text:
$F_{ST}$ and the genetic variance in metapopulations
From this video (21'15''), the speaker gives the following formulae in order to calculate the between and among populations genetic variance from the $F_{ST}$:
$$V_{Among Pop} = 2 F_{ST}V_G$$
$$V_{Within Pop} = (1-F_{ST})V_G$$
, where $V_G$ is the total genetic variance of this population if it was well mixing. $V_{Among Pop}$ is the variance among populations and $V_{Within Pop}$ is the variance within populations.
In this same video, the speaker defines $F_{ST}$ as:
$$F_{ST} = \frac{\text{Var}(p)}{\bar p (1-\bar p)}$$
, where $p$ is a vector of frequencies of a given allele and $\bar p$ and $\text{Var}(p)$ are the mean and variance of this vector.
For example, consider a metapopulation made of 4 subpopulations. The allele frequencies in these 4 subpopulations are p=[0.2, 0.5, 0.8, 0.3]. $\bar p$ is the mean of $p$ ($\bar p = 0.45$) and $\text{Var}(p)$ is the variance of $p$ ($\text{Var}(p )=0.07 \space$).
Can you help me to make sense of the formulas for $V_{Among Pop}$ and $V_{Within Pop}$?
Can you prove these formulas? I would expect that $V_{Among Pop} + V_{Within Pop} = V_G$ but it doesn't! Maybe the issue has to do with the fact that $V_{Within Pop}$ as defined above fit to haploid population and not diploid populations. Then, I would expect that for diploid populations $V_{Within Pop}$ becomes $(1-2F_{ST})V_G$. Is that correct? Just in order to make it more general, how do you extrapolate these definitions for a tetraploid population? Also maybe I misunderstand the meaning of $V_G$. Is the variance within population the sum of the within populations variance or is it the average (or something else)? Thanks for your help!


text:
$F_{ST}$ when considering a multi-allelic locus
Sewall Wright defined the $F_{ST}$ in a metapopulation as being:
$$F_{ST} = \frac{\text{Var}(p)}{\bar p (1-\bar p)}$$
, where $p$ is a vector of frequencies of a given allele and $\bar p$ and $\text{Var}(p)$ are the mean and variance of this vector.
For example, consider a metapopulation made of 4 subpopulations. The allele frequencies in these 4 subpopulations are p=[0.2, 0.5, 0.8, 0.3]. $\bar p$ is the mean of $p$ ($\bar p = 0.45$) and $\text{Var}(p)$ is the variance of $p$ ($\text{Var}(p )=0.07 \space$).
Question
Can we define $F_{ST}$ for a multiple allele locus? Or should $F_{ST}$ be defined for each allele independently?

Can you provide a cite for the idea? The form of these things varies with the source. $F_{ST}$ is a symbol. What is it supposed to stand for, in English?

@daniel $F_{ST}$ is also called fixation index. It is an index used in population genetics in order to describe the population structure (non-random mating throughout the population) of a metapopulation. Here is the wiki page. I think there is only one definition of $F_{ST}$ but several ways to equivalently understand it. There are a bunch of ways to measure and approximate the $F_{ST}$ but this is the matter of another discussion.

@daniel You may also want to have a look to the table and to the slide that follows this table on this video at 31'44''. It gives an explanation of where the definition I wrote in my post comes from. I am personally not really able to give you a good intuitive explanation of what $F_{ST}$ is. I am only able to give the mathematical definition of it. Here is a related question I recently asked that might help a bit!

Short answer: yes, people have formulated ways to estimate $F_{ST}$ for multiallelic loci, e.g. microsatellites. For a review, see here.
Specifically, Nei could define $F_{ST}$ for multiple alleles as
$F_{ST} = \frac{(H_t - H_s)}{H_t}$,
which is to say the proportion of total heterozygosity that is across rather than within populations. This is agnostic to the number of alleles, as it just uses heterozygosity. I believe there are other formulations as well.
There exist alternate statistics such as $G_{ST}$ and $R_{ST}$ (links under each) which are devised specifically for the multiallelic problem, see also the review for further discussion. Basically, microsatellites have high mutation rates such that they deflate the statistic; this will likely be the case for most multiallelic loci.
It's not clear though which statistic works best in practice as far as I can tell.

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text:
Do primitive lymph nodes exist in 12th week embryo?
Someone told me that primitive lymph nodes do not exist during this week.
However, others say they can.
Here is a picture about inguinal lymph nodes from here.
No primary lymph nodes are visible (like circular) at 56th day:

When are the primitive lymph nodes formed?

Have a look at this webpage. I think it answers your question.

@Chris I would like to have some trustworthy source, because the one who claimed that there is no primitive lymph nodes at that time is a smart person. There is something recent research going on by which you can say that those lymph nodes at 3rd month cannot be anymore called primitive lymph nodes. Something new has been discovered by which you can reject the primitive lymph nodes that early. However, I was not told the reason for that. However, this is only research so can be false too; still the claim which I heard today was expressed very strongly.

Then do it the usual way: A person which makes strong claims needs to have strong proofs as well. In this case the original studies. I can have a look later...

@Chris Anything found?

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How do GPCRs transmit a signal across the plasma membrane?
How do G-coupled protein receptors (GPCR) transmit signals through the plasma membrane?
Links containing information about this and pictures will be very helpful.

The G-coupled protein receptors (GPCR) transmit signals from outside of the cell into the cell and activate downstream signalling pathways. These change for example the expression of certain genes.
The whole process is a coorperation between the receptor, a G-protein, GTP as a co-factor and the ligand of the receptor (which starts the whole process). An extensive description (including much more images) is available in the Wikipedia, but in short, it looks like the images below (from the Wikipedia article on GPCR):

To answer how this signal is tranferred from the outside to the inside look at the first image: Upon ligand binding the conformation of the receptor changes its conformation and brings some of it transmembrane helices together so the G$\alpha$ subunit can bind here and activate downstream signalling.

The whole process happens in a few steps:

In the resting state the receptor has a trimeric G-protein (consisting of the subunits $\alpha, \beta$ and $\gamma$ bound on its cytosolic site. The G-protein also has a GDP molecule bound to it $\alpha$ subunit.
Upon binding of the ligand, the receptor changes its conformation, and G$\alpha$ exchanges the GD against GTP, which activates the complex.
The G-protein dissociates into the active G$\alpha$ the G$\beta\gamma$ subunits, which signal to downstream signal transduction pathways like the MAP-Kinase pathway.
Binding of RGS (regulator of G-protein signalling) to the g$\alpha$ subunit activates the intrinsic GTPase function of the subunit and hydrolyses GTP into GDP and P. The GDP stays bound to the G$\alpha$ subunit, which changes its conformation and forms the G-protein trimer at the receptor. At the receptor itself this induces also a change in conformation which makes the ligand dissociate from the receptor.

At the end of the fourth step the receptor has returned into its inactive form and stays there until the next ligand binding.

Thanks for your help.but intracellular signal transduction is well known property of gpcr i know the mechanism of that.i asked how gpcr transmit signal through plasma membrane

@N00B I added some information. But the whole process (especially the involvement of G-alpha) is connected and can not be seen seperated.


text:
Diffusion of Hypotonic solution into solution with glucose and starch
Cell walls are selectively permeable to ions and organic molecules. Sometimes the selectivity is passive and a reflection of the physical laws governing diffusion. We can do simple experiments that strengthen intuition about transport across biological membranes. The following homework question concerns a situation which tests understanding of the basic ideas of osmosis and diffusion generally.

A bag made of a flexible semipermeable membrane is filled with a 10% glucose and 5% starch solution. This bag is permeable to water and glucose but NOT to starch. The bag is suspended in a a beaker containing a 10% glucose solution. In 30 minutes the bag can be expected to

(A) swell
(B) shrink slightly
(C) collapse entirely
(D) become impermeable to glucose
(E) remain the same

Since the bag is impermeable to starch, I know that the solution in the bag isn't going to diffuse outside so it won't shrink, but would water from outside flood into the bag to try to dilute the starch concentration to the point that it's isotonic? Or am I not understanding some fundamental principle of diffusion?

The question is clever but I think you are right. It's the osmotic concentration that drives the movement. The 10% glucose has no net effect. The added starch means the osmotic conc. in the bag is higher and so water from the outside would enter the bag.

@daniel Note that starch will not form a true solution and cannot contribute to osmotic pressure. Colloidal dynamics are a little more complicated.

@WYSIWYG: I'm confident colloidal dynamics were not what the question contemplated, so if you are correct the question was badly written.

yes.. I understand that @daniel but if not looked at as a homework question, there are some interesting aspects to it.

This question appears to be off-topic because it doesn't have fit with the topics listed in the help center. Great question, though. Maybe better suited to Physics or Chemistry?

@jmusser: Every basic 1-year biology course with lab covers osmosis. There are currently 14 questions dealing directly or indirectly with osmosis on this site. The help center says questions have to be about biology, which this is. A basic grasp of osmosis is crucial to understanding membranes in a biological context.

Link to Meta discussion

The answer by @Allan Boyd is correct and well stated, you should accept it.

The bag will swell.
Diffusion results in molecules moving down their concentration gradient.
In the set-up described only glucose and water are able to diffuse. Glucose is at the same concentration inside and out so there will be no changes in glucose concentration. Water will move into the bag because it is effectively at a lower concentration (more correctly  - chemical potential) inside due to the presence of the starch. As water moves into the bag, increasing the volume, glucose will also move so that the glucose concentration remains equal on both sides. Thus there will be net movement of water and glucose into the bag.
@WYSIWYG has raised the spectre of colloids in the comments. I don't understand colloids so cannot comment, but I think that in the context of problems like this we are usually dealing with "soluble" starch. Here is an example of a calculation in which starch is treated as an osmolyte.

It should depend on the chemical nature of the suspended macromolecule (in this case starch and it will form a colloidal mixture). If the macromolecule is inert then it will just reduce the effective volume inside the bag.

@WYSIWYG are you saying that my answer is incorrect and the correct answer is E?

I think A) swelling is right answer. The water is at lower concentration in the bag than outside the bag so it will diffuse passively into the bag. Glucose concentration drops in the bag, but at the same time, glucose is diffused passively from outside into the bag so keeping the potential stable between glucose. Water will mostly diffuse, and some water.

@AlanBoyd.. I am not sure.. that is why I commented. Considering that starch has polar groups it can interact with water and may reduce the bulk water - in that case your answer will hold correct. I cannot conclusively say if it can give rise to oncotic pressure. I am not an expert in this area but this is what I understand. If we are really interested in that aspect we can migrate this question (with appropriate edits) to ChemistrySE/PhysicsSE

glucose will equilibriate.. that's what Alan Boyd said in his answer

@daniel can you explain what 'force' would prevent glucose from diffusing to equilibrium (= same concentration in both compartments)?

But, by definition, if the glucose concentration is higher on the outside then the rate of movement inwards will be greater than the rate of movement outwards. In my view the presence of the non-diffusible solute inside the bag will cause a net movement of water into the bag until this is exactly counteracted by the pressure created. The glucose is simply a passive observer and will equilibrate (equal concentration inside and outside). As I say, this is my view, and I am happy for someone to explain why this is incorrect.

DIY Diffusion Experiment
This procedure was done to see what happens qualitatively when semipermeable (dialysis) tubing containing a solution of  glucose and protein is immersed in a solution of glucose alone. Given that water would diffuse into the bag, the question to be answered was whether there would be an equilibrium increase of sugar concentration outside the bag.
Equipment: one-inch dialysis tubing, bovine serum albumin (BSA), dextrose, an inexpensive commercial glucose meter, test strips for the meter.
General procedure:  A control dextrose solution was divided between a sac made of dialysis tubing and a drinking glass.  A small mass of powdered BSA was added to the sac. The sac was suspended in the sugar-only solution and the solution outside the bag checked at 13 times during a 33-hour period. At about 8 hours protein was added to the bag since neither diffusion nor osmosis was being observed. After this the bag began to swell. Due to concern that BSA would affect the reading the measurements were compared with the control solution and not the inside of the bag$^1$.
Results: Results are given in the table below. Addition of protein is indicated by the arrow in the graph.
Discussion: This procedure was suggested in this answer at the Chemistry SE. The meter requires some practice to use. Protein was added to the bag in roughly 200mg increments until an influx of water occurred. The solutions had probably reached equilibrium within a few hours of adding the extra protein but fluctuation in temperature made this difficult to determine. The gross trends correspond to air-conditioner use.
Conclusion: This procedure was done twice with similar results. The results are qualitative and suggest that sugar diffuses out through the membrane. This result is consistent with the answer at PhysicsSE and also this website (Figure 4.1) which indicates that diffusion and osmosis (diffusion of water) both occur. At equilibrium the concentration of sugar is slightly higher outside the bag.
Problems/issues :  (1) The meter is very sensitive to temperature $^2.$ (2) Perhaps because the dextrose was incompletely dissolved the measurement of control solutions took about an hour to stabilize. That is why the measurements begin at 110 minutes. (3) The meter gave errors outside a range of 30-500 mg/dl and after checking the standard deviation for a few concentrations of dextrose a concentration of 90 mg/dl was chosen. (4) It was not assumed that the meter functioned properly in the presence of BSA. Except for the last measurements, the glucose was measured outside the bag only.
$^1$ Four measurements were taken with the meter within 2 minutes of the last measurement to check variability of the meter. The numbers [mg/dl] were: 90, 94, 93, 89, $\mu = 91.5, \sigma = 2.38.$ At the last measurement the glucose concentration inside the bag was checked twice and the meter gave: 72, 80.
$^2$ Concentration should remain the same after equilibrium [Fick equation] and should not be affected by temperature. Manufacture information for the meter omitted for this reason. Caveat emptor.
Table 1. Min.= minutes, contr. = control [mg/dl], dextr. = dextrose [mg/dl].
$$\begin{array}{c | c | c | c | c | c |c | c | c | c | c | c | c | c | } min. & 110 & 145 & 296 &  356 & 686 & 776 & 802 & 832 & 862 & 1352 & 1393 & 2053 & 2069 \\ \hline
dextr. & 90 &  80 & 88 & 83 & 90 & 91& 88 & 88 & 89 & 84 & 93 & 86 & 90 \\ \hline
contr.& 91 & 83 & 83 & 86 & 82 & 87 & 83 & 85 & 80 & 77 & 89 & 82 & 82   \\ \hline\end{array}$$
A graph (mg/dl v. minutes) was made from this table. The arrow indicates addition of protein to the bag.


text:
Why are different lengths of nucleotides taken for structure prediction from an miRNA match area after BLAST analysis?
Generally in miRNA prediction most researchers do as Blast search with a set of miRNAs downloaded from miRBase with the parameters they require. Later on usually custom methods are utilized to get an area around the match area for structure prediction.
In one paper, I found that ~70 flanking nt of match area was taken as pre-miRNA for structural analysis while in this paper ~100 flanking nt of the match area was taken for pre-miRNA structure prediction. Any idea why so?

There is no hard and fast rule for how many nucleotides you have to select. If your miRNA is ~20nt and you take 70nt from both sides (average length of hairpins is ~84nt in humans), your total length will be 160nt. The point of taking $\pm70nt$ is that you don't know if your read is -3p or -5p. So take 70nt from both sides.
The maximum length of a human miRNA hairpin is 180nt for mir-3648 (90nt per half hairpin). In such cases you may take more flanking residues. But these cases are rare.


text:
Assumptions of the models for haploid and diploid selection
For a bi-allelic locus, the model for haploid Natural Selection is:
$$\frac{dp}{dt} =  \frac{pW_A}{pW_A + (1-p)W_B}$$
, where $p$ is the frequency of the allele $A$, which relative fitness is $W_A$. $W_B$ is the fitness of the allele $B$, which frequency is $1-p$. $\frac{dp}{dt}$ is the change in allele frequency through time.
The same model for diploid selection is:
$$\frac{dp}{dt} = \frac{p^2W_{AA} + p(1-p)W_{AB}}{p^2W_{AA} + 2p(1-p)W_{AB} + (1-p)^2W_{BB}}$$
, where $W_{AB}$ is the fitness of the diploid genotype carrying the allele $X$ on one chromosome and the allele $Y$ on the other chromosome. We define $W_{AB} = W_{BA}$ and therefore we use only the symbol $W_{AB}$ in the above calculations. Note: This equation assumes Hardy-Weinberg equilibrium.
Those equations can be found in any introductory courses in population genetics. For example, here is a source where you can find this same equation for diploid selection. They just express $q$ instead of $1-p$.
My questions are:

Do these models assume constant population size? Why?
Do these models assume threshold selection? Why?

Thank you!

See my updated question!

Unless I am missing something the equations you have posted are incorrect. The second equation should be:
$$p' = \frac{p^2 W_{AA} + p(1-p)W_{AB}}{p^2W_{AA}+ 2p(1-p)W_{AB}+(1-p)W_{BB}} $$
$p'$ is not interpreted as $\frac{dp}{dt}.$
$p'$ is the frequency of allele A in the next generation. If zygotic frequencies via random mating are
$p^2(AA) + 2pq(Aa)+q^2(aa) = 1$
then all of AA individuals and 1/2 the Aa gametes bear the A allele. So we can find $p$ in the next generation as
$p^2+pq = p^2+p(1-p) = p^2+p-p^2 = p$ which shows that in a Hardy-Weinberg population the frequencies are stable.
The assumptions here are those underlying the HW model, which includes infinite population size (hence constant).

Yes indeed you'r right. I was curious about how changing in population size may change selection pressures and change allele frequencies, but the model I gave assumes infinite population size. And yes, dp/dt is not the same as p'. Thank you!


text:
Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?
Background
The standard definition of species refers to the concept of reproductive isolation. If two lineages are found to be reproductively isolated, then we consider these two lineages to belong to different species. My question concerns evolved reproductive isolation in Drosophila sp. following labs due to experimental evolution.
Question
Have we ever demonstrated that two Drosophila sp. lineages that could initially interbreed (in nature or in labs) evolved through artificial selection (and drift and mutations) in labs to finally not be able to interbreed anymore either due pre- or post- zygotic isolation (see wiki)? Or, in other words, have we ever demonstrated that two drosophila lineages evolved to become different species (reproductive isolation definition) in labs experiments?
If not, have we ever observed some partial reproductive isolation such as inbreeding depression for example?

Note: This question is motivated by @LotusBiology that could not receive the answers she/he was waiting for because he/she failed to ask questions that are possibly answerable! So I wanted to ask this question that somehow addresses this question he/she asked (now on-hold)
For more information about the concept of species, please have a look at How could humans have interbred with Neanderthals if we're a different species?

Reproductive isolation in not only Drosophila but other species is the basis of Daniel Matute's research (http://dm-incompatibilities.org/).

Rice and Salt$^1$ bred fruit flies for 35 generations and from one line of flies created two groups that were isolated from each other reproductively. They could not interbreed because they no longer bred in the same environment. Depending on one's definition of 'species' this could be a case of artificial speciation.
$^1$Rice WR, Salt GW (1988), Speciation via disruptive selection on habitat preference: experimental evidence". The American Naturalist 131 (6): 911–917.

Also there was one experiment by diane dodd...mate preferences of fruit flies changed.

Diane Dodd's experiments on Drosophila pseudoobscura would be another example of lab-based speciation.
http://www.jstor.org/stable/2409365?__redirected
To summarise - four populations each adapted to feeding on a starch-based diet and a maltose-based diet were evolved in the lab to test effects on mating preferences; compared to what is expected by random, using chi-squared tests, 11 of 16 combinations showed greater isolation than expected by chance - strong evidence for assortative mating.
An alternate link to the PDF of the paper is here http://www.sulfide-life.info/mtobler/images/stories/readings/dodd%201989%20evolution.pdf

Reference:
Dodd, Diane M. B. (September 1989). "Reproductive isolation as a consequence of adaptive divergence in Drosophila pseudoobscura". Evolution 43 (6): 1308–1311. doi:10.2307/2409365.

Can you summarize the results so that if the link dies the answer will still have value?

@AnkurChakravarthy The link no longer works I am afraid. Can you please edit it and as JamesJenkins asked, can you please add a short summary of this article or post your link in a comment. Thanks a lot!


text:
Can a postsynaptic neuron 'shut itself off?
I am an amateur interested in neuroscience and was curious whether there is a process by which a neuron or group of neurons would close their receptors and stop receiving signals from specific synapses for a temporary period?

I think you might be onto the desentization of neurons. Here's a not very helpful Wiki link and a paper

AFAIK, receptors can not respond to stimuli if 1) they are modified in some way that it no longer binds its ligand, 2) modified in some way that the binding does not induce a change detectable inside the cell, 3) the old ligands are not cleared so any new signals are not noticed...these are the things I can think of right now...

drugs can apparently have this effect of decreasing synaptic sensitivity due to habituation! also see anaesthesia

An example would be the neurons that switch off/switch on based on our sleep cycle. Nerve-signaling chemicals called neurotransmitters control whether we are asleep or awake by acting on different groups of nerve cells, or neurons, in the brain. Neurons in the brainstem, which connects the brain with the spinal cord, produce neurotransmitters such as serotonin and norepinephrine that keep some parts of the brain active while we are awake. Other neurons at the base of the brain begin signaling when we fall asleep. These neurons appear to "switch off" the signals that keep us awake. Research also suggests that a chemical called adenosine builds up in our blood while we are awake and causes drowsiness. This chemical gradually breaks down while we sleep (reference and reference). Here is a study based on switch on/switch off of fear i mice (reference).
There are also artificial ways in which to shut down receptors like our sweet receptors (reference). There have also been studies done on other organisms where one particular study showed the switch on/switch off of olfactory receptors in cockroach antenna (reference).


text:
What do the Clustal Alignment Symbols Mean?
Occasionally I will run protein alignments on peptide families and I can never remember what the symbols mean to show degrees of identity. What do they mean?

From the FAQ for the Clustal-W2 program:

An * (asterisk) indicates positions which have a single, fully conserved residue.
A : (colon) indicates conservation between groups of strongly similar properties - scoring > 0.5 in the Gonnet PAM 250 matrix.
A . (period) indicates conservation between groups of weakly similar properties - scoring =< 0.5 in the Gonnet PAM 250 matrix.

Therefore the hierchy of conservation using these symbols is * (identical) > : (colon) > . (period).


text:
When infected with malaria, how many parasites are within a human host?
When infected with malaria, how many P. falciparum cells are within a human host? And how does this compare with the average infection parasitemia of A. gambiae? I can't seem to find a reliable source to guide me on this question.

The uninucleate sporozoites are injected by the mosquito into a human host. They mature in the liver parenchymal cells in schizonts. Each schizont releases into the blood flow 2,000 to 40,000 uninucleate merozoites. Each of them can infect a red blood cell. Here, a merozoite can release other 10 to 36 merozoites [1].
The numer of injected sporozites depends on the bite and the number of bites [2]. And it seems that a parasitemia greater than 5000/microliters which is usually achieved by 10 infective bites during a 28-day period triggers the signs and symptoms [3].
I couldn't find any data on the mosquito parasitemia. It has been found that the infected mosquito and the parasite mutually benefit each other and thereby promote transmission of the infection. The Plasmodium-infected mosquitoes have a better survival and show an increased rate of blood-feeding, particularly from an infected host [4].
References:

James M. Crutcher and Stephen L. Hoffman. Medical Microbiology. 4th edition. 1996, The University of Texas Medical Branch at Galveston.
Garrett-Jones C, Shidrawi GR. Malaria vectorial capacity of a population of Anopheles gambiae: an exercise in epidemiological entomology. Bull. World Health Organ. 1969 Apr;40(4):531-45. PubMed PMID: 5306719.
McElroy PD, Beier JC, Oster CN, Beadle C, Sherwood JA, Oloo AJ, Hoffman SL. Predicting outcome in malaria: correlation between rate of exposure to infected mosquitoes and level of Plasmodium falciparum parasitemia. Am. J. Trop. Med. Hyg. 1994 Nov;51(5):523-32. PubMed PMID: 7985743.
Dr. B.S. Kakkilaya's Malaria Web Site. Life Cycle of Malaria.


text:
Alleles notation in SNPPedia criteria
I can understand the allele notation when is in the form rs8176719(T;T) or rs8176719(G) but recently i found this ones rs8176719(T;-) or rs8176719(-;T).
So im confused, rs8176719(T;-) is the same as rs8176719(T)? or is the location is important ?
Thanks .

The '-' means that that allele has a single base deletion.


text:
What does "regulatory genomics" mean?
I have read about basics of molecular genetics ,although its not a thorough in-depth knowledge. I would like to know about "regulatory genomics". What is it actually?

As I understand it, it is the study of regulatory mechanisms in gene or protein expression in populations and especially how these mechanisms vary between closely related lineages.

Can you tell us, in which context you read about it?

@Chris : I was going through an institute website ( http://www.imsc.res.in/biology_imsc ). There a professor is specializing in regualatory genomics, and research programme for computational biology is going on.

The genome may be divided into two classes of sequences - those that code for proteins and those that do not. Those that do not code for proteins may be again divided into classes consisting of actively transcribed sequences that have biological activity (such as long noncoding RNA, microRNA, competing endogenous RNA and so on) and those that aren't.
These untranscribed noncoding regions may be involved in regulating the activity of protein coding and actively transcribed regions by binding to transcription factors or transcriptional coactivators/corepressors that control whether certain genes are expressed or not - this can happen close to the start of the gene (i.e, promoters) or far away (at enhancers). Distant enhancers can still affect gene expression because they and the genes they affect can be close together in three-dimensional space (The genome is folded in cells!).
Regulatory genomics is, simply put, the study of these regions, which are called genomic "features" and how they regulate genes. A great example of studies in this area are offered by papers published as part of the ENCODE project http://www.nature.com/encode/#/threads

Thanks for the effort in answering. Good answer too, I got the essence. But I didn't completely understood. Since my subject is not biology I don't understand things like binding. Can you suggest me some reference for beginners other than papers.

Not to discourage you, but you're getting into some fairly advanced topics in molecular biology so you may want to read some basic biology/biochemistry textbooks first to get the prerequisite knowledge.

@canadianer : I completely agree with you. I will have to see the basics.

Alberts' Molecular Biology of the Cell or Lewin's Genes would be a good starting point if you are looking for textbooks; alternatively, check out Scitable http://www.nature.com/scitable/topic/gene-expression-and-regulation-15


text:
What is the definition of a stringent/relaxed plasmid?
I have found a publication which proposes some definitions, including a definition for strict and relaxed replication. The definitions are:

Relaxed control of plasmid replication. Relaxed control should be used in reference to plasmid replication that is not obligatorily coupled to chromosome-replication.
Stringent control of plasmid replication. Stringent control should be used in reference to plasmid replication that is obligatorily coupled to chromosome replication.

However, the publication is from 1976. Are these definitions current? If no, what is the current definition?

In short, yes, the definitions are still correct:
The number of copies of a plasmid in the cell is determined by the mechanism of its replication: whether it is synchronized with the replication of the bacterial chromosome or is independent of it.
In the first case, the initiation of replication is performed by the same mechanisms of replication of the bacterial chromosome. This means that the origins of replication, as well as all proteins involved in the initiation of replication, are shared between the plasmid and the bacterial chromosome. For plasmids, which replication is synchronized with the replication of the bacterial chromosome are under stringent control of replication. The stringent control of replication is characteristics of plasmids with low copy number. These plasmids contain DNA regions called par-locuses (from partition) that control the correct division of the plasmids in the two daughter cells.
Plasmids with high copy number are under relaxed control of replication. These plasmids are replicated independently of the replication of the bacterial chromosome. They have individual mechanisms for initiation of replication. The plasmids themselves encode the initiation factors for replication, which are mainly RNA molecules. Once the plasmid replication is initiated, it continues with the same machinery used by the bacterial chromosome.
Reference (Textbook): Bacterial Genetics, Margarita Pesheva (2000)


text:
Is the number of legs in myriapoda determined entirely by the genome?
Myriapoda (comprising, among others, millipedes and centipedes) can have hundreds of legs (Illacme plenipes having up to 750 legs). Interestingly, the number of legs (or leg pairs) appears to differ not only between myriapod species, but even between individuals of the same species:

Body light cream-colored, thread-like, extremely narrow and long (max. width: ♂ 0.55, ♀ 0.64; max. length: ♂ 28.16, ♀ 40.40). Adult individuals with 84 – 192 segments, and with 318 – 750 legs (VMNH paratype ♀ with 192 segments and 750 legs, more than any other organism known on Earth).
Source: "A redescription of the leggiest animal, the millipede Illacme plenipes, with notes on its natural history and biogeography"

This raises the question: Is the number of legs in myriapoda determined entirely by the genome, or do environmental factors play a role in precisely how many legs eventually develop?

Note: Myriapoda generelly hatch with very few legs, and more legs develop during successive moults. Some examples can be found here.

Your question is "How much of the variance in number of legs is explained by genetic variance versus environmental variance?". If needed, you will find here and here some basic information in order to understand the concepts of phenotypic, environmental, genetic variances and the different concepts of heritability.

It seems that this would be fairly easy to test(we have guesses for what they eat) with a small colony of I. plenipes kept under observation. Unfortunately, considering how rare it is, that experiment seems not to have been conducted. It's also possible that I. plenipes simply continues adding legs indefinitely.

Three factors that influence the number of legs are:
1) Sex : In some species of myriapoda, the females have been found to have more leg segments than males (reference) eg: Himantarium gabrielis
2) age

Growth is by adding segments and legs with successive molts
  (anamorphic), and myriapods continue to add additional segments and
  legs after they have reached sexual maturity (reference).

3) Working of a "segmentation clock" (set of genes) that periodically adds segments (reference).


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Does urine therapy really work?
I heard a lecture from a supporter of urine therapy and he claimed that urine is not only good disinfection but also as rich source of minerals. To me, these two advice seemed contradictory.
In addition, the supporter emphasized one should use his own urine - and yet, as an example of the magical effect of urine therapy we got a story of a boy who was hooked by jellyfish but was saved by a nearby doctor who used urine of his own. Apart from that I see no reason why urine should work against toxins better than a water or a disinfection (they don't).
Though, I know a very qualified doctor who advocated this treatment. What do you think?

There are people for both for and against in the case of urinating to cure the pain from jellyfish stings. There is no research supporting the claim though.

I think skeptics.se would be a better relevant for this question. Is that?

@TheLastWord May be it works in exact same mechanism as Vinegre?

This is at best anecdotal evidence. First of all, urine is, although it has been thought otherwise for decades, not sterile. The bacteria in it just don't grow under the conditions used in the lab which are used to proof bladder infections. See these two articles:

Evidence of uncultivated bacteria in the adult female bladder.
Urine is not sterile: use of enhanced urine culture techniques to
detect resident bacterial flora in the adult female bladder.

When you take into account that bacteria grow on almost all surfaces which have a connection to the outside (like mouth, stomach, gut and so on) this is not really surprising that this is true for the bladder as well.
Urine might be a relatively low risk solution of choice to rinse a wound when nothing else is available, but otherwise I wouldn't recommend it.
Then think of what urine is used for: it is the way our body excretes all the water soluble stuff it doesn't need any more. The body makes a lot of effort here to concentrate the primary urine in our kidneys to recover all the stuff which is still needed and to save water. I wouldn't drink it and make my body go through the whole process of excretion again.
About the doctors: is there any hard evidence for that or is this only an anecdote? I get highly skeptical when I hear about such stories.


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Activity of DNA glycosylase
I am wondering how DNA glycosylase works from the chemical point of view. Sometimes in papers I can see that they are doing activity assays with 1M NaOH and I am trying to understand why using 1M NaOH is more factual? Thank you for any help.

DNA glycosylases bind to dsDNA, flip a base out of the base-paired double-helical structure and cleave it off, leaving the sugar-phosphate backbone intact. This base removal renders the DNA susceptible to alkaline cleavage.
In this recent paper:

Miyazono et al. (2014) A sequence-specific DNA glycosylase mediates restriction-modification in Pyrococcus abyssi. Nature Communications 5: #3178

the authors monitor the activity of a DNA glycosylase using this phenomenon: after treating an oligonucleotide with increasing amounts of the enzyme R.PabI they treat the DNA with NaOH so that the oligo is cleaved, allowing detection of the result of enzyme action on a polyacrylamide gel, as you can see from this image, taken from their Figure 3.

Incidentally the same phenomenon is exploited when DNA is transferred to a membrane for Southern blotting. After electrophoresis the gel is soaked in acid which causes depurination (analogous to DNA glycosylase). It is then transferred to an alkaline solution. Although protocols often refer to this as a neutralisation step it actually breaks the DNA at the apurinic sites and separates the strands. This cleavage is important for effective transfer of larger fragments from the gel to the membrane.


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How deep does water have to be so a mosquito can lay viable eggs in it?
I read about this idea for a mosquito trap (with a rather tactless name) where the idea seems to be that because the water available for the mosquito eggs is so shallow, they will die somehow or not be viable. Mosquitos are pretty small though, wouldn't they not need much water for the eggs to hatch?

very little.. even a cup of water is fine for them.. I have seen larvae in the rain water accumulated in old tires as well.  I don't know the exact measure though..

Very litle. The small puddles which are left after big rainfalls or floodings are usually enough.

The main constraint is shallow water will evaporate more quickly. The depth that the larve themselves need is very little.

From own observation: about 1-2 cm is enough to live and hatch.

They can survive fine in 1cm of water, they just stay at the surface and feed from microrganisms, and a mosqito would probably lay viable eggs in 1cm stagnant water if you forced it to in an aquarium, it may even lay in 0.7mm of water, it depends on the species. Mosquitos probably have some way of judging if a water source is stable and if it is likely to evaporate. The larger the body of water, the less it is vulnerable to sudden changes in pH and Temps, aglification, cloudings.

Many mosquitoes, such as Culex quinquefasciatus, lay their eggs on the surface of fresh or stagnant water. The water may be in tin cans, barrels, horse troughs, ornamental ponds, swimming pools, puddles, creeks, ditches, catch basins or marshy areas. Mosquitoes prefer water sheltered from the wind by grass and weeds (reference). There are mosquitoes like Aedes taeniorhyncus (floodwater mosquitoes) which can even lay eggs in moist soil (because the eggs need to dry out before they can hatch) which then waits for the rainy season for hatching. These eggs are capable of surviving through summer, winter and spring to find the right time to hatch (reference). Water is necessary during the life cycle of a mosquito but how much is never an issue. Even the top of some mushrooms can be a place for mosquitoes to lay eggs (reference).

I have them in my property breeding in my containers all the time. From a few inches gets the best results (more mosquitoes) but I’ve gotten colonies in water up to 2-3’ deep.


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What is in Mosquito bites?
I was wondering what is in the mosquito bites, which causes the swelling of the skin at the bite and also the itching. I know that the mosquito injects some stuff, but what is it?

a study on the major allergens in mosquito saliva... http://www.ncbi.nlm.nih.gov/pubmed/21038786

When female mosquitos bite to suck blood, they need to overcome the body reaction against it. So when they found a bood vessel, they inject their saliva into the wound. This saliva contains substances which affect blood clotting and platelet aggregation (so the blood will stay liquid which is essential for sucking) and a vasodilatory substance (which widens the blood vessel and prevents contraction of it). The exact composition depends on the exact mosquito species.
These "foreign" substances cause a local immune reaction which results in the release of histamine in the skin. The itching and also the red skin and the swelling are a result of the histamine release. See the Wikipedia article on mosquitos for more information.
If you are interested in a deeper look on the composition of the mosquito saliva have a look at these two articles and their references (if there is help needed in getting the articles, let me know):

Role of arthropod saliva in blood feeding: sialome and post-sialome
perspectives.
Toward a description of the sialome of the adult female mosquito
Aedes aegypti.

Since the substances affect the blood coagulation cascade, there is some research going on if and how this can be used clinically. See this article for an overview or have a look at the original publication here ("Unique thrombin
inhibition mechanism by anophelin, an anticoagulant from the malaria vector")

So this is comparable to what is used in medicine? Can this be used in medicine?

It is comparable in the way that it keeps the blood from coagulating. Regarding the reasearch, I updated the article.


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How does the counter current mechanism concentrate urine?
The movement of ions like sodium into the interstitial space causes water to passively diffuse out the descending loop of Henle. How does this concentrate the urine? The solvent is removed at one place, and the solute at another. Shouldn't the concentration remain the same? Or does the removal of a little solute remove a lot of solvent? Why?

There are actually two places where water is removed (Descending limb and the Collecting tubules) and only one where solute is expelled(Ascending limb). Does this help? Ask If you want further clarifications.

Have a look at this figure (from here):

In the descending loop the NaCl concentration is lower than in the surrounding tissue which leads to a passive water transport along the gradient, which leads to a concentration effect. In the ascending loop then NaCl is actively transported out of the loop which then prevents the diffusion of water back into the loop.
In the collecting tube water is actively transported out leading to an even higher concentration effect. A nice animation of this can be found here.


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I2D vs STRING for protein-protein interactions
Can someone clearly explain me the differences between STRING and I2D(Interlogous interaction database) ? What does each database do best ? Which database is better for what kinds of studies etc ?

I just looked and it seems I2D use the PPI from 5 organisms to predict interactions in those organisms, which have not yet been experimentally demonstrated, so its interolog PPI prediction tool by design (http://genomebiology.com/content/pdf/gb-2007-8-5-r95.pdf), where as STRING can be used to see what proteins are known to interact with a given protein, and what evidence is present for a particular interaction, which you then get a (confidence like) score.

So I2d is STRING + some interologous interactions without any scoring parameter. Anything wrong in what I just said

Yes, that's essentially correct although STRING is a lot more comprehensive in terms of the number of species it has PPI data for.


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Why the plants are not black but green?
if the evolution makes the species better then why the leaf and trees are not black??
black colour absorbs more ligth than simply the green color so a black plant should make photosinthesis better then why aren't the plants black ?


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Applying saliva to mosquito bites
Is it true that; when you apply your own saliva to a mosquito bite it would stop itching ?

There have been many personal experiences documented where people have experienced relief from itching of mosquito bites on the application of their own saliva to the itchy spot (reference 1, reference 2) It helps to reduce the itching because saliva has been proven to speed up tissue repair and has antibacterial properties. It also provides a moisturising effect on the itchy spot (reference). Salt is also known to provide relief to itching (reference) and the slight salt content of saliva helps in that respect too.

If the skin is broken from scratching, though, it would also be inoculating an open wound with oral bacteria - which can lead to infection.

@DoctorWhom Most of what I found on the advantages of applying saliva to reduce itching is based on personal experiences and I couldn't find any reliable source or research for the same. I wouldn't depend on it as a sure fire cure for itching as such. Of course, in the case of open wounds there definitely is a risk of infection. Might work as a first stage to reduce itching before scratching your skin off.

Agreed - I hadn't heard of it before actually, so it's an interesting concept.  I just wanted to mention infection to go along with the saliva, because a lot of people suck on skin-breaking injuries (and to put a plug in for that, the best thing (even more than antibacterial ointment, which has limited utility and isn't often recommended) is washing it IMMEDIATELY with soap and lots of water).   Our mouths are quite full of life - microorganism life ;)


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How are cyclic hormones characterized?
I have a question regarding the description of a subset of peptide hormones, called cyclic hormones. Two examples of cyclic hormones would be somatostatin and melanin-concentrating hormones. I know the definition is not applied based on observations of oscillations in biologic levels of the hormones, rather, it is applied to the structure. These hormones possess a single disulfide loop, giving them a cyclic (circular) topology.
My question relates to the chemical definition of cyclic in this context. Does the word cyclic imply any chemistry that forms a single loop topology, arising from any kind of chemical bond (e.g., C-C bonds in carbon rings, or S-S bonds in these hormones). Or, does the word cycling only apply to S-S bonds in the context of these hormones?  I have not seen it defined in the literature, and my inclination is that it is more a definition of topology than any specific chemistry.

Cyclic mostly refers to topology and not particularly any bond. Check this. BTW cyclic peptides (including amide linked) can be studied using mass spectrometry.

@WYSIWYG - can mass spec differentiate between the reduced (acyclic) and oxidized (cyclic) forms of somatostatin?

If fragmented then it should but I am not sure how robust the disulphide bond is to the fragmentation procedures. LC should be able to resolve it.

If you look in the results section of this paper on somatostatin-14, they explain that s-14 "is a fourteen residue peptide hormone where Cys$^3$ is disulfide bonded with Cys$^{14}$ to form a cyclic structure.
So your inclination is correct. The structure is cyclic and it is the cyclic structure which is responsible for the terminology. I don't know if there are exactly analogous structures with other than disulfide bonds but they would be cyclic for the same reason.
Another paper at page S1 talks briefly about the linear version of the same hormone, contrasting it with the cyclic form, again confirming that it is the structure that gives rise to the name, and not some other property.
It is the second reference that I think also answers the broader question: 'cyclic' is generic usage to describe a (simple or) complicated molecule containing a cyclic structure of joined atoms. Yet another paper (abstract) talks about cyclic vs. branched in a general way with respect to somatostatin and others:
"The aim of this contribution is to offer an unambiguous and general nomenclature system that enables researchers to represent all cyclic and branched homo- and hetero-detic peptides in a coherent manner in one-line text - as long as their as constituents can be represented in (three)-letter codes."
In this somewhat dated paper containing proposed IUPAC nomenclature for cyclic organic compounds, in cases in which there is a question whether a molecule is cyclic or not the prefix "cyclo-" enters the formal name. But in the title the origin of the issue is clear: "Nomenclature for cyclic organic compounds..." and again confirms that the usage is not based on the elements bonded but the ringlike structure.
There is a paper in which 'heterocyclic' (vs. 'carbocyclic') is used as a subclass of cyclic to refer to rings containing other than carbon. But the term cyclic applies to both.
Finally there is discussion of 'cyclic peptides' (wiki entry) generally which are classified 'according to the types of bonds that comprise the ring.' But they are cyclic because of the circular molecular structure notwithstanding considerable variation in the atoms (or multiplicity of bonds) comprising the ring.
Biochemistry has inherited much nomenclature from organic chemistry, and informal usage in textbook organic chemistry is that ringlike structures are called 'cyclic' whether they are comprised entirely of carbon or contain another element (typically N,O,S, etc.); for example 'cyclic ethers'--oxacyclopentane is a cyclic molecule containing oxygen.


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Plant's phylogeny tree to identify which of them are closer (genetically) with another plant
I'am trying to create a phylogeny tree from some plants, as the post's title says, to help me conclude which of those plants are closer genetically with another one plant.
So let's say that this is the plant list:
Nicotiana tabacum , Zea mays, Oryza sativa, Solanum lycopersicum,    Solanum tuberosum, Erythranthe guttata, Hordeum vulgare, Vitis vinifera, Prunus persica, Glycine max, Populus trichocarpa, Medicago truncatula, Phaseolus vulgaris, Morus notabilis, Citrus clementina, Setaria italica, Theobroma cacao, Acacia mangium, Cicer arietinum, Triticum urartu, Brachypodium distachyon, Aegilops tauschii, Panax ginseng
and i want to see which of those species is closer with Sorghum bicolor.
Is there any easy way to conclude something like that or it needs to get results out of bioinformatics using a specific gene , align it , and then see the tree ?

If you want to compare the relationship, you need to use a gene which is present in all plants you list here and then do a comparision. This will allow you to build such a tree.

Ok. i have took one gene and translated into protein for all these plants. Aligned them and now which algorithm should i use to produce the phylogeny tree ?

Single gene trees are unreliable. You should concatenate and align at least 50 genes, e.g. ribosomal proteins, and then build a tree with e.g. RAxML and PhyloBayes. Be sure to pick an out group wisely too..

In general for plants, before you start trying to make your own phylogeny, you should try to find an existing phylogeny. Phylogenetics is complex, and a lot of people have already done the hard work. You can start by looking at the Angiosperm Phylogeny to figure out which species are most closely related. To make use of the tree you will usually have to look up each species to figure out what order or family it is in.

In this particular case, Sorghum bicolor is a grass, so of course it's going to be closed to Zea, Oryza, Setaria and Brachypodium (all grasses) than any of the others. You can see where it places relative to the other grasses by looking at a grass-specific phylogeny. Because all three are model species, their phylogenetic placement relative to one another is well established. A simple Google image search for [grass model species phylogeny] gives you your answer (from the Setaria genome paper):

This shows you that Sorghum is closest to Zea out of the species you listed.

authors: Мікалас Кaрыбутоў


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Resting and action membrane potential..?
In the resting membrane potential of neurons the inside of membrane is kept negative and outside of membrane is kept positive by the utilization of energy through Na-K Atpase pump, While during action membrane potential through the opening of specific gated ion channels inside of membrane is made positive while outside is made negative, What is the significance of specific charges across the membrane, does these specific charges across the membrane play any role in the passage of neurotransmitters ? or these charges are just arbitrary ?does this can happen that during resting membrane potential the inside will become positive and outside will become negative and vice versa, I want to know that what is the significance of these specific charges across the membrane ..?

I'm not sure how far back your confusion goes.

A membrane potential is defined as the difference in charge across the memb. Do you understand that?
The charge diff is not just the NaK Pump, but leaky K channel. Do you know that?
Have you looked at youtube videos of action potentials leading to neurotransmitter release? What part confuses you?

I m not confused about the points that you have written above, I m clear about these points, I just want to know the significance of These specific charges across the membrane..? That why there is need to maintain negative membrane potential by using Atp..?What is Significance of Negative membrane potential?

Just wanted to point out that the K channel open near the resting potential isn't "leaky". Like all other ion channels, it allows a passive flow of ions so it's not actively pumping but just allowing things to happen. If you like, you can call that "leakage" but then you'd also have the leaky sodium current, leaky calcium current etc. What's more, there are already things called "leak currents" which are currents caused by ions slowly permeating the membrane through other means than the main pump, exchanger or ion channel currents.

I've tried to split this into the answer to three questions:

Why does a membrane potential arise at all?
Why does it happen to be around -80mV
How does the cell use its membrane potential

(1) You've indicated that you know this one already, but I'd still like to point a few things out: The NaK pump not only creates a negative resting potential, it also seriously unbalances the Sodium and Potassium concentrations on each side of the cell. Even without any voltage, diffusion forces would cause an inward sodium current and an outward potassium current if you made holes in the membrane. The NaK pump (and the other active pumps/exchangers) are much slower than the passive currents through ion channels when they open.
(2) The resting potential is a dynamical equilibrium. This means that the potential you end up with is simply the one where all the opposing forces are equal. If you were designing a new cell from scratch you could put it at other values than around -80mV without too much trouble. In the cells we have, there's this region around -80mV where sodium and calcium channels are closed but a particular Potassium channel is wide open. Because there is much more Potassium inside the cell than out, diffusion drives Potassium out of the channel. However, because K+ has a positive charge the negative potential drives the K+ right back in. These two forces are able to balance each other out at around -80mV.
(3) A cell uses its membrane potential in two important ways: Firstly, when you trigger an action potential (AP) in one cell, it almost immediately triggers an AP in its neighbours. This allows rapid communication between neurons in your brain, but also allows for the coordinated contraction of your heart. Secondly, the action potential opens up Calcium channels which let Calcium flow into the cell. The free calcium concentration within a cell acts as a second messenger initiating all sorts of actions. For example, in muscles the increased Calcium triggers a contraction: muscle cells contract during their AP. In neurons, the presence of Ca2+ in a cell strongly increases the release of neurotransmitters.

Answering the question: "Why is a negative membrane potential important?"
I don't think cells have strong feelings about being slightly negative inside its membrane. I'm guessing these are the driving factors:

the cell membrane is nonpolar, so charged particles can only pass via transport proteins. This makes ion gradients an easy way to maintain a source of (literally, in the physics sense) potential energy.
the cell needs to control its environment and send signals to other cells. The particle gradient (sodium, for example), allows it to accomplish these tasks: bring in glucose by co-transporting with sodium, send an action potential by triggering voltage-gated ion channels.
Therefore, the Na/K pump is a way to "charge" the ability of the cell to perform various types of work in the future.

To risk an analogy, a cell having a membrane potential is like you charging your cell in the morning. You aren't quite sure what exactly you'll be doing with your phone all day, but it will be many different tasks and all will be doable because you've got a controlled energy source.


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Is it possible to combine live attenuated and non-live vaccines?
There are many combination vaccines available but I've noticed that there don't seem to be any with both live and non-live components, e.g. DTaP/IPV/MMR. Such combinations could be useful in some cases, since most developed countries give a second dose of MMR (or MMRV) at the same time as DTaP/IPV. Is there a biological reason that this is difficult?

by live, do you mean attenuated vaccines?

@The Last Word: Yes

typically the manufacture and storage of live (attenuated) and inactive (killed, dead, kaput) vaccines is rather different, and the effective shelf lives can vary significantly. For example, inactive vaccines often have preservatives in them, which may be incompatible with live viruses. A killed vaccine may be stored at room temp, while an attenuated one may require refrigeration.

+1 It's not actually difficult, it's more a question of practicality (when the vaccinations are given), and which vaccines actually work (live attenuated almost always elicits a stronger immune response, but can have more complications).  Working on a detailed answer now.

I'll make the comments into one nice answer.

@Chris thanks for that.  Sorry I went AWOL.  Turns out I had to have surgery on myself for once.  Truncated the answer I was going to write to what's below.

@AtlLED I hope you are fine. I was browsing through unanswered questions....

First let me point out that for the US, I'm not knowledgeable enough to speak for the rest of the world, you are correct.

There are no approved live attenuated vaccines mixed with componet/subunit/inactivated vaccines.

Background:
Before we go into why that's true, let's work a little to show that's true.  The FDA publishes a wonderful list of every approved vaccine for use in the US.  Of the 78 vaccines listed (and there is a lot of redundancy due to different manufacturers etc), only 16 are live attenuated (or about 20%).
Another thing to notice is that we have vaccines to both viruses and bacteria.   Technically, some of the vaccines are to bacterial toxins, not bacteria themselves, but for the sake of simplicity, we're going to group all bacterial component, subunit, and inactivated vaccine preparations together in one group.
First you will note that there is only one live attenuated vaccine for bacteria, Mycobacterium bovis (more on this exception later).  There are several reasons for this, but as a general rule, you don't want to put a foreign object capable of self replication inside a person.  Viruses cannot self replicate, they are obligate parasites by definition, so they don't fall under this rule.  One could, however engineer bacteria that were sufficiently deficient in replication that this might not be an issue.  Another safety concern with live attenuated bacteria is sepsis.  Again by choosing a delivery route that doesn't involve injections, you might be able to mitigate this risk.
I also want to be clear that I think live attenuated bacterial/fungal (yeast mostly) vaccines can work more broadly, and are likely to be used in innovative vaccine strategies.
The main obstacle to a live attenuated bacteria vaccine is that the component and subunit vaccines work.  Sometimes they work even better by only supply the part of an organism that is known to provide broad neutralization (getting rid of) of the pathogen.  And if you know that you can provide protection with out the risk of putting the live organism in a person, why would you take that risk?
Quite simply you don't.  Back to M. bovis.  For the most part, humans are not vaccinated with M. bovis (BCG) to prevent M. Bovis infection (though zoonotic infections can occur).  Instead it is to prevent M. tuberculosis (MTB) infection.  Attenuation of MTB is difficult, and not complete.  Indeed we don't have a subunit or component vaccine that has worked for MTB, and an inactivated MTB has more safety concerns than BCG.  Thus we choose a related organism, M. Bovis, which naturally doesn't cause disease in humans (or rarely), but can provide some protection against TB.  Even the product insert admits that efficacy of the vaccine is in question.
The same pattern of necessity holds true for viral live attenuated vaccines.  They are used when you need a more immunogenic vaccine, and where we haven't been able to make safe and effective, inactivated, subunit, or VLP vaccines.  Thus when you need a live attenuated vaccine, you really do need it to be alive for it work.

Answering the core question:
As @MattDMo pointed out, the storage conditions are very different for live attenuated vaccines.  Not only that, but most of the preservatives used in many inactivated vaccines cause titer loss (though there is work to find alternatives).
On the theory that a picture is worth a thousand words, I did a little experiment just for this post (and also I was cleaning out an -80).  I took a high titer stock of measles virus that has a protein tag on one of the proteins so we can easily detect it (F is Flag tagged).  Then I spiked 3 different tubes of virus in ether PBS (saline) or DTaP (an actual dose, just past expiration), and left them in the refrigerator (4oC) for 8h.  Note that Merk thinks you should toss the measles vaccine if you don't use it within 8/hours (also note their comment on preservatives).  Then I infected some cells that grow up measles, and harvested the cells in a total cell lysate.  Finally I ran equal amounts of total protein form each preparation on a gel for a western blot:

You should notice the three pairs of bands, in each case the lighter band (indicating less protein) belongs to the DTaP group.  That is to say less measles F protein (something you want to make antibodies to) came from the samples that were put into the DTaP vaccine compared to PBS.
Another serious problem is cold chain:
Again we need the virus to be "alive" when we give a person a vaccine.  This almost always means that we have to keep it frozen or at least refrigerated from the manufacturer, all the way up until moments before it goes into a person's arm.  There are many good reviews on cold chain to be found.  Quite simply, inactivated and component vaccines do not have the thermo-stability requirements that live vaccines do.  It would be a waste of energy in most cases to chill all of the vaccines which could be left at room temperature, and it would remove one of their clear advantages.
As far as the immunology is concerned, there is probably not a real limit on what the body can react to.  Indeed, as you point out, they are often administered at the same time in developed countries.  It is merely a question of how you can keep live-attenuated vaccines "alive" in the same preparation.  It is certainly possible that there is a solution to this, and vaccine stability is an active field of research.  Hopefully in 10-20 years we will be able to adjust this answer to say that such a vaccine has been made, and that it's safe enough for approval.

It would be interesting to see, how these mixed vaccines perform in tests.

The major reason for this are differences in the preparation methods. Live (attenuated) vaccines need permanent cooling, which makes their use in third world countries difficult.
Inactivated vaccines are inactivated either by heat, radiation of chemicals and are often freeze-dried after purification (removal of chemicals used for killing). In this condition, they have a very long shelf-life and need no cooling. Before use they are dissolved in water and then administered.
There is another problem with mixing these vaccines: Live vaccines can not be given to anybody, people which have a weakened immune system (because of an infection like HIV, chemotherapy or the adimistration of drugs, which downregulate the immune system after an organ transplantation) are not able to receive them. The attenuated pathogen which replicates usually only slowly would still be a possible danger for these people. So they can still be vaccinated with inactivated vaccines to provide at least some protection.
For more information on this topic see the chapter on immunization in "Microbiology and Immunology online" and this information from the National Institute of Health.


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Identify this large exotic bird spotted in Taipei, Taiwan
A few months ago while backpacking in Taipei I found this very intriguing large bird facing off a curious puppy in a fairly busy pedestrian area.
The bird did not attempt to fly. None of the Taiwanese locals could tell me what it was and attempts to Google it via description all failed.
I'd appreciate learning the species name, common name in English, and/or common name in Chinese:

For me it looks like a Malayan Night Heron, Gorsachius melanolophus.
They seems to be common in this part of Asia, see the distribution.
It looks strange because he probably get scared.

It seems to resemble the birds in this photo online. It's labelled "黑冠麻鷺", which seems to be the Chinese translation for "Malayan night heron".


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Protein structures given in PDB and SNP's
There are millions of proteins given in PDB, the sequence for which we can download in FASTA format. There are also hundreds of SNP's given in NCBI dbSNP. My question is whether the proteins in PDB incorporate the SNP's into their structure? If not, is there a way to visualize protein structure using any tool after a SNP on the protein? I know that tools like SIFT exist but they only say whether or not a SNP is harmful or not. They don't comment on the structure of the protein in anyway.

its not a given that you can look at a protein structure and tell whether a mutation is going to change the properties of the gene.

There's only about 100 000 deposites in PDB - everything other one need to simulate and there are lots of tools to do this.

Swiss PDB Viewer allows you to mutate residues in an existing structure and explore the effects.
I'm pretty sure that UCSF Chimera does too.

Solving the 3D structure of a protein is hard and a lot of work, doing that for every common SNP of a protein would be excessive in most cases. So you generally won't find such structures unless the structure of the specific mutated version is particularly interesting.
In many cases it is also not structurally interesting what happens, there is no point in trying to get the 3D structure if an SNP leads to a frameshift or an early stop codon.
What you can do is simply load the PDB structure of the wildtype protein into a viewer like PyMol and look at the amino acid that is changes by the SNP. Read the associated paper to find out if that residue is important in some way. This won't be always possible, but if e.g. the amino acid is in the catalytic center of an enzyme, this would explain how the SNP affect the function of the protein.

check out the sequence page at RCSB PDB, it can show SNPs mapped onto 3D for some of the proteins (you need to enable the SNP annotations in the drop-down)
http://www.rcsb.org/pdb/explore/remediatedSequence.do?params.showJmol=true&structureId=4HHB


text:
Is the default kmer 25 value in Trinity still ok for assembly of 150bp reads from Illumina HiSeq 2500?
I will soon be receiving Illumina HiSeq 2500 data (150bp PE stranded reads). In the past we have been using Trinity as our assembler of choice, but it uses a default kmer value of 25. I believe this may have been optimal for GAIIx data (35bp) but is it still ok to use such a kmer for 150bp data?
All inputs will be greatly appreciated!
Thanks!

what sequencing are you doing- WGS/RNAseq/... ?

I am doing RNA-seq of multiplexed samples in order to determine differential expression between different samples

I have't used trinity.. I use cufflinks and for longer reads (>50nt) this is not really necessary (by default off in cufflinks for reads >50nt)..

As far as I know, Tophat-cufflinks require a reference, don't they? I am working on a non-model organism so will be doing de novo assembly, hence the use of Trinity. What do you mean is not necessary?

Oh okay.. In that case I cant say. I have some acquaintance with velvet but not trinity. In tophat (I am sorry I said cufflinks) that is used for enhanced prediction for splice junctions.
For de-novo assembly the choice of k-mers should be such that it maximizes your N50 but does't consume a lot of resources. You can see this post

Thanks for the link and your explanation. Yes, resources and N50 maximisation are definitely factors to consider, though probably not the only one. Using only a single kmer value Trinity may be a bit less greedy in resources, making it attractive to use whereas velvet is known to require lots of RAM, hence my initial question ;-)


text:
What does "thermodynamic equilibrium" mean for an enzyme-substrate complex?
From Fersht, Enzyme Structure and Mechanism p. 87:

The Michaelis-Menten mechanism assumes that the enzyme-substrate
  complex is in thermodynamic equilibrium with free enzyme and
  substrate.

In my understanding what this means is that the (E-, S- and ES-concentration dependent) rates of association and dissociation have equated.
So we're kind of in this situation:

where "product" would be referring to [ES] and "reactant" to [E] and [S]. Does that make sense?

Product is still $P$; $ES$ is the transient Enzyme-Substrate complex. If you mean product in the sense of product of a reaction then yes but it is a confusing usage. So stick to calling $ES$ as a transient state

@tmottm Can you please accept answers, which answer your question satisfactory? This is a nice gesture towards the people who write the answers. You can find all your questions in your User menu.

Thermodynamic equilibrium means that:
Rate of forward reaction = Rate of backward reaction
In this case:
$E + S\xrightleftharpoons[k2]{k1} ES\\ \ \\
 \ \\ \\ at\ equilibrium:\\ \  \ \\ \ k1.[E][S] \tiny{\ (forward\ rate)}\normalsize=  k2.[ES] \tiny\ (backward\ rate)
$
This was the initial assumption in the Michaelis-Menten model.
Later on this was improvised by assuming pseudo-steady state of ES complex. This means that $[ES]$ does not change over time, which is both as a result of its production by the reversible reaction:  $E + S \leftrightharpoons\ ES$ and consumption by the irreversible reaction $\ ES\ \xrightarrow{k3} E+P$
that is:
$k1[E][S]\tiny\ (production)\normalsize=(k2+k3)[ES]\tiny\ (consumption)$


text:
Religion and Genetics
Are there studies that investigate the heritability of "believing in supernatural" (or related concepts)?

the perception of paranormal perception can be due to some brain development disorders. (At least I know that they arise because of lesions in certain areas). In such cases if there is a gene involved, these traits may be heritable.

sorry the perception got repeated.. another sort of impairment of brain function :P

How do you define a measurable scale for believing in supernatural things?

Oh there are some tests for self transcendence.. not for religious beliefs though..

This is an interesting idea, I'll just watch and see what happens with it!

See this related CogSci question, but the answer cites the same references as below.

There are several twin studies showing, that the tendency to be religious has a genetic component. Not which religion you choose, because that is a cultural thing, but how serious you are abot it. I am lazy for a detailed report, but this blog can lead you to the studies: http://www.scilogs.eu/en/blog/biology-of-religion/2011-03-12/religiosity-genes-again-confirmed-by-another-twin-study
Also this article: http://www.popsci.com/science/article/2013-08/what-twins-reveal-about-god-gene
EDIT after a few years - I was informed one link is broken and the other contains no citation. So I checked for new material today and wikipedia has a cool passage how genes and environment affect religion. Wikipedia saves the old version, so this is from March 8 2018, article Religiosity.
"
The contributions of genes and environment to religiosity have been quantified in studies of twins (Bouchard et al., 1999; Kirk et al., 1999) and sociological studies of welfare, availability, and legal regulations [15] (state religions, etc.).
Koenig et al. (2005) report that the contribution of genes to variation in religiosity (called heritability) increases from 12% to 44% and the contribution of shared (family) effects decreases from 56% to 18% between adolescence and adulthood.[16] "
15 Nolan, P., & Lenski, G. E. (2010). Human societies: Introduction to macrosociology. Boulder, CO: Paradigm Publisher.
16 L. B. Koenig, M. McGue, R. F. Krueger and T. J. Bouchard, Jr. (2005). Genetic and environmental influences on religiousness: findings for retrospective and current religiousness ratings. Journal of Personality, 73, 471-88
https://en.m.wikipedia.org/wiki/Religiosity#Genes_and_environment

Sadly the first link is now broken (and the second link does not contain any reference to peer-reviewed paper). This is a common issue with referring to popular science articles.

You updated your question shortly after I updated my answer. Did you feel misunderstood by my update ?


text:
Transportation of bacteria
I would like to take an apparatus containing bacteria to another country (Bolivia) from the U.S.. How do I determine whether I am allowed to do this?
The bacteria are:
http://www.atcc.org/Products/All/49787.aspx,
http://www.atcc.org/Products/All/53774.aspx,
http://www.atcc.org/Products/All/51573.aspx,
http://www.atcc.org/Products/All/700550.aspx
Also... What is the best way of transporting bacteria from one country to another?

there are some regulations w.r.t pathogenic strains.. you have to get a certificate issued that says that the sample that you are carrying is non-pathogenic non-hazardous etc

@WYSIWYG Can you give me the contact information of someone who could help me with that?

it depends on the laws of different governments. Ask someone in the customs.

Please go through this link http://www.dehs.umn.edu/bio_pracprin_std_ship_guide.htm and this pdf ( www.ncsu.edu/ehs/dot/Bio_shipping.pdf ). Since all of the microbes are Biosafety level 1, you shouldn't have much problems.

@okarin  That's actually bad advise.  I would actually recommend that you ship them ahead of yourself.  Not al microbes are Biosafety level 1, and their BSL level is not actually what is considered (risk level by CDC in the US, IATA has set standards as well).  You need to determine if your bacteria are UN2814, UN2900, or UN3373.  IF they are not pathogenic (not just to humans, but animals) but are GMO then they will be UN3245. Remember dry ice by itself is considered a hazardous material.  Post specifically what you're moving and I'll give you an answer.

@TheLastWord That's a good link to what needs to be covered, but your later comment is not entirely correct, and might cause confusion as BSL is not directly correlated with Risk Group Classification

@AtlLED What do you mean by post specifically what you're moving? Is there information that you need other than the names of the bacteria?

@okarin names of the bacteria, are they GMO (transformed with a plasmid counts unfortunately), the transport media, and transport temp.  Ie. NEB 10b's transformed with HIV-env in a glycerol stock transported on dry-ice.


text:
Tap vs. mineral water for drinking
I was told a human should drink a small glass (0,3 liter) of mineral water per day to get the minerals. What is the rationale behind this? What is the difference between tap water and mineral water in terms of nutrition facts and effects on human health?
Values for tap water in my area:

How good are the values regarding nutrition facts?

it all depends on where you live and how your neighborhood water supply is..

You physician is the best one to answer questions about the rationale behind this recommendation.

We spent all but the last few thousand years or so of our evolutionary history exclusively drinking mineral water so it is reasonable to suspect there may be things that benefit us in naturally-occurring, mineral-laden water. If you live in the US there is also a lot of discussion about the health effects of chlorine in tap water as it may be a carcinogen and have a lot of other possible bad effects. I could also write a book about the tremendous amount of incompetency I have witnessed surrounding the management of public drinking water. I try to consume tap water in moderation.

@Kozuch I propose you change this question to discuss about necessary minerals and their role with necessary hormones in human body. The only necessary hormones are Insulin (glucose), Parathyroid hormone (calcium) and aldosterone (Na ad K). Pay attention to Calcium especially. Please, see this http://ajcn.nutrition.org/content/71/4/999.full

The mineral content in tap water differs from area to area as well as the source. The mineral content in bottled water is regulated by the companies that manufacture them, in particular the Mg and Ca content(reference).

Death rates tend to be lower in areas with tap water containing higher
  levels of Ca and Mg. It has been shown that deficiencies in magnesium
  are capable of producing heart disturbances, including 215,000 fatal
  heart attacks in the U.S. each year, and as many as 20,000,000 fatal
  heart attacks worldwide (reference).

Different brands of bottled water will differ in their mineral content as well (reference). The place where you stay might be lacking in a particular mineral that your body requires which is why your doctor has specified the use of a particular brand of mineral water.

The main minerals in tap water are calcium and magnesium, which determine the hardness of water. The main minerals in mineral waters are calcium, magnesium, sodium, chloride, carbonate and sulfate. Tap water from different regions and various brands of mineral water can contain very different amounts of minerals, so it is impossible to make a general recommendation to drink more mineral water.
Mineral water high in calcium or magnesium can be a good source of calcium and magnesium for people who do not get enough calcium from foods. Foods are much better source of calcium and magnesium than water, though.
Researchers from the World Health Organization (WHO) claim that water hardness (calcium and magnesium content) has no effects on health (positive or negative).
Foods high in calcium, beneficial and harmful effects of calcium and references to claims I made:
http://www.nutrientsreview.com/minerals/calcium-ca.html
Calcium concentration in bottled and mineral waters (US, Europe):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2488164/table/Tab2/

Agreed, if foods high in calcium and magnesium are touted as "super foods" then it is illogical to reprimand water for the same thing. its all going in the same place lol


text:
Are Lambic beers the product of quorum sensing?
Lambic beers are a Belgian specialty which is still made by open-air "inoculation" by airborne microbiota first, followed by additional yeasts, LAB bacteria and more joining in at the time of transferring to used wine barrels. (No yeast is "pitched" or added intentionally.)  As many as 200 organisms may play a role, and they seem to take turns, partly regulated by rising acidity and alcohol probably, but with some such as Brettanomyces seeming to simply wait their turn compared to what they will do in a single strain fermentation.
Lambic (or American Coolship Ale hereabouts) fementations can take up to 3 years.  Often a thick fluffy "pellicle" or "film" forms on the top of the barrel, like "flor" on sherry, evidently in response to and protection from oxygen. (Sure seems like a bio film.)
(There have been a few studies tracking the staggered blooms of various organisms, including one done 2 years ago at Allagash and one this year at Cantillon, but no discussion about how the sequence is orchestrated. So this is a speculative question about the evolution of these beers.)
Could interspecies quorum sensing be at work?    How could that be confirmed?

First it is important to identify the species that co-habit the fermenting malt.

That's the part that's been done. (The numbers of different yeasts and bacteria are high.Each fermentation allows wind borne contributions and differing communities in second use barrels, so there are differences between batches.) Actually, I just thought of something from watching a Bonnie Basler video: Could anything be learned by looking for one of the sensing molecules? And found a paper about Acyl homoserine lactones found on surfaces in a modern brewery not trying for ambient brewing. I so want to state that these fermentations are timed by Quorum Sensing. Almost certainly, right?

can you add that information. What are these microbes?

ok, two studies.  The newest one, which I am struggling to grasp, is http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3991685/

That Belgian study showed "diverse members of the Enterobacteriaceae" (month 1), Saccharomyces cerevisiae and S. pastorianus (mos 1-3) then Saccharomyces spp. decreases and Pediococcus damnosus increases from 3 mos, followed by highly acid- and ethanol-resistant Dekkera bruxellensis, (aka Brett) which dominated from 6 mos onwards together with P. damnosus. (plus N. castellii, Hanseniaspora spp, Kazachstania spp, Acetobacter spp, Etc.)
The earlier study, from the US: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3329477/

Almost certainly not. Species occupy different niches due to their differing growth rates and tolerances. Interspecies quorum sensing and the symbiotic relationship that implies do exist(see: lichen), but open-air inoculation is unlikely to produce them.
Why would the Brettanomyces simply kill time waiting for 'their turn'? It's likely they don't grow as fast as S. cervisiae or other early fermenters, and as a result they're outcompeted until alcohol content rises enough to slow or stop other species. Brettanomyces isn't 'waiting', they're eating and growing as fast as they possibly can.
Many microorganisms form spores or simply hibernate until conditions are favorable for growth. For highly acid and alcohol-tolerant species, perhaps they sporulate until the mix is acidic enough to guarantee them habitat. This is a form of quorum sensing, but the transmission medium is pH and alcohol concentration.


text:
What is the fastest but not venomous snake?
Is it known which non-venomous snake can attack most quickly? I guess it is a snake that attacks its opponent by bites, and not some kind of constrictor.

black mamba (?)

@WYSIWYG Its venomous.

ohh okay.. I missed it... sorry..

The fastest non venomous snake is arguably the Eastern Coachwhip with a top speed of upto 10 mph (reference). If it feels cornered, it will attack with bites but otherwise, it prefers to flee.


text:
Why are there no tree-like plants that grow in lakes?
Looking at aerial photos of boreal forests, with dense woods clear-cut by quiet lakes, I wondered why exactly are the woods so clear-cut at the edge of water? Why won't trees develop adaptations that will let them grow from a shallow lake bottom, with the lower part of the trunk in the water and the crown above the water?
It seems to me that this would give them some significant advantages. Lake bottoms are rich in organic nutrition, and insolation will also be plentiful above water, at least at first when there's little competition. So why are lakes' surfaces so clear and open, instead of overgrown? Of course there are aquatic and semi-aquatic plants like water lilies, Scirpus or Typha, but they are a far cry from the nearby terrestrial forests, in terms of biomass. Why don't they develop into large amphibian trees, or why don't terrestrial trees try to re-colonize lakes?

Just a guess really, but maybe for whatever reason they can't outcompete aquatic plants.

Mangroves grow in the water...

@MattDMo Think he is talking about boreal forests while  Mangroves belong to the tropics

http://www.mangrove.at/images/mangrove/forests/overwashed/overwashed%20mangrove%20community.jpg

Up in cooler areas, I bet that when winter rolls around and freezes the water, the ice would crush any plants coming through it. I suppose the plant could drain it's sap like a deciduous tree but even so the vascular system could still be crushed. The first years when the tree isn't very thick could spell it's demise. It would be easier to crush when it's so small. My 2c.

I remember seeing a documentary (David Attenborough perhaps?) that showed a particular plant where part of the plant grows underwater and part grows above water (i.e. not just floating on the surface). The stem is strong enough to support the weight of the plant above water and the airborne leaves are radically different from the aqueous leaves. Still, it is not big enough to be called a tree.

Trees need:

Deep roots to get more water and anchor their growth.
Strong trunks to support themselves against gravity.
A vascular system to move water and nutrients throughout the tree.
Small leaves that can be supported high by the trunk to compete for sunlight.

Water plants need:

Just enough root to anchor its location.
No vascular system. Water is everywhere.
Leaves that are more substantial than the stems to gather as much sunlight as possible through the cover of water.

So the kind of body that has to develop under water to thrive is in many ways the opposite of the kind of body needed to thrive on land.
Water plants would have to waste energy on

Vast roots.
A strong trunk.
A vascular system.

...Things it wouldn't need till later while receiving little sunlight on small leaves. It would have to shed its thirsty skin like a snake on the above water parts. Too complex and little or no demand for it.

If water plants had evolved a way to turn oxygen into helium and keep much of it trapped within its leaves, then we'd have tall ocean forests. The plants could grow just like they do now  but with slightly fluffy leaves. As soon as it broke water surface, the abundance of oxygen would ramp up helium production and really fluff them leaves. The slight stems would have to be scrappy instead of massive.
There would be Greek mythology that Gaia was married to Helios but left him for Poseidon the Gaia-Shaker. Poseidon and Gaia were cursed with children (the vast ocean forests) who rebel against them and adopt a lifestyle where they are always reaching out to Helios and later in life shedd their bodies to be closer to him in spirit. Some early humans tried to rob the Helium spirits of the ocean forests by inhailing them out of their plant bodies. They were cursed and turned into chipmunks with only their hands to remind them of their past humanity.

Edit to add reference: A piece by Mickey Walburg on eHow.com
Though I would call mangroves amphibian trees, I wouldn't call them large and I was trying to ascertain the spirit of what @kai teorn was asking rather than let the question sit unanswered when I believe I can answer it.
You learn something new often if you're looking and today @MattDMo introduced mangroves into my awareness. If he thought it was the answer to the spirit of the question post, he might have elaborated on it as an answer instead of a comment. I could be wrong about that.
Mangroves are mostly coastal. They are usually at the edges of the water. The ones that are a few meters in the water are usually more like shrubs than majestic boreal forest trees. They end up shooting roots everywhere and kinda lounge around compared to the typical tree standing straight reaching for the sun. Also the incidences of Mangroves in the ocean away from the shoreline are of maybe a handful bunched up, hardly a species wide return to the the oceans. Seen from aerial photos, Mangrove concentrations look like boreal forests surrounding lakes, not swamp lands.

Why are there no tree-like plants that grow in lakes?
Looking at aerial photos of boreal forests, with dense woods clear-cut
  by quiet lakes, I wondered why exactly are the woods so clear-cut at
  the edge of water?

I think the spirit of the next question is about trees in general in lakes. Not the few instances peppered around the world. Also some lakes grow and shrink throughout time, sometimes long enough for trees to gain a little ground and survive lake growth. But I don't think those trees as a species have developed adaptations to grow from shallow lake bottoms.

Why won't trees develop adaptations that will let them grow from a
  shallow lake bottom, with the lower part of the trunk in the water and
  the crown above the water?

... and from the end of the post ...

Of course there are aquatic and semi-aquatic plants like water lilies,
  Scirpus or Typha, but they are a far cry from the nearby terrestrial
  forests, in terms of biomass. Why don't they develop into large
  amphibian trees, or why don't terrestrial trees try to re-colonize
  lakes?

... I eliminated mangroves from qualification. Interesting but I still don't think it's what @kai teorn had in mind. I think @MattDMo introduced mangroves as a comment to enhance our knowledge.

Please consider adding references. I dont think u can generalize trees that way as one of the comments do mention that mangroves send roots in water

For boreal forests, lake freezing is probably also hindering mangrove-like growth: freezing may be resisted if you're wholly out or wholly in the water, if crossing the air/water interface then there's much more danger of mechanical damage to a plant.

The question of "why are there no/few aquatic trees?" can be approached in two ways.

Why are land trees tall?
Is it harder to be tall in a lake?

Land trees are tall to shade competitors and spread their seeds and fruits. To get tall, they need extensive root structures to anchor and provide enough water to the trunk. If there are no competitors to shade out and the water provides long-distance seed dispersal, why bother growing tall?
It's much harder to be tall in a lake. Nutrient uptake is a problem, as is proper anchoring. Large amounts of organic biomass may exist, but iron, phosphorus, and other micronutrients are more important. A large oak can be 15 tons, which is harder to support using only sediment on the lakebed. It's also understandably difficult to germinate and sprout if you're an aquatic tree. See mangrove propagules for an example of the problems and how to get around them(sort of). Most mangrove species need lenticels in the trunk to provide enough oxygen, and long roots require periodic pneumatophores to provide oxygen to the roots.
Looking at all the pressures on plant life in lakes, it's a lot of work to be a tree, and much easier to be a lilypad. More of the biomass can be concentrated on photosynthesis, and structural concerns are a lot less troublesome. Additionally, many lakes simply do not have the nitrogen or phosphorus content to support tree-sized growth. See trophic state index in lakes. If the lake can't support algae, there's no way it can support a tree.

Cypress swamps are an example of tree like plants in lakes. There is even a lake in Louisiana called  Cypress Lake


text:
Is the tomato a very very close relative of the pepper?
I ask because if you look at a tomato, the way it grows on a vine, its color, the texture, and make up of its skin and internal structure it seems very much like a pepper.  The only thing I can think it lacks that a pepper has is any amount of spice.  I wouldn't be surprised to learn that it has trace amounts of capsaicin.

There are different unrelated plants called "pepper" in English. Black pepper (species of the Piper genus), as indicated by Chris, is not related to tomato and doesn't "look alike".
I guess the OP meant actually a different plant (Capsicum genus), to which the common bell pepper (Capsicum annuum) belongs. This one is similar to tomato and they both belong to Solanaceae, the same subfamily Solanoideae, but different tribes: tomato is classified in Solaneae and Capsicum in Capsiceae.
In this study you can see, how distant phylogenetically the two genera are. Currently accepted classification generally reflects phylogeny, and there are three more tribes that are closer to Capsiceae, to which Solaneae is nevertheless a close relative.
The most striking morphological difference between Capsicum and Solanum is that the first one is characterized by hollow fruits, while tomato and other Solanum species have fleshy berry-like fruits.
EDIT: It's actually not a difficult task for one's imagination to see that the two types of fruit are structurally very similar. In reality a pepper-structured tomato cultivar is known, and even quantitative trait loci underlying this morphological trait were already found.

They are not related, both plants belong to different taxonomic orders:
Pepper belongs to:

Order: Piperales
Family: Piperaceae
Genus: Piper

Tomatoes belong to the

Order: Solanales
Family: Solanaceae
Genus: Solanum

If you look at Capsicum (as MattDmo suggested) then this is different. These peppers belong to the same order (solanales) and family (solanaceae) as tomatoes. They form a different tribe (Capsiceae).
Wikipedia states on this:

The name "pepper" came into use because of their similar flavour to the condiment black >pepper, Piper nigrum, although there is no botanical relationship with this plant, or >with Sichuan pepper.

I think OP is referring to Capsicum sp., not black pepper...


text:
Difference between flexion and contraction?
i asked this to my anatomy teacher and he said there is no difference but when it comes to specialy in body building when you say to flex their bicep they freeze their upper limb in order to do that but when you say contract your bicep they only isolate it an shortens it.
am I right with my reason?

Flexion: the movement that decreases the angle between two parts [1]. Examples: clenching the hand into fist, sitting down.
Contraction: the property of muscle to generate tension when actin and myosin filaments are crossing. There are a few types of contractions. The isometric contraction is when the muscle generates tension but its length doesn't change (for example when you try to lift something that you can't). The isotonic contraction is when the muscle changes its length [2]. This kind of contraction leads to movements and can lead to flexion too.

References:

Wikipedia contributors, "Anatomical terms of motion," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Anatomical_terms_of_motion&oldid=612679254 (accessed June 26, 2014).
Wikipedia contributors, "Muscle contraction," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Muscle_contraction&oldid=609265714 (accessed June 26, 2014).