty much the same, but with some flash tweaking. For a size estimate, they appear to be between half and 1 cm long, and the distance between the bars of the grill is about 12 cm or so. Are they some kind of bees? Would they leave eventually or is this a long term thing. Also, the length of the hive appears to be growing at ~ 1-2 cm per week.

(crop of larger picture found below)

p.s. the images are quite large, drag onto a new tab to see in full size

I suggest killing it with fire. Paper wasps in North America can be very aggressive and their stings hurt.

These are certainly paper wasps (Vespidae) building their paper nest. Looks like a species of Ropalidia, which are known from Singapore.
I know little about Ropalidia, it seems to be rather small and probably harmless, but our larger European wasps can sting and bite and are sometimes quite aggressive (this refers first of all to Vespula germanica).


text:
List of np-hard problems in biology/bioinformatics
I'm not sure if this is the right place for this but...
I am looking for a list of computationally "hard" problems such that if a problem from this list could be solved effectively, it would be (significantly, or otherwise) beneficial in some form or another to the biology community.
Some examples I have found (or atleast were tagged as "np-hard" problems):
Multiple sequence alignment problem
Protein threading / design problem
Map / sequence assembly problem

The list does not have to be extensive, but hopefully more than a few.
Thank you!
(Also, I couldn't think of any more tags to add so feel free to help out there as well.)
Note:
Same question at biostars: https://www.biostars.org/p/98112/

Try asking this on http://www.biostars.org, the people there probably have thought more often about the question if a problem is np-hard.

Why has this question been downvoted? btw, this post might interest you @Colton

Just a curiosity: an NP-complete problem (Hamiltonian path) solved with molecular computing http://www.ncbi.nlm.nih.gov/m/pubmed/7973651/

Hope the below answer is somewhat helpful.

@MattiaRovetta Here is a related paper

Molecular distance geometry problem is well known to be NP hard, in 3 dimensions.

I think this is a great question but it may have been misunderstood to mean literally NP-hard problems in bioinformatics, whereas it is really seemingly asking about hard computational problems that would be of great use in biology or bioinformatics. Perhaps it should be reasked here.

I'm no expert in computational biology but I am very much interested and do some big data analysis using R for my own projects so I will try to provide some information.
This (http://www.ncbi.nlm.nih.gov/books/NBK25461/) is an excellent book talking about all the grand challenges in computational biology and the emerging fields so I definitely recommend looking through at least the list on the page, if you don't want to read the entire book. To me all this points to the fact that we are in the big data era, where we have masses of data but making sense of them all and putting them into prospective and analysing them in a way to show us new insights into problems is difficult.
You might also be interested in BOINC, which runs a few computationally challenging projects through crowd sourcing/grid computing (http://boinc.berkeley.edu/projects.php). In more theoretical aspects, here is a list of unsolved problems (http://en.wikipedia.org/wiki/List_of_unsolved_problems_in_mathematics), solving of which will excel our understanding of many modelling problems, which percolate in biological problems as well although I'm not at all an expert in biological systems modelling.
Hope this helps!

De-novo assembly
To construct a genome from short reads, it's necessary to construct a graph of those reads. We do it by breaking the reads into k-mers and assemble them into a graph.

In this example, we have a k-mer of 3. We can reconstruct the genome by visiting each node once as in the diagram. This is known as Hamiltonian path.
Unfortunately, constructing such path is NP-hard. It's not possible to derive an efficient algorithm for solving it. Instead, in bioinformatics we construct a Eulerian cycle where an edge represents an overlap in two k-mers.

This is more of a long comment than an answer, but I thought it might still interest you. We usually care about NP-hardness because it means that we can't do something or solve some problem. But that isn't the only intractable complexity class that should be important to biologists.
If we re-frame NP problems as optimization problems (instead of the strict definition as decision problems) then what NP-hardness usually says is that we can't (in general and in reasonable time) find the global optimum. However, in a lot of evolutionary settings we wouldn't even care about a global optimum, we'd be happy with a local one.
The difficulty of finding local optima is captured by the complexity class known as Polynomial Local Search (PLS). And here we also have surprising complexity barriers. For example, Kauffman's NK-model of static fitness landscapes (also, see this blog post and SE question for overview) is not only NP-hard [Weinberger, E. (1996), "NP-completeness of Kauffman's N-k model, a Tuneably Rugged Fitness Landscape", Santa Fe Institute Working Paper, 96-02-003] but also PLS-hard (Kaznatcheev, 2017; see here for an overview or here for the final paper). This means that not only can arbitrary evolutionary dynamics not find global optima, but in general they can't even always find local optima on these finite (but exponentially large) landscapes. Suggesting that local optimality might not be a reasonable assumption even on static landscapes.

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


text:
How are new chromosomes replicated into the next generation via sexual reproduction?
If an individual has a new chromosome, which is very unlikely to happen, he will not have any luck in finding a sexual partner with this same trait. How will the offspring inherit this trait. And given that extra/fewer chromosomes are often undesirable traits (e.g. Turner Syndrome) how can it propagate?
I assume that humans and rats have different number of chromosomes, so a common ancestor must give a lineage where some individuals had a different number of chromosomes than their parents.

You are right that a person with an abnormal number of chromosomes will be unlikely to find an "equal" partner to mate with. This does not prevent a chromosome aberration from spreading though, and it is not necessary that the mutation is initially beneficial for it to spread. While it is true that many chromosomal aberrations may be detrimental and cause various syndromes, a chromosome split or multiplication may also be netural except for the matter of reproduction. A change in chromsome number will not be inherited deterministically, but can give rise to various new permutations in the offspring due to the mechanics of chromosome segregation during meiosis.
You can find a good explanation at Scienceblogs.com: http://scienceblogs.com/pharyngula/2008/04/21/basics-how-can-chromosome-numb/ :

The net result [of a chromosome split] is that although this
  individual is fine and healthy, a significant number of his or her
  gametes may carry serious chromosomal errors, which means they may
  have reduced fertility. They aren’t sterile, though; some of their
  gametes will have the full complement of genes, and can similarly
  produce new healthy individuals who will probably have fertility
  problems. (...)
  So our two chromosome individual will have a reduced fertility as long
  as he or she is breeding with the normal one chromosome organisms, but
  those split chromosomes can continue to spread through the population.
  They are not certain to spread — they’re more likely to eventually go
  extinct — but by chance alone there can be continued propagation of
  the two chromosome variant. Which leads to another misconception in
  the question: something doesn’t have to provide a benefit to spread
  through a population! Chance alone can do it. We don’t have to argue
  for a benefit of chromosome fission at all in order for it to happen.


text:
Why haven't land animals evolved beyond urination?
It occurred to me (while urinating) that this would seem to be selected against because water is a scarce resource.   Why are we constantly losing water we don't need to through urination?   What is it about the chemistry of urine and the waste products eliminated that make urination necessary as opposed to eliminating them through defecation and recovering the water on the way out?

Actually this process (in the kidney) helps saving a lot of water. The primary urine is concentrated about 200x before it is excreted into the urinal bladder.

I would hardly call water scarce in the natural world…

Many have, see birds and most reptiles, what white stuff in bird poop is their nitrogenous waste. please do a little background research before asking a question.

It is probably true that toilets and other resting-ish area are always a great place to think about biology, I agree $\ddot \smile$.
Why do we urinate?
In short, urine contains the waste from our blood while defecation is just the stuff that we haven't digested. Kidneys are the organs responsible for draining wastes (mostly nitrogen-containing, or nitrogenous, wastes) from our blood.
Trade-off: energy cost vs. water loss
You're correct that the loss of water through urination is a considerable cost for an organism (especially those living in dry environments). But the amount of water used to excrete nitrogenous wastes is negatively correlated with the energy it costs to perform this excretion. In other words, there is a trade-off between water and energy loss during nitrogen excretion. Also, the question of toxicity is important.
Three ways to excrete nitrogenous wastes
Animals basically have three choices to excrete nitrogenous wastes:

Uric acid (excreted by uricotelic organisms)

Solid (crystal) with low water solubility
Low toxicity
Little water is needed
Lots of energy is needed

Ammonia (excreted by aminotelic organisms)

Highly soluble in water
High toxicity
Lots of water is needed to dilute it because of the toxicity
Not much energy is needed

Urea (excreted by ureotelic organisms)

Solid but highly soluble in water
"medium" amount of water is needed
"medium" toxicity
"medium" amount of energy is needed

What method is most beneficial for a given individual?
The amount of energy and the availability of water are very important aspects to understand whether a species is ureotelic, aminotelic or uricotelic. Another developmental constraint must be considered too. For example, birds are uricotelic (uric acid) probably because during the development of the embryo the wastes cannot be excreted outside the egg and therefore, excreting uric acid allows to greatly decrease the toxicity of the embryo's environment. In short, we must consider

Water availability
energy loss
developmental constraints

Note: This domain is not at all my field of study and I have no reference, typically for what concerns the toxicity, water amount and energy amount. One should not take my words for granted!

This is an interesting answer.   But it doesn't explain why nitrogen can't be excreted in solid or gaseous, rather than aqueous, form.

@ThePopMachine Well, Amonia is a gaz, Urea is liquid and Uric acid is solid (it makes cristals if I'm not mistaken). So, yes it can be excreted through solid form but it cost lots of energy (ATP). But you're right that my answer does not explain why it is more costly. But I know nothing about physiology and I can't give this answer $\ddot \smile$ I'll let someone else to give info about that if you're waiting for them.

@ThePopMachine You might want to create another post and to ask a more specific question about the physiology of Nitrogen excretion and why different solutions (Ammonia, Uric acid and Urea) are differentially costly in terms of energy. Consider this post as it had answered the evolutionary part of the question.

Yes, okay this has been here a while, so I will accept.   But this answer can be improved further by talking about nitrogen chemistry.   Any takers?

Are you asking why is amonia gazeous while uric acid is solid? If so, you may want to make another post on Chemistry.beta. I personally know very little about chemistry and won't be able to help you further with that.

As I have already mentioned in my other post, the most important role of urea synthesis by humans is blood pH regulation and urine concentration, so it is not just about excreting a waste product. I don't think human body is very special in this case, so I think most of the urea excreting mammals use urea for the same purposes.
The urea is created from NH4+ and HCO3- in the liver (mostly) and the kidney because of blood pH regulation purposes. It neutralizes the HCO3- created by the lungs from CO2 and OH -.

The urea cycle (also known as the Ornithine cycle) is a cycle of
  biochemical reactions occurring in many animals that produces urea
  ((NH2)2CO) from ammonia (NH3). This cycle was the first metabolic
  cycle discovered (Hans Krebs and Kurt Henseleit, 1932), five years
  before the discovery of the TCA cycle. In mammals, the urea cycle
  takes place primarily in the liver, and to a lesser extent in the
  kidney.
In chemical terms, urea synthesis is an irreversible, energy driven
  neutralization of the strong base HCO3– by the weak acid NH4+, and the
  average daily excretion of 30 g of urea is equivalent to the disposal
  of about 1 mol of HCO3– per day. Thus, a major function of hepatic
  urea synthesis is to effect this neutralization, without which the
  body would otherwise be confronted by a major load of alkali.
Urea is excreted by the kidney, and is normally present in plasma and
  body fluids at a concentration of 3.0–6.5 mmol/L.

wikipedia - Ornithine cycle
Textbook of Hepatology - Ammonia, urea production and pH regulation - Dieter Häussinger
1984 - The role of ureagenesis in pH homeostasis

The kidney reabsorbs urea in order to concentrate the urine

2007 - Critical Role of Urea in the Urine-Concentrating Mechanism

Evolution is reactive, not proactive. While clean water may be becoming scarce, it wasn't previously. Having to pee had no negative effect (probably positive ones) on being able to reproduce, so people that do urinate reproduced.
Now let's imagine a world where we get to people evolving to not having to urinate.
First, water has become extremely scarce, and most of the human race and other animals have died of dehydration. But some people who are very effective at retaining water (who urinate less) make it through the lack of water. They have kids who carry this water retention gene, and some probably have slight mutations that make them even better at it. Since the slight mutation group is better at retaining water, they can live longer and have more kids that may also have a slight mutation that allows them to live longer and have more kids, and so on and so forth until eventually, you might have a human that doesn't pee.

Water scarcity is now and has been forever an issue for land animals, this is not something "new". Different animals handle this challenge differently, as described in the existing answers. I fail to see what new value this answer adds, it seems not up to the standards of this site.

Welcome to Biology.SE. We're looking for answers that provide explanation, context, and include references to reliable sources. Don't just give a short opinion or speculate — instead explain why your answer is right with appropriate citations. Answers that don't include explanations may be removed especially when they are a poor duplicate of an already existing answer. Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then delete or [edit] your answer accordingly. ——— Also note the question was not about humans ...

authors: მამუკა ჯიბლაძე


text:
Heterozygosity and overdominance
Consider $m$ loci with heterozygote advantage (overdominance) such that the fitness of the two homozygotes is $1-\frac{s}{2}$ and the fitness of the heterozygotes is $1+\frac{s}{2}$, where $s>0$. We'll assume that the fitness of an individual is given by the multiplication of the fitness component on each locus. In consequence, the fitness of the best possible genotype is given by $\left(1+\frac{s}{2}\right)^m$.
According to this book, an individual is heterozygote at $j$ of these $m$ loci with probability
$${m\choose j}\left(\frac{1}{2}\right)^m$$
and the equilibrium population mean fitness $\hat w$ is
$$\hat w = \sum_{j=0}^m {m\choose j}\left(\frac{1}{2}\right)^m  \left(1+\frac{s}{2}\right)^j  \left(1-\frac{s}{2}\right)^{m-j} = 1$$
I don't understand any of these two equations! Can you help me to understand how they have been calculated?

For the moment I just enjoyed proving that $\hat w = 1$. We can reformulate $\hat w$ as
$$\hat w = \left(\frac{1}{2}\right)^m  \sum_{j=0}^m {m\choose j} \left(1+\frac{s}{2}\right)^j  \left(1-\frac{s}{2}\right)^{m-j} = 1$$
,then using the binomial identity
$$ \hat w = \left(\frac{1}{2}\right)^m \left(\left(1+\frac{s}{2}\right) + \left(1-\frac{s}{2}\right)\right)^{\space m}$$
$$\hat w = \left(\frac{1}{2}\right)^m 2^m$$
$$ \hat w = 1 $$

Am taking another stab at this. I think that derivations in the refs are simpler and overall it's an interesting question.

If the fitness of a heterozygote is $(1+s/2)$ and of a homozygote is $(1-s/2)$ then why is the probability for a given state $(1+s/2)^j(1-s/2)^{m-k}$
$$\binom mj (1/2)^j(1/2)^{m-j}= \binom mj (1/2)^m~~ ?$$
As you pointed out earlier, in the general case it need not be true that $p = q = 1/2$ but that is what the form of the probability above implies. So the threshold question is why this particular heterozygous-dominant model implies equilibrium probabilities $p = q = 1/2.$ I think the ideas below begin to address this.
The simplest case is for one locus, two alleles, and there are many good derivations online. I think if you understand the situation for one locus you can generalize to higher numbers. (Hopefully I will supplement this answer, time allowing. I think a shortcut would be to assume $p = q = 1/2$ and use your fitness weights. That gives us $\bar{w}=1$ as a denominator. Now for reasons of symmetry I think you can show that the relative frequencies of $p$ and $q$ are equal and so $p' = p.$ Then you have to show that this equilibrium solution is unique.)
For a single locus the derivations of `heterozygote advantage' I have found,(1)(2), assign fitness weights as follows:
AA = (1 - s),     Aa = 1,       aa = (1 - t )
in which $s,t > 0, s \neq t$ in general, from which they derive as a condition for equilibrium
$$\Delta q = \frac{pq(sp-tq)}{\bar{W}}  = 0$$
so
$$\hat{p} = \frac{t}{s+t} ~~~\text{and}~~~ \hat{q} = \frac{s }{s+t}$$
in which $\hat{p}, \hat{q}$ are equilibrum frequencies for each allele, respectively, and s and t are rates of mutation. Nowhere did I see a model in which they had assigned the same fitness to both homozygous cases (AA, aa) but it's just a special case of the heterozygote advantage model.
fitness (AA) = fitness(aa) = (1 - s/2), fitness(Aa) = (1+ s/2).
So if we subtract s/2 from each fitness score (or normalize with respect to Aa to the same effect), we get:
fitness(AA) = fitness (aa) = (1- s ) and fitness (Aa) = 1 as in the two references above, except that now the two homozygous states have equal fitness.
But then we have $$\Delta q = \frac{pq(sp-sq)}{\bar{W}} =  \frac{pqs(p - q)}{\bar{W}} $$
and the only nontrivial solution is $p = q = 1/2.$
So what I am suggesting is that when you assign the same fitness to both $AA$ and $aa$ you no longer have the general case. As for the value of s being forced, the following seems relevant.
The full expression from (2) for the equilibrium condition is
$$p' = \frac{p^2 W_{AA}+ pq W_{Aa}}{\bar{W}} \hspace{10mm}(1)$$
in which$ W_{AA} = W_{aa} =  1- s$ and $W_{Aa} = 1$ and
$\bar{W} = p^2 W_{AA}+2pqW_{Aa}+q^2W_{aa}$
If the homozygotes are assigned the same fitness and $p = q = 1/2$ , equation (1) above becomes:
$$p' = \frac{\frac{1}{4} + \frac{1}{4}(1-s)}{\frac{1}{2} + \frac{1}{2}(1-s)} $$
The program on page 583 of (1) is helpful. Let h:= heterozygous and m:= homozygous. If $p = q = 1/2$ then as long as fitness(h) and fitness(m) are equal the system is in equilibrium immediately.
If $p\neq 1/2$ then as long as f(h) = f(m) the system reaches equilibrium at $p = 1/2$ asymtotically. If $p = 1/2$ but f(h) $\neq$ f(m) the asymtotic limit has to be calculated.
See also http://evol.bio.lmu.de/_teaching/evogen/Evo8-Summary.pdf

Thanks a lot for your answer. I'm traveling right now and I don't have time for reading up your answer. I'll read it wednesday or thursday probably.

Great answer. In addition to your (now deleted by yourself) other answer, you perfectly answered my question. Thank you. +1

@Remi.b: Appreciate the feedback. It was an interesting question and I am still learning about this broad subject.


text:
How do exon tandem exon duplications occur in the genome?
By this I mean in cases where tandem exons are introduced by replication slippage how would a DNA polymerase by chance duplicate an entire exon cleanly (i.e. from exact start to exact end) when it doesn't even know what an exon is?

I dont think it would happen because of slippage. It should happen via recombination. Can you indicate the source of this information ?

i guess I was thinking of somatic cancers but the question still stands: how does the recombination machinery know what an exon is?

There is a section in the Human Molecular Genetics textbook about how such repeats do occur. Like the commentor said, it is likely a result of recombination. If there are repeats flanking a gene or an exon there can be paring between sister chromatids / chromosomes, which can result in the duplication. See Figure 9.7 here http://www.ncbi.nlm.nih.gov/books/NBK7566/#A1095
As for how does it "know": It doesnt. Its not just the exon that is duplicated though. It is also the DNA before and after the exon, which contains cis-elements that splicing factors bind to, which results in the exon being spliced into the transcript.
Splicing is pretty complicated but if just 50 bp upstream and downstream of the exon was also duplicated, it would probably be enough to cause some splicing of the exon. U1 and U2 snRNP bind immediately at the exon-intron junction, and the polypyrimadine tract is about 30 bp or so upstream from the exon. U1 and U2 and the polypyrimadine tract are all vital to splicing. I dont know of any work that shows the minimum requirement for splicing but if you have those 3 you will probably splice the exon at least part of the time. So in sum, its probably not just the exon that is duplicated. It is probably the exon plus the cis elements involved in splicing.

I'm going to speculate that exons that are not cleanly duplicated activate the cell death machinery. We see the clean exon duplications because they are able to survive.


text:
Detecting a Fasting State in the Body via Lasers
I was just wondering wether it would be possible to detect if the body is in a "fasting" state, via lasers attached to the body. If it is possible, what sort of laser would be needed?

If by a fasting state, you mean blood glucose levels, researchers seem to think it is feasible. See for example Pleitez et al. (1) and Guo et al. (2). Their designs both utilize infrared IR laser light to measure glucose levels in the skin.