text:
What are the pros and cons of eating earth (soil)?
I wonder if there are any benefits to eat earth. What I mean by earth is the topsoil that is sometimes on vegetable (I eat organic vegetables and some of them like spinach are full of topsoil).
I found this article (a study about why people, in certain culture, eat earth) but it doesn't clearly answer my question as it's about clay and not topsoil. Topsoil has a highest concentration of organic matter than clay.
I wonder if we can digest the soil nutrient (Phosphorus, Potassium, Calcium, Magnesium, Manganese, Zinc, Copper) just as we would if there were coming from vegetable and fruits.
What are the other pros and cons of eating earth (soil)? (I am aware of the cons about parasite and bacteria but my question is not about these risks. It's about nutritive value of earth.)

The article (a PDF can be found here) suggests that this happens neither for feeding reasons (to get your belly filled, when anything else is available) nor that this is done for supplemental reasons.
They suggest that this happens more for protective reasons. In the abstract they write:

Our results indicate that human geophagy is best explained as
  providing protection from dietary chemicals, parasites, and pathogens,
  whereas animal geophagy may involve both micronutrient acquisition and
  protection.

In the paper they give a few examples for this. First the earth eaten is usually digged up from deeper layers of the ground and sometimes even cooked. Then they bring in the example of people, which eat soil, when they have gastrointestinal problems as a kind of medicine to calm down the problems.
In my opinion there is not much nutritional value in eating soil. Organic compounds can usually not be metabolized (for example we don't have the possibility to break down cellulose). I am not sure, if we can get minerals from clay into our body, since a lot of them is present in soil as unsoluble minerals.

Thanks a lot Chris! You wrote "I am not sure, if we can get minerals from clay into our body, since a lot of them is present in soil as unsoluble minerals." Is it the same for topsoil ? Are its minerals also present as unsoluble minerals ?

In the topsoil probably not (though I haven't found any data on that yet) since a lot of the minerals is set free from organic matter. But it also gets washed away with rain if it is soluble.

A/ stronger immune system. children without soil environments are weaker, and the immune memory doesn't last forever across the decades, so it's good for adults too.
http://www.npr.org/sections/health-shots/2017/07/16/537075018/dirt-is-good-why-kids-need-exposure-to-germs
B/ Stronger bones and nerves and mineral content. We get calcium from milk, according to our culture, which is stupid because, if you have a soft water source or rain, milk is more harmful for adults that water treated with clay/chalk etc. Magnesium is important to nerves and it's one of the biggest mineral defficiencies in people. the main mineral that doesn't dissolve well is Silicon Si (same reason why there wouldnt be silicon based life in a water soluble animal). If you eat chalky clay, your body can dissolve it with the HCL ann digestive acids, and get many times more calcium than from milk. the body contains 1.2 kilos of calcium. crystals with lattice energy dissolve less easily than less structured stones, permeability helps a lot to dissolve stones/sands, so small particles like clays release a lot more minerals in water than rocks and sands do.
C/ better digestion. If you leave a bit of soil microbiota on your potatoes, and make a soup, and let that soup ferment for a few hours, you will have many times more microbiota in your gut that can eat potatos, than if the potatos were totally washed of soil. https://www.thecandidadiet.com/soil-based-organisms/


text:
What does this sentence about toxemia and Clostridium tetani mean?
I know that Cl tetani is not invasive and strictly localised.
I think toxemia means spread in the blood.
I am thinking this sentence

The volume of infected tissue is small, and the disease is almost entirely a toxemia.

Cl tetani has spores.
This suggests me that these spores spread through blood.
They then open and become pathogenic in some tissues where they remain strictly locally (so small area/volume of infected tissue; I think area is better word, since the disease is not invasive) and pathogenic.
How do you understand the quoted sentence about pathogenesis of Cl tetani?

Clostridium tetani produces a protein toxin, tetanospasmin which causes the major symptom of tetanus, namely involuntary muscle spasms. C. tetani is an aerobic species, does not infect the blood, and apparently only produces toxin in anaerobic conditions.
If a pathogenic bacterium propagates through the bloodstream this condition is referred to as bacteraemia. In the case of C. tetani it is the toxin which enters the bloodstream, not the bacteria, hence toxaemia. The bacteria, being anaerobic, are inhibited from spreading through aerobic tissues.

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text:
Genotypic distribution of a population with two characteristics and linkage
I am currently doing some research into distributions and probabilities with Mendellian genetics. I came across this problem that I cannot seem to wrap my head around.
Given that the population has two characteristics, they are color and texture. Supposed two dihybrids reproduce (AaBb x AaBb) and if the dominant form of the
color gene is contributed, then the dominant form of the texture gene is three
times as likely to be contributed as the recessive form. If the recessive color gene is contributed then the dominant and recessive genes for texture are equally likely.
From this the geneotypic distribution has to be calculated.
I know the solution is:
[9/64   6/64   1/64   3/16   1/4   1/16   1/16   2/16   1/16]

 AABB   AABb   AAbb   AaBB   AaBb  Aabb   aaBB   aaBb   aabb

When I performed the punnett square I got the distribution of:
 [1/16   2/16   1/16   2/16   4/16   2/16   1/16   2/16   1/16]

 AABB   AABb   AAbb   AaBB   AaBb  Aabb   aaBB   aaBb   aabb

and did not know where to go from there.
My question is how did they incorporate the "times as likely" condition into the solution.

What are these traits exactly ? just colors ?
From the data it seems that homozygosity is not preferred

You are...  done. You fully answered the question; if I were you, I might just put it in ratio format instead of probability, just to be safe.
The three times thing is a bit weird, but I have seen it before. First, let's look at the phenotypic ratio of the progeny: 9:3:3:1 for Dominant Both:Dominant A Recessive B:Recessive A Dominant B: Recessive Both.
Let's find out how many dominant and recessive there are for each trait. For the dominant A trait, you add up the 9 and 3, because they are the only two types of dominant phenotypes, and find that 12 different organisms of the 16 possible are dominant for Trait A, so the probability of getting trait A is 3/4 or 75%. This means that 4 of the 16 orgamisms are recessive for Trait A, so the probability of being recessive for Trait A is 4/16, or 25%. Therefore, the ratio of Dominant Organism probability:Recessive organism probability is 75% to 25%, or 3:1. This means that it is 3 times as likely to get the dominant trait than the recessive trait. Make sense?

Hi, I understand what you are telling me there but what I really wanted to know is how to move from the punnett square distribution I got ( [1/16 ... 1/16] ) to the distribution that was stated in the solution ( [1/64 ... 1/16] ).

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text:
Distribution of genotypes after adverse selection
I am doing some research into Mendelian genetics and came across this phrase called adverse selection.
I found a few questions but I am unsure of the calculations. For example given a distribution

[0.36 0.48 0.16]

it is stated that 25% of individuals with Aa(middle) genotype dies. The distribution changes to

[0.4091 0.4091 0.1818].

I initially thought to just take off 25% of the middle becoming 0.36 and equally distributing the 0.12 change to the other two geneotypes. Can someone explain how they did this computation.

If you distribute the 0.12 equally to the two other genotypes you change the relative frequencies. You have to withdraw 0.12 to 0.48 and then set the three frequencies so that they sum up to 1. Therefore, the correct calculation is the following:
If we set $fAA = 0.36$, $fAa = 0.48$ and $faa = 0.16$ and then simulate the death of 25% of the Aa individuals, the same variables at the next time step (without reproduction) will be...
$$faa = \frac{0.16}{0.36 + 0.36 + 0.16} ≈ 0.1818$$
$$fAa = \frac{0.36}{0.36 + 0.36 + 0.16} ≈ 0.4091$$
$$fAA = \frac{0.36}{0.36 + 0.36 + 0.16} ≈ 0.4091$$

Thank you so much, you made it very clear to me and showed how my thinking was incorrect.


text:
Gloves for Cell Culture?
I always wear gloves when I'm doing cell culture. Moreover, I always spray my gloves with ethanol to disinfect, so that I don't contaminate everything.
However, I recently heard the argument that EtOH could impair the integrity of the glove, making it an unsuitible barrier between your hand and the culture. According to this argument, the best idea is to not wear gloves during cell culture, but instead thoroughly spray your hands with EtOH to ensure decontamination.
I don't believe it, but I'm wondering if anyone else has heard a similar argument and if there is any truth to the claim.

In my opinion wearing gloves during cell culture is a good idea. It works both ways as a protection: For your cells since you are not loosing small danders from your hand and for you since you are not getting media or chemicals used in cell culture on your skin when you are uncautious.
I usually prefer nitrile gloves over latex, since nitrile gloves are ways more stable and pose no risk for allergies (I am not allergic, but minimizing risks is always a good idea). The downside of nitrile is, that they are a bit more expensive (thats the point where you need to argue with some coordinators about what to buy).
I never had problems with desinfectants and gloves, but this is my personal experience and probably not more than an anecdote. I desinfect my gloves, since I touch different things with them, but I usually don't spray everything which comes around with alcohol since this is usually pointless. To be useful, it needs to reach all points of a surface and also needs to stay there for a while. What I make sure is that all the stuff, which goes into the hood is either very clean or packaged sterile anyway.
After my experiences some data, this PDF has quite a lot of information. The list below is taken from the PDF:
Nitrile gloves:

Acetone - fair
Ethanol - excellent
Isobutyl - alcohol excellent
Isopropyl - alcohol excellent
Methanol - fair

Latex gloves:

Acetone - good
Ethanol - excellent
Isobutyl - alcohol poor
Isopropyl - alcohol excellent
Methanol - fair

I second that.. Nitrile gloves are also good against many acids. Only chloroform destroys it. plus, even if alcohol did affect the gloves it wont do it immediately and in any case you wont use the same pair for more than a few days..

Chloroform (and other halogenated solvents as well) also break Latex gloves very fast. So if these are used, different security measures are needed. Or you have to work very clean (which is always good :-) ).

Assuming you use latex or nitrile, you're probably good.  Nitrile does hold up better than latex in many situations, so if you're worried about it, switch to nitrile.  This is a good quick guide to glove materials and their resistance.  For some of the applications we do in our clinic/lab, we use thick >6mm nitrile gloves.
Your needs all really depend on your application.


text:
MTT assay normalization
Since the precise amount of cells in each well of an MTT assay varies, how can I normalize the results by cell number/concentration?
How can I take into account the number of cells that have already disappeared due to the action of a toxin applied previously as part of this assay?


text:
What is the relation between plasmid concentration and mRNA levels?
Suppose a simple synthetic construct, consisting of a constitutive promoter and a single gene:

One of the simplest ways to model GFP transcription is to use an ODE:
$\frac{d [GFP_{mRNA}]}{dt} = a - b{\cdot}[GFP_{mRNA}]$
where $a$ is GFP transcription rate and $b$ is GFP mRNA degradation rate (both constants). Normally, we assume $a>>b$.
Suppose we wish to account for plasmid concentration with the value of transcription rate $a$ - e.g. with higher plasmid concentration, the ratio $a/b$ should increase as the mRNA saturation levels are expected to be reached faster. In other words, suppose we transfect 2 individual constructs depicted above, 10 ng of one and 30 ng of the other - how should this difference in concentration impact the rate constants values, assuming the constructs are otherwise identical?
Assuming this, approximately how does gene transcription rate $a$ change as a function of the amount of transfected plasmid containing the above construct? Ideally, I'd be interested in knowing this for HEK 293 cells, but any other decent estimation is acceptable. One simple option is to simply assume linear relation, but I think that's too simplistic: e.g. if we say $a=1$ at 10 ng plasmid concentration, then $a=3$ at 30 ng plasmid concentration. Note that I'm not necessarily limiting myself to ODE models, just looking for some kind of relation.
I have so far not been able to find anything useful in papers I've examined, so any help would be appreciated.

The amount of transfected plasmid does not correlate at all with the protein expression level. After transfction, usually each cell is going to get and keep only one copy of the plasmid. Once the plasmid is in the cell, it will be replicated and the cell will contain X copies of it, depending on the plasmid copy number. In general, plasmids with low copy numbers correlate with lower protein expression compared to plasmids with high copy number. But there are also exceptions:

Expression of genes under control of EF1α promoter appears to correlate with plasmid copy number.  In contrast, expression driven by the more traditional CMV immediate early promoter appears less plasmid copy number dose-responsive (ref).

Well.. the copy number does matter in case of CMV also. I had observed normalized luciferase activity in HEK cells at different amounts of transfected plasmid- it shows difference. Also, the effect on an miRNA on the luciferase is better as the concentrations decrease. It is not strictly linear, though.


text:
Is there a standard reference for the importance of tumor heterogeneity?
In a recent post, Philip Gerlee highlighted the two biggest contributions of mathematical oncology to cancer research: (1) increasing focus on the progress of cancer as an evolutionary process, and (2) looking at the importance of tumor heterogeneity.
For the first point, the standard historical reference is: Nowell, P. C. (1976). The clonal evolution of tumor cell populations. Science, 194(4260): 23-28.
However, for the second point, although I am vaguely familiar with modern work, I don't know of a historical reference. When was tumour heterogeneity first recognized as important to cancer dynamics and treatment? Was this work related to mathematical or other modeling insights? If not, what is the first important mathematical (or computational) modeling work on tumour heterogeneity?

I more confident about the experimental evidence being older. The histological evidences are even presented in pathology books. The whole field of systems biology is relatively new- most cancer mathematical models have been published in the last decade only.
The oldest model that uses the concept of tumor heterogeneity is this- published in 1996. [ Based on google search ]

you might look for 'clonal selection' and cancer.  I've heard the term bandied around.

It's quite interesting that the first reference that come to mind is not a mathematical/theoretical one (which is, in all likelihood, going to be a lot older than the one I am going to mention) but a clinical one. That would be Gerlinger and Swanton and their paper in the New England Journal of Medicine.

This paper is quite recent. The concept of tumor heterogeneity was in discussion since long time back. I can't recall references but I have heard people talking in seminars about genome sequencing different regions of cancerous tissue to look for heterogeneity.
Histological evidences are even older. I guess pathology books also have it.

That paper is very well cited (over 1000 times!), but I agree with @WYSIWYG that 2012 seems too recent. Is there a richer history with Gerlinger and Swanton that you could expand on in your answer? Or did you intend this as a comment?

The idea of tumour heterogeneity has been around for a long time (look at the below review and the refs therein), but the underlying causes have been revised in the light of theoretical advances and the novel (Gerlinger et al.) genetic data.
Firstly genetic heterogeneity was largely believed to be the cause of genetic instability (an increased mutation rate), and hence being attributed to drift rather than multiple fitness peaks (i.e. selection).
Secondly there was no evidence to determine if the observed phenotypic heterogeneity (from histology slides) could be attributed to genetic changes, or if it was the cause of phenotypic plasticity.
Alexandrova, Tumour Heterogeneity, Exp. Pathol. Parasitol (2001).

Welcome to the site! Do you know any other sources for Alexandrova's essay apart from a dropbox link? I know a lot of people are unwilling to click those. Also, could you make your answer a bit more self-contained by taking a reference or two out of Alexandrova's essay for when you say "has been around for a long time", for example? That way people can have an idea of the timeline without having to leave this answer.

Actually it's a google drive link. In any case I uploaded it because I couldn't find a pdf of the manuscript anywhere. Do you know of a place that is considered "safe" in terms of downloading?


text:
Are recessive, deleterious alleles less common on the X chromosome than the autosomes in humans?
As there is a potential for them to be more readily purged in hemizygous males (and in cell lineages in females with the deleterious-allele-bearing chromosome activated), I would expect the frequency of deleterious alleles to be lower on this chromosome than in autosomes. Is this information known?

Just to make sure I understand the question. When you say "Is this information known", you actually ask "Are empirical observations coherent with this hypothesis?"

Yes, that's at least in part what I mean. Thank you, @Remi.b. I imagine other hypotheses might also explain this empirical observation, if it indeed exists. I would also be interested to know whether this particular hypothesis has found stronger support than alternative hypotheses. But I would be most curious, as you say, about whether empirical data supports this prediction.

"Monosomy for the X chromosome in humans creates a genetic Achilles' heel for nature to deal with."
The article I quoted1 tackles this issue.  It's from the turn of the century, though, so quite old in sequencing/genetic terms, but the science is still sound as far as I can tell.  Here's the money quote:

Hence, the X chromosome appears to have a lower gene density and should yield fewer deleterious mutations per megabase of DNA.

In short, yes, you're correct.  There appears to be less overall information on the X-chromosome, deleterious or not, and selection is faster; the X chromosome is just flat-out less diverse.  This article goes into quite a bit more but says essentially the same thing: "On one hand, the greater effectiveness of selection on males due to the hemizygous expression of the X, which may be further reinforced by sexual selection, is expected to lower the mutation load for females at shared loci."  Here is a more recent article stating the same: "This finding [X-chromosomes with lower linkage disequalibrium] is consistent with more rapid selection against deleterious mutations when the X is monosomic in males, and to a lesser extent, under random inactivation (Lyonization) in females."
Finally, here is a piece written a few years back by a colleague of mine that goes into depth on the subject.  The second half deals with population differences (also fascinating), but the first part has a lot of good detail on what you want.


text:
How to check if a fastq file has single or paired end reads
I am trying to check if a fastq file has single or paired end reads. How can I achieve this with an error-proof method?
I checked wikipedia and MAQ but I want to know if is there a reliable document that describes all possible variants in sequence ID to check for single/paired end reads.
I am searching also for a library, better in Python, to achieve this.
Thanks

You might be better off asking this question on http://www.biostars.org/

See for example this question: http://www.biostars.org/p/45961/

Thanks @jarlemag. I did some research earlier and I noticed that answer. However there are two problems: first I am not fluent in Perl and it is hard to me to deciphers the content of the accepted answer (not to mention that not being able to check the code could lead to run into bugs that you cannot predict). Second, I read the answer and wikipedia page for FASTQ format but I am searching for the real reference. So I decided to ask a new question not to have a script (related but not main question) but the idea behind that, that could possibly cover all possible variants in this scenario.

I see. I found some info on the read identifiers, but held off from answering since it seemed you wanted a complete script. Have you checked out the SeqIO interface in BioPython?

Not yet, sorry.. I am quite a noob in BioPython.. now I'll try it. Thanks

By now I got some interesting answers in this question on Biostars
Basically what I did is the following:

First of all, I checked if Sequence Id contains paired end notation. As described in this wikipedia page, for Illumina reads there are two possible notation for single/paired end reads:
@HWUSI-EAS100R:6:73:941:1973#0/1
If the last number is /2 in some reads then the reads are paired end; otherwise they can be single end.
The second notation is:
@EAS139:136:FC706VJ:2:2104:15343:197393 1:Y:18:ATCACG
If the first number in the second group is 2 in some reads then the reads are paired end; otherwise they can be single end;
Then I checked for multiple files. If a sample has two fastq files it is likely that the reads are paired end. It is to note however that with a single file it is not possible to exclude that paired end reads can be interleaved in one single file, even if it is not common (in my opinion);
The most general method is to cross check each single reads with the whole set of reads. If the first part of the sequence ID (in this case the field starting from @ and ending before the # - in the first notation - or the whitespace - in the second notation) is unique among all the reads (for each read) it is likely that the reads are single reads, otherwise - if can be found a duplicate for each reads - the reads are paired end.
In this case, on *nix systems it can be achieved with the following command (thanks to the biostars answers):
grep --no-filename @HWUSI-EAS100R:6:73:941:1973 *.fastq | cut -d' ' -f1 | sort | uniq -c | sort -rgk 1,1 | head
If the result shows in the first lines a result like this:
1        read1_ID
1        read2_ID
...
It is likely it is single end. Otherwise:
2        read1_ID
2        read2_ID
...
it is paired end.

I skim read BioPython API documentation but I cannot find something useful to do it.
Suggestions and corrections are welcomed.
Thanks

This is complementary answer to what @gc5 provided.

For cases that are using "the second notation" which looks like:
@EAS139:136:FC706VJ:2:2104:15343:197393 1:Y:18:ATCACG`
                                        ^
                                        |________________what we are
                                                         trying to extract

The following code will go through all the files iteratively and produce one output per file:
grep -P "^@" *.fastq | grep -oP "\s\d+" | sort | uniq -c

or if you have .fastq.gz files:
zgrep -e "^@" *.fastq.gz | grep -oP "\s\d+" | sort | uniq -c

if you have single-end you will only see ones and if you have paired-end you will see ones and twos. Also as sanity check, you can see how many of each you have:
zgrep --max-count=10000 -e "^@" *.fastq.gz | grep -oP "\s\d+" | sort | uniq -c

6333652  1
6333652  2

Note that I added --max-count=10000 to the last one. This is particularly useful if you have paired-ends in separate files as you will get all ones form one and all twos from the other. This will only go through the first 10'000 lines which makes this one-liner much  much faster.

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text:
Plasmid maintenance
I have obtained some plasmids used as integration vectors, this question may apply to all plasmids. I would like to have a somewhat continuos source for these plasmids, let's say that the origin of replication is e-coli specific and can i then just transform the e-coli with the plasmid, let it grow to some density and then do miniprep? or can i also create glycerol stocks out of the bacteria that contain the plasmids and then harvest more plasmids as needed? i realize that both things are possible, but is this a good reasoning to follow?
Thanks

What I would usually do is transform E. coli with the plasmid, grow an overnight culture and mini prep the plasmid in the morning. Before you do the miniprep save a glycerol stock. Thus, you would have some plasmid to work with in the next couple of weeks, and also a glycerol stock to come back to. You can also keep the plate with your transformants, as you can go back to it within a month.

I'll add to this as well. Always keep a small aliquot of your miniprep DNA in a stock box, and keep it frozen, just in case the glycerol stock fails for some reason (e.g., freezer failure). The DNA is more forgiving of freeze-thaws and offers one more backup. I only do this with final (or destination) vectors that I have finished manipulating.

Yeah, I think this is a good backup.


text:
How many transcription factors are there?
In molecular biology and genetics, a transcription factor is a protein that binds to specific DNA sequences, thereby controlling the flow (or transcription) of genetic information from DNA to messenger RNA.
My question is simply how many transcription factors are there in the genomes of:

Humans
Anopheles gambiae (or it's close taxonomic relatives)
Less prioritized: any other species

This is the Curated database of mouse and human transcription factors. And this is the paper in which they describe how they curated the database. In summary, there are 3230 putative mouse TF, 1200 of which are described in scientific papers.

As the number of human TFs have been discussed by the previous answers, I'll limit myself to Anopheles gambiae.
In the same issue of Science in which Holt et al. published a genome sequence for Anopheles gambiae (1), Zdobnov et al. published a comparison of the A. gambiae and Drosophila melanogaster genomes.(2) While the two species diverged about 250 million years ago, and the D. melanogaster genome is about twice the size of the A. gambiae genome, the two species still show broad similarities and a similar number of proteins.
The authors identified 6089 protein pairs as "clear orthologs", corresponding to 47% and 44% of the of the Anophelesand and Drosophila proteins respectively. One might thus be tempted to estimate the number of TFs in A. gambiae as similar to that in D. melanogaster. For the latter, the FlyTF database (http://www.mrc-lmb.cam.ac.uk/genomes/FlyTF/old_index.html) currently lists 753 putative site-specific TFs and 454 "well supported" candidates. More recently, Hammonds et al. identified 708 melanogaster genes "likely to encode sequence-specific DNA-binding TFs".(3)
Edit: You may also want to check out the following question on Biostars: http://www.biostars.org/p/53590/

Pretty interesting question. There are a few numbers out, I remember that round about 10% of the human genes are coding for transcription factors (unfortunately I don'T remember the source for that).
This paper from 2002 estimates between 2000 and 3000 factors:

Signal transduction and the control of gene expression.

This paper from 2009 states a number of 1391 manually curated factors and also speculates about a number of 2000 - 3000 factors in total. This is definitely interesting to read.

A census of human transcription factors: function, expression and
evolution.

Amos Bairoch, of SWISSProt/UniProt fame has set up the nextprot database, a manually curated repository of knowledge for human proteins. While that won't help you get a number for the mosquito, it does make it easy to retrieve a list of human proteins that are annotated as transcription factors.
Searching for "Transcription Factor" in the "Function" tab returns 1405 hits. You'll notice that most answers are in the same ball park despite small differences, but bear in mind that many of these are assumed TFs and it will be a while before all of them have been experimentally confirmed to act as such in vivo.


text:
How host defends against S. pneumoniae capsule?
The host response involves at least phagocytosis and probably localised acute inflammatory response at least after the colonisation.
I am thinking how the host can defend against pneumolysin which helps the streptococcus pneumoniae invasion.
How can the host defend against Streptococcus pneumoniae capsule?

According to the two papers listed below, this is mostly done by a neutrophilic inflammatory response. The response is regulated by mechanisms of the innate immune system and is mediated by receptor like TLR2, TLR4 and SIGN-R1.

Role of Dectin-2 in the host defense against Streptococcus
pneumoniae infection
Dectin-2-dependent NKT cell activation and serotype-specific antibody
production in mice immunized with pneumococcal polysaccharide
vaccine.

There are a few papers which go deeper (reviews, so you will probably have to go through the reference lists):

Mechanisms of host defense against infection with Streptococcus
pneumoniae.

This paper mentions specific antibodies later on in the reaction and finally the opsonization by immune cells.
These two papers tal specifically about pneumolysin:

Pneumococcal virulence factors and host immune responses to them.
Pneumolysin as a vaccine and drug target in the prevention and
treatment of invasive pneumococcal disease.

This seems to be localised acute inflammation what they describe. Probably, first fibrous type of acute inflammation.

@Masi I expanded my answer.


text:
How do TLR1/TLR2 activate the MyD88 dependent pathway
Recently, I've been reading about the MyD88 dependent signalling pathway, with particular reference to its activation in Macrophages and other cells of the immune system on recognition of a pathogen. I understand that when a PAMP (Pathogen Associated Molecular Pattern) binds with a PRR (Pattern Recognition Receptor), the receptor undergoes a conformational change, which precipitates a cascade of chemical reactions between various proteins, which eventually leads (inter alia) to the translocation of NF-κB to the nucleus, which leads to the production of cytokines. My question is about the finer points, particularly with respect to TLR1 and TLR2.
My reading suggests that these generally form a heterodimer - is this always true? Are both required for a pathogen to be recognised and an immune response produced?
Upon the pathogen binding with TLR1 (whether in a complex with TLR2 or not) what precisely happens to the receptor. I understand that MyD88 is, ultimately, recruited, but by what means?
I believe I understand everything that happens after the recruitment of MyD88, but I am less clear on everything before that. I had initially understood that the recruitment of MyD88 was the immediate next step, but other sources make reference to two proteins which I was initially unaware of: TOLLIP and TIRAP. What, if anything, is their role?
I'm still a little new to stackexchange so I apologise if this question is not up to standard, in which case, let the question simply be: 'How do TLR1/TLR2 activate the MyD88 dependent pathway?'

The TLR are usually working as homodimers (Toll-like receptors), although TLR2 can cooperate with TLR1 or 6.
Upon binding of its ligand (this is called pathogen associated molecular pattern) the receptors change their conformation and allow binding of TIRAP (TIR adapter protein) to their Toll-interleukin 1 receptor (TIR) domain. TIRAP then recruits MYD88, which then recruits IRAK1 or 4. The signal is then passed down the pathway as shown in the figure below (taken from the Wikipedia article on TLR).

Pretty good, but a correction - MyD88 recruits both IRAK1 and IRAK4. 4 then gets phosphorylated, and in turn phosphorylates 1 at Thr209 and Thr387. This in turn activates 1's kinase activity, and it hyper-autophosphorylates. 1 (and maybe 4) then dissociates from the complex, becomes ubiquitinated, and goes on to recruit the membrane-bound TAB/TRAF complex, which facilitates activation of TAK and RIP, leading to the NF-kB, PI3K/Akt, and MAPK pathways.

Thats correct. I updated the answer. Thanks for it.

I really enjoyed your link but I remain a little confused by sentences such as "Lipopeptides and other components of Gram-positive bacterial cells activate TLR2 in conjunction with either TLR1 or TLR6." Should I understand by this that you either have two TLR1 monomers which, together, form a homodimer, or you have a TLR1 monomer and a TLR2 which, together, form a heterodimer? Also, does dimerization occur only after binding with the ligand?


text:
What prevents predator overpopulation?
I've often heard that a population, human or otherwise, will continue to grow as long as there is food available (assuming nothing else is killing them off).  It makes sense: if you have food you can live, and if nothing is hunting you you'll survive to reproduce.
I recently designed a piece of software to simulate an ecosystem, with groups of creatures of different species eating and hunting and reproducing alongside each other.  It was very simplified (each animal had simple attack/defense/speed/stealth values, etc), but something became rapidly apparent: in every simulation the predators overwhelmed the prey, reproducing until their numbers could not be sustained by the herbivores, and leading to an inevitable die-off of both groups.  I could delay the die-off by adjusting different values and initial population counts, but it would always happen eventually.  The predators would eat and breed and eat and breed until the entire system collapsed.
At first I thought it was just the product of my over-simplified system, but it got me thinking: what prevents predators from overpopulating in real life?
It seems like the natural tendency would be for (for example) the sharks to continue breeding and eating until all the fish are gone, or the wolves to eat all the deer, etc.  Obviously some predators have predators of their own, but that's just putting off the question: if the hyenas don't overpopulate because the lions eat them, then what's keeping the lions from overpopulating?  I can't come up with anything that would prevent the apex predators from growing too numerous, then fighting each other over a dwindling prey population, then dying off entirely when there was no more food to find.
Do predator populations self-regulate to prevent putting undo stress on their prey populations?  Or is there some other mechanism to keep the predator hierarchy from becoming top-heavy?

As a supplement to Remis answer, here's a link to the Nature Knowledge Project page on population dynamics: http://www.nature.com/scitable/knowledge/library/dynamics-of-predation-13229468

In history, there are also mass extinctions very well outlined by this video: http://www.youtube.com/watch?v=FlUes_NPa6M. They "reset" the world and allow everything to start over again.

aka - they tend to starve to death when there are too many

Starvation, diseases and bigger predators.

Can you be more specific regarding your model?  Did the prey reproduce with its offspring possessing the same abilities as the parent(s)?  You said you could "delay."  What marked the time?

It sounds like you made it to easy for your predators to kill prey, Predators tend to fail to catch prey a large percentage of the time, and a small percentage of the time they get injured themselves. The more predators there are the more common failure and injury becomes. Predators that attack healthy prey in the middle of a herd have a decent chance of being killed by the prey.

@Nerrolken Be more specific regarding your model?  Did the prey reproduce with its offspring possessing the same abilities as the parent(s)? You said you could "delay." What marked the time?

relevant, @remi.b ?
https://www.sciencemag.org/news/2015/02/do-big-carnivores-practice-birth-control

A fun fact, the human is ultimate predator, and it is overpopulating.

No, I don't think auto-regulation explain much in the population sizes of predators. Group selection may explain such auto-regulation but I don't think it is of any considerable importance for this discussion.
The short answer is, as @shigeta said

[predators] tend to starve to death as they are too many!

To have a better understanding of what @shigeta said, you'll be interested in understanding various model of prey-predator or of consumer-resource interactions. For example the famous Lotka-Volterra equations describe the population dynamics of two co-existing species where one is the prey and the other is a predator. Let's first define some variables…

$x$ : Number of preys
$y$ : number of predators
$t$ : time
$\alpha$, $\beta$, $\xi$ and $\gamma$ are parameters describing how one species influence the population size of the other one.

The Lotka-Voltera equations are:
$$\frac{dx}{dt} = x(\alpha - \beta y)$$
$$\frac{dy}{dt} = -y(\gamma - \xi x)$$
You can show that for some parameters the matrix for these equations have a complex eigenvalue meaning that the long term behavior of this system is cyclic (periodic behavior). If you simulate such systems you'll see that the population sizes of the two species fluctuate like this:

where the blue line represents the predators and the red line represents the preys.
Representing the same data in phase space, meaning with the population size of the two species on axes $x$ and $y$ you get:

where the arrows shows the direction toward which the system moves. If the population size of the predators ($y$) reaches 0 (extinction), then $\frac{dx}{dt} = x(\alpha - \beta y)\space$ becomes $\frac{dx}{dt} = x\alpha \space$ (which general solution is $x_t = e^{\alpha t}x_0$) and therefore the populations of preys will grow exponentially. If the population size of preys ($x$) reaches 0 (extinction), then $\frac{dy}{dt} = -y(\gamma - \xi x)\space$ becomes $\frac{dy}{dt} = -y\gamma \space$, and therefore the population of predators will decrease exponentially.
Following this model, your question is actually: Why are the parameters $\alpha$, $\beta$, $\xi$ and $\gamma$ not "set" in a way that predators cause the extinction of preys (and therefore their own extinction)? One might equivalently ask the opposite question? Why don't preys evolve in order to escape predators so that the population of predators crushes?
As showed, you don't need a complex model to allow the co-existence of predators and preys. You could describe your model a bit more accurately in another post and ask why in your model the preys always get extinct. But there are tons of possibilities to render your model more realistic such as adding spatial heterogeneities (places to hide for example as suggested by @AudriusMeškauskas). One can also consider other trophic levels, stochastic effects, varying selection pressure through time (and other types of balancing selection), age, sex or health-specific mortality rate due to predation (e.g. predators may target preferentially young ones or diseased ones), several competing species, etc..

I would also like to talk about other things that might be of interest in your model (two of them need you to allow evolutionary processes in your model):
1) lineage selection: predators that eat too much end up disappearing because they caused their preys to get extinct. This hypothesis has nothing to do with some kind of auto-regulation for the good of species. Of course you'd need several species of predators and preys in your model. This kind of hypothesis are usually considered as very unlikely to have any explanatory power.
2) Life-dinner principle. While the wolf runs for its dinner, the rabbit runs for its life. Therefore, there is higher selection pressure on the rabbits which yield the rabbits to run in average slightly faster than wolves. This evolutionary process protects the rabbits from extinction.
3) You may consider..

more than one species of preys or predators
environmental heterogeneity
partial overlapping of distribution ranges between predators and preys
When one species is absent, the model behave just like an exponential model. You might want to make a model of logistic growth for each species by including $K_x$ and $K_y$ the carrying capacity for each species.
Adding a predator (or parasite) to the predator species of interest
... and you might get very different results.

Another factor that the asker's model might not have considered is predator-against-predator action. Territorial conflicts would become more common as the predator-prey ratio increases. Another possible factor might be reduced hunting ability from malnutrition.

This is a great answer, another key factor (perhaps even more important than some mentioned) is - "handling time". Your simulation likely allows a predator to eat a prey infinitely quickly when there are lots of prey around. But even if prey are hitting the predator in the face, it still takes time to eat, and while you are eating one you aren't eating another. Look up Rosenzweig-MacArthur predator-prey model - this modification of Lotka-Voltera which includes handling time prevents your die off problem!

@cell0 please don't edit correct american english spellings to british english variants. Either are correct, but one shouldn't be edited to the other.

Remi.b's answer is an excellent one, and this should be taken as a supplement to it:
It's possible your simulation is correct
The Lotka-Volterra equations are what is known as a deterministic model, and it describes the behavior of predator-prey systems (in a somewhat simplified fashion) in large populations. Small populations are subject to what is known as stochastic extinction - as the predator and prey curves approach their minimums, they may predict populations less than 1, which in reality are either 0 or 1, and when they're 0...well, someone's gone extinct.
Odds are your simulation is on a small population, and if its a simulation, rather than calculus, you should be seeing those stochastic effects (to be sure - if your simulation keeps track of integer animals, rather than continuous animals, and random chance is involved, this is going to be something you have to worry about).
In a similar model I've been working with, that's a pretty simple adaptation of a L-V model that should, deterministically, result in a stable system like in Remi.b's picture, the predators go extinct 20% of the time, and the prey 80% of the time.

What does a continuous animal look like?

@JAB Usually proportions of a population

One of the possible adjustments of these mathematical models is to introduce a "place to hide", making some (small) percent of the prey population not accessible (or much more difficult to access) for predators. After the number of predators decreases from starvation, prey individuals are relatively safer outside the "place to hide" and can grow over this limit before the number of predators increases again.

An excellent notion!

You need to add Bell curves to your simulation. The most important curve to simulate is the nutritional quality of the prey though there are plenty more thing to curve like speed and virility for prey and predators both. Nature uses lots of Bell curves so they must be good for something, such as softening the harsh effects of pure exponential growth. I suspect that the more Bell curves you implement the more stable your populations will become.
If the food value of your prey is all equal then there's no reason for your predators to not eat every last one. That's what I do with a plate full of foodstuffs, all equally delicious and with enough surplus that all the bad food can be thrown in the trash. Problems arise when you are forced to eat the trash because there's nothing else to eat.
Let's eat our prey from all 3 sides of the curve. If we eat from the weakest and easiest to catch on the left this makes the prey population stronger and more resistant to the predator. If we eat from the most common on the top the prey rebound more rapidly. If we eat from the most desirable on the right the rapid quality (but not the virility) reduction of the prey population has serious negative health consequences for the predators. Notice how each direction we eat has the necessary corrective action against the predator as a response. Due to the wild randomness of genetics the weak population can always rebound in quality when the predatory pressure eases. Looks like Nature didn't screw that one up either.
An easy example is seen in the human vs plant food supply. Population should rise with no detriment as we produce more and more food, and it would if the quality could stay the same. The population does rise but because the nutritional quality keeps dropping, the detriment is rapidly increasing on numerous health and population charts.
When plants are forced to make do with what little they have, you are forced to make do with what little they provide.

This boils down to one main reason: competition.
Animals, in general, don’t like sharing resources with direct competitors, but this violence over food, territory, and in the case of intraspecific relations, breeding rights seems to be more extreme the higher up you go on the food chain.
An excellent example of this regards cougars. A dominant tom cat in Montana, for instance, rules over a domain that can easily exceed a hundred square miles. This territory is several times larger than what he’d require just to feed himself, so why is it so large? It’s quite simple: breeding rights. Within the borders of his, hundred or so square miles of territory are lands also used by two or three females and the cubs he’s fathered with them. Other tom cougars enter at their own risk, as he’d be more than happy to run them out or kill them. The same fate befalls any of his sons who reach maturity, so they either disperse to lands unknown or die trying. Dispersing males naturally die frequently in most species as a result.
Females also defend their territories, but since it’s not advantageous for them to have multiple potential breeding partners, their lands aren’t near as large (maybe forty square miles or smaller), just big enough to keep them and their offspring safe and well fed with all the deer, elk, coyotes, and/or bighorns they need, in addition to smaller prey. Female offspring who disperse have an easier time finding territories than their brothers and are less likely to disperse widely because of this fact.
To answer your question, predators self regulate their populations, often violently. In a stable ecosystem, there’s enough of them to keep their prey in check, but due to factors of real estate, breeding rights, and interactions with other predatory species, they simply don’t overpopulate.

I think self-regulating is a confusing term in this case. The individuals absolutely do not self-regulate, it is only at the species level that it occurs.

What you are missing is that not all prey are equally easy to catch. The old, sick animals living in exposed places are much easier to catch than animals that are young, healthy and living in well-protected places. As the predator catches the easy meat, it becomes progressively harder and harder for the predator to get a meal.

If I missed seeing this in one of the other answers, I apologize, but I don't believe anyone has mentioned a very relevant fact about some predators that directly affects their populations at any given time. The fact is that wolves and probably other predators living in a pack-style grouping, allow only the alpha male and female to mate. This obviously severely limits the number of offspring born each year as well as leaving the pack vulnerable to catastrophe when something happens to either or both alphas. This mode of self-regulation is independent of food availability so works in years of abundance as well as famine.

Welcome and +1 for this answer. However, we do ask for any answers to be accompanied by the appropriate references to allow other users to background read on your material.

@Deborah Stephenson , it is not "obvious" that restricting mating to the alpha male and female limits the number of offspring born because the limiting factor in offspring production is commonly the food available to support those offspring.  As long as the group's other members can still hunt, the same food that was available for all offspring would be available for the offspring of the alpha individuals.


text:
How do mosquitoes maintain telomere length?
While the vast majority of eukaryotic organisms maintain their chromosome ends (telomeres) via telomerase, an enzyme system that generates short, tandem repeats on the ends of chromosomes, other mechanisms such as the transposition of retrotransposons (e.g. Drosophila) or recombination (e.g. Yeast) can also be used in some species.
I would like to know of your thoughts on the possible mechanisms that regulate telomere lengths in mosquitoes.

It seems that the current model is that recombination is the mechanism by which telomere length is maintained in the malaria vector Anopheles gambiae. Here is an exerpt of Roth et al paper that proposed the recombination mechanism:

The insertion of a transgenic pUChsneo plasmid at the left end of chromosome 2 provided a unique marker for measuring the dynamics of the 2L telomere over a period of about 3 years. The terminal length was relatively uniform in the 1993 population with the chromosomes ending within the white gene sequence of the inserted transgene. Cloned terminal chromosome fragments did not end in short repeat sequences that could have been synthesized by telomerase. By late 1995, the chromosome ends had become heterogeneous: some had further shortened while other chromosomes had been elongated by regenerating part of the integrated pUChsneo plasmid. A model is presented for extension of the 2L chromosome by recombination between homologous 2L chromosome ends by using the partial plasmid duplication generated during its original integration.

You might also be interested in this paper: Genes required to maintain telomeres in the absence of telomerase in Saccharomyces cerevisiae and then look at whether there are mosquito homologs of the identified yeast genes that might be involved in telomere maintance.

Cheers @Gergana Vandova Do you think this mechanism of telomere length maintenance would require any specialized enzymes?

mm that's a good question. My first thought would be no, as eukaryotic cells are in general capable of  recombination. I am not really familiar with mosquitoes, but would assume that applies for them as well. But again, it might be possible that there are telomere-specific recombination enzymes. Worth looking into.

May I ask, are you a telomere biologist?

No I am not but I know the principle. You should just read this paper and try see whether you believe the interpretation of their data. Also just wait to see what other people might say about that.

Oh sorry I didn't mean to question your thinking... We are actually working on a manuscript based on genetically engineering telomere length regulation for pest control, the next stage is to carry out experimental work and so we're seeking expertise in telomere experimental work :)

I can actually help you with that! Steve Artandi (Stanford University) is working on telomeres. You might be able to talk to one of his students... Email me at gvandova@stanford.edu if you are interested.


text:
Electronic cigarettes (e-cigs), any health risks?
Background:
An electronic cigarette (e-cig or e-cigarette) is a battery-powered device which simulates tobacco smoking patented in 1963 by Herbert A. Gilbert.
It generally uses a heating element known as an atomizer, that vaporizes a liquid solution. Some solutions contain a mixture of nicotine and flavorings, while others release a flavored vapor without nicotine.
Question:
Are there any health risks uniquely associated with e-cigs as compared with normal cigarettes?

There is a really good sciam article on this in April 2014 issue.

Since the question is about risk specific to e-cigarette as opposed to classic cigarettes, what's left is the potential harm from the chemicals in refill-fluids (apart from nicotine): polyethylene glycol, glycerol, alcohol, linalol, flavours. You can find cytotoxicity experiments (e.g. http://www.sciencedirect.com/science/article/pii/S0890623812002833), that show that the most harmful components may be the flavouring compounds. Some other articles (I can't find a reference right now) point out that the moderate heating of the fluid might create harmful byproducts, differently from those in regular cigarette: acroleine, formaldehyde. The use of e-cigarette is probably too recent to have long-term studies that answer your question.

The e-cig possess potential risks for healthy people as well as for a ill ones.
It contains nicotine which still reaches the lungs and causes its negative effects as oxidative stress.
In addition, because one can smoke e-cig anywhere there is potential risk for nicotine intoxication for smokers using e-cig nonstop.
There is a risk of paradoxical conversion from e-cigs to regular ones by teenagers/beginners because starting smoking with e-cigs can increase tolerance to nicotine and raise the need to higher concentrations of it to achieve the desired sensation of "smoking", thus the user can replace the e-cigs to regular and more toxic ones.
In Feb 2014 a special article was published
Ann Am Thorac Soc. 2014 Feb;11(2):236-42. Electronic cigarettes. Potential harms and benefits. Drummond MB1, Upson D which abstract I place here -
"Use of electronic cigarettes, devices that deliver a nicotine-containing vapor, has increased rapidly across the country and globally. Perceived and marketed as a "healthier alternative" to conventional cigarettes, few data exist regarding the safety of these devices and their efficacy in harm reduction and treatment of tobacco dependence; even less is known about their overall impact on population health. This review highlights the recent data regarding electronic cigarette toxicity, impact on lung function, and efficacy in smoking reduction and cessation. Studies show that the vapor generated from electronic cigarettes has variable amounts of nicotine and potential harmful toxins, albeit at levels lower than in conventional cigarettes. The long-term carcinogenic and lung function effects of electronic cigarettes are not known. Although some data demonstrate that electronic cigarettes may be effective in reducing conventional cigarette consumption, there are no data demonstrating the efficacy of electronic cigarettes as a tool to achieve cessation. Until robust longitudinal evaluations demonstrate the safety of electronic cigarettes and efficacy in treatment of tobacco dependence, their role as a harm reduction tool is unclear."

It must be stressed that the only consensus is that "no one knows yet" how much e-cig is more/less dangerous. You cite the risk of conversion from e-cig to real smoking. Other studies show that e-cig could help smoker temporarily or permanently quit (e.g. http://www.sciencedirect.com/science/article/pii/S0306460313003304). And you are right to underline that any product containing a high level of nicotine must me considered harmful a priori.

Please source your claims. You mention a risk of "nicotine intoxication". What's that? The nicotine high is precisely the reason why people smoke. Nicotine is not in itself particularly harmful, the dangers of smoking are primarily related to imperfect combustion and the subsequent production of CO and free radicals, not to the ingestion of nicotine as such. I have read pretty much everything published on the subject and have yet to see any evidence that e-cigs are harmful and have seen a lot of evidence that they are much safer than normal cigs.


text:
How does the telomere repeat sequence vary in Eukaryotes?
Question:
How does the telomeric repeating sequence vary in non-vertebrate Eukaryotes? If you know the repeating sequence of a given species I would appreciate hearing it.
Background:
Telomerase is a ribonucleoprotein enzyme that adds DNA sequence repeats to the 3' end of DNA strands in the telomere regions, which are found at the ends of eukaryotic chromosomes.
In vertebrates the conserved telomeric repeating sequence is "TTAGGG".

A database that answers the question, charting telomere repeat sequences for all known species, is: http://telomerase.asu.edu/sequences_telomere.html
For example in Yeast:

TTAGG telomeric repeats have been found in several insects. From Sahara, Marek & Traut (1):

(TTAGG)n-containing telomeres were found in three Lepidoptera species,
  the silkworm Bombyx mori (in which the telomeric sequence was recently
  discovered), the flour moth Ephestia kuehniella, and the wax moth
  Galleria mellonella, in one species of Hymenoptera, the honey bee Apis
  mellifera, in one species of Coleoptera, the bark beetle Ips
  typographus, in one species of Orthoptera, the locust Locusta
  migratoria, and in a crustacean, the amphipod Gammarus pulex

C. elegans have TTAGGC repeats.(2)
The TTAGGG motif is also common in filamentous fungi, while Saccharomyces cerevisiae telomeres have TG(TG)(TG) repeats. Many plants have TTTAGGG repeats.(3)

For additional references, see the introduction in Wu et al.(4)

Cheers jarlemag, +1. I wont tick yet till more answers come through :)


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Gene Complementation Question

Hi everyone! Here is a diagram of a genetics complementation problem. My main concern is regarding number 3d. I'm assuming that in this case, it would be complementary interaction and thus exhibiting a ratio of nine to seven. because if we cross F1, 3 will be mutant while one will exhibit wild-type phenotype. Is this right? Thanks in advance!

Yes 9:7 seems to be the right answer.
F1 progeny should be AaGg... and crossing it will give a ratio of 9:7 as is of any complementary genes


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Parasitism and mimicry
I was reading this article which states this:

Classical Batesian mimicry, in which an undefended mimic evolves to
  look like a toxic model, is a parasitic relationship in which the
  mimic gains an advantage at the expense of the model

I don't understand why this mimicry is equivalent to parasitism. Do the authors call it parasitic because eventually it may cause threat to the model, as the predator learns that it is being fooled around ?
I don't see a clear and certain antagonistic relationship here. Can someone please explain.
EDIT
If it is the case that the mimic reduces the likelihood of the model being preyed then then outcome of this is dependent on multiple parameters.
The +/- effect of this interaction is not always certain (which on the other hand is usually certain in the case of a typical parasitism). The uncertainty can arise not just by evolution of the predator but by other factors such as population size and structure.
Considering all this is it correct to call a relationship as parasitism just based on one of the many possible outcomes ?

A parasitic interaction is when one species has a fitness increase (benefit) from the interaction while the other has a fitness decrease (cost). Note: you don't need to have physical contact to have an interaction. As soon as the presence of one specie influence the fitness of the other, it is enough to consider that there is an interaction.
In the case of Batesian mimicry, I think it is obvious to understand why the non-toxic species gain from this interaction. Let's imagine the toxic (model) species is blue. Predators learn to avoid blue species because they feel very sick right after eating it. In other words, the predators have a bad experience or even better we can say that the predator receives a punishment or a negative reinforcement (instrumental conditioning). In consequence the predator that got this negative reinforcement will probably avoid blue individuals in the future.
When a predator eats an individual from the mimic non-toxic species, he got a positive reinforcement. In consequence the predator learns that the prey tastes good and in consequence it is more likely to eat a blue prey next time it encounters one, which obviously has a negative impact on toxic model organism.
Now, I have two issues with this concept.

The interaction is not one-to-one and we can consider that the presence of a species that use Batesian mimicry influence the variance in fitness of the toxic species only if (actually you might argue differently by not assuming infinite population size) the distribution ranges are not completely overlapping or if there are some kind of population structure.
If the toxic species causes death to the predator, then the predators never get the opportunity to learn. But one can consider the same mechanisms at evolutionary timescale than at the time of the lifespan of the predators. It is also possible that the predators have higher cognitive abilities allowing them to gain insights concerning the toxicity of one species without having to taste it.

EDIT

What if predators can tell the difference between the two prey species?

Your point, if I understand it, is that if the predators manage to sense (or to evolve sensing) the two prey species differently (in consequence the non-toxic species does not mimic the other prey species anymore), then the toxic species will not suffer anymore from the mimicry. So in other words, mimicry is a parasitic interaction but predators might evolve ways to sense the two species differently in which case there would have no mimicry anymore. Note: the predator is more likely to evolve good sensing abilities if it forages on few species only.
I think your issue is that you should not consider a species to be mimicry if the predator can tell the difference between the two prey species. It is not to the human eyes that the mimicry makes sense but only to those of the predators. So, batesian mimicry is a parasitic interaction and if the predators evolve so that they can sense the difference between the two species, then there is no more Batesian mimicry and there is no more parasitic interactions between the two prey species.

Why do you say that  "physical contact" not necessary for two species to have a parasitic interaction?

The interactions between species are defined as follow:

The benefits and costs (harmed) are defined in terms of fitness. These definitions do not involve any physical interactions. And to the eyes of the evolutionist at least, that would not make much sense to add a notion of physical interaction into these definitions.

In the case of Batesian mimicry the ± effect is not always certain (while it is certain in common parasitic interactions)

The point is interesting. I think it just mean that the non-toxic organism is a facultative parasite (a species that can live with or without the parasitic interaction). Statistically speaking, if you have enough preys of each species and especially enough predators, then the consequence is certain.
Consider the common Ivy. It is a parasite of other plants but can also live on human-made walls in which case the negative effect on other plants is not always certain either. The difference between the Ivy and the non-toxic prey is that the fitness of the non-toxic prey depends on whether it parasites the other species while the Ivy is doing just fine on human-made walls.
You can think about the interactions between rabbits and wolves. They share a prey-predator interaction which is a special case of the parasitic interaction according to above diagram. In a particular environment the wolves might be absent and so predation does not occur, just like the non-toxic species might be absent species might be absent and so the parasitic interaction does not occur anymore.

Nicely summarized. But one doubt still remains. The +/- effect of this interaction is not always certain (which on the other hand is always certain in the case of a typical parasitism). The uncertainty can arise not just by evolution of the predator. As you pointed out it is also dependent on the population sizes and structures. Also a predator may not evolve and continue to be fooled.

another clarification.. i was discussing this with a friend and another point emerged: in the case of predator not updating its knowledge of a certain appearance associated with toxicity i.e predator still wont attack the mimic and the model both. In this case also the model is in disadvantage that it invests in production of toxin whereas the mimic doesnt. is this a valid point ?

I think you say: "If the predator, for some reason, cannot associate toxicity with appearance, then the toxic species pay a cost of producing the toxin while the mimic species doesn't have this cost." Yes! Note: there might have some cost for "looking" like the other species. And cost for displaying some shiny structure. Also, this interpretation might be a bit too simple. Producing toxin might be beneficial under kin selection if the survival of the predator is reduced so that it won't kill the brothers of the prey and stuff like that.

I meant that the predator has strongly associated the appearance with toxicity and will not attack the mimic. In this case the model produces color/pattern + toxin but the mimic just produces colors. So the model has an additional cost of living. But it is likely that there might be other confounding factors.

Ah ok. I missunderstood what you said. Well, yes indeed the toxic species would have an additional cost compare to the non-toxic prey species. I think that comparing their costs only make sense if these two species have a relatively high overlap of ecological niche (due to principle of competitive exclusion).


text:
Looking for a DNA sequence
I am not a biologist. Please pardon me, if my question does not make sense.
I am trying to obtain a DNA sequence for pattern analysis in Matlab. I used to generate random sequence randseq in Matlab. However, I am trying to obtain some real dataset.
Any idea where I can obtain the DNA dataset. I am looking at a dataset having acgt patterns
Thanks
EDIT : Thanks a lot guys, I found it here. : http://www.ncbi.nlm.nih.gov/nucest?term=((human%5BComponent+Accession%5D)+AND+normal+Breast+gene+sequence)+AND+1000%3A10000%5BSequence+Length%5D

There are several nucleotide sequence datbases available. One of the largest is the NCBI GenBank at http://www.ncbi.nlm.nih.gov/genbank/
You may use the search bar at the top to search for nucleotide sequences belonging to a certain organism or gene. For example, searching for "E coli" will give you the full genome sequences for several bacterial species, with a strain of E. coli as the top result. The E. coli genome is about 5 MB large. If you want a single gene sequence, searching for "sonic hedgehog" (without quotes) will return the human hedgehog gene as the top result, which is 1,481 basepairs long.
To get a sequence in raw format, select "FASTA" below the entry. At the page you get sent to  , chose "send" in the upper right corner and under "Choose destination", "file". This will give you a .fasta file, the standard raw sequence format. The first line, starting with ">" will be metadata, while the rest of the file consists of the nucleotide letters only.
Note that in addition to a,t,g and c, you may also find other characters, most often "n". These characters describe ambiguity in the sequence (meaning that the nucleotide at that position could not be determined). For a full description of the FASTA format sequence representation, see http://en.wikipedia.org/wiki/FASTA_format#Sequence_representation

You guys are the best. You are so unlike the IT guys. :) Always there to help.

Try Wolfram|Alpha at www.wolframalpha.com.  On the home page is Examples.   Click it.  One of the boxes on the next screen is Life Sciences. Within that box is a choice of Human genome. Click on that. You will then see examples of searches.  Those include sections of the human genome and even sequences for specific genes.   Choose an existing one or modify.  Then submit the query clicking on the = at the right hand side of the (sample) query.  When you get a result from such a search, mouse over the ATGC sequence and you will see a menu appear. The icon "A" allows you to copy the plaintext.  That should quickly give you sample sequences for further processing.

you can download real sequences from GENBANK. You can search model organism(s) or genetic marker(s) and download it in *.fasta or other format. Good luck!
http://www.ncbi.nlm.nih.gov/genbank/

Searching the database was really complicated. Thanks a lot for your support.

Since you don't seem to care what sequence you have as long as it is a real sequence, here's the (one of them anyway) mRNA sequence of the human tumor suppressor TP53, perhaps the most studied gene in the world:
http://www.ncbi.nlm.nih.gov/nuccore/371502115?report=fasta
If you prefer genomic sequences as opposed to mRNA:
http://www.ncbi.nlm.nih.gov/nuccore/383209646?report=fasta&from=5001&to=24149
And if you are looking for a larger sample size, here's the entire sequence of the human 22nd chromosome (careful, largish file, ~30MB)
http://www.ncbi.nlm.nih.gov/nuccore/568801965?report=fasta
Finally, if you want a lot of sequence, you can download the entire human genome from here (careful: 905MB):
ftp://hgdownload.soe.ucsc.edu/goldenPath/hg19/bigZips/chromFa.tar.gz

No, I do, I am looking for a very particular pattern from humans suffering from cancer. Thanks a lot

@www.sapnaedu.in huh? What pattern? You don't mention anything like that in your question. The sequences you are using are not from cancer, do you want sequences from cancer patients?

Yes, I am sorry, I was not aware of it earlier. Now that I am able to find the sequences, I am particularly looking for patterns from Humans suffering from cancer.

@www.sapnaedu.in please explain what you are actually trying to do. There are hundreds or thousands of available cancer datasets but which one is good for you will depend on the analysis you will perform. Most sequences will be identical in cancer and healthy tissue. If you want to find patterns characteristic of cancer you will need to be more specific.

I am really sorry, I donot have much information to share apart from what I have already mentioned. I will post it later once I have it.


text:
Why do 6-8% of diphtheria patients do not develop natural immunity after being affected?
I am thinking of why some patients do not have natural immunity after exposure to the A-B toxin of diphthria.
I think the A-B exotoxin is the key factor causing this disease and should trigger memory cells to form.
DT has both local and systemic effects.
Locally, its action on epithelial cells leads to necrosis and inflammation, forming a pseudomembrane composed of a coagulum of fibrin, leukocytes and cellular debris.
Absorption and circulation of DT allow binding throughout the body.
Local effects produce pseudomembrane.
The major impact of transduction in pathogens is the introduction and stable inheritance of virulence genes such as those coding for toxins.
C diphtheriae is lysogenic with a phage containing the diphtheria toxin gene.
Diphtheria toxin is produced by C diphtheriae only when infected with a bacteriophage that integrates the toxin-encoding genetic elements into the bacteria
The toxicity for intact cells depends on toxin binding and uptake.
In other words, the net effect of the toxin depends on the function of the target protein and the function of the cell.
B subunit binds to receptors that regulate cell growth and differentiation, thus exploiting a normal cell function.
A subunit inhibits protein synthesis.
B subunit binding determines cell susceptibility.
Absorption and circulation of DT allow binding throughout the body.
I think this uptake does not occur sufficiently with patients without natural immunity stimulation.
I think the reason for no natural immunity for some patients after toxin exposure is that the host does not stimulate enough adaptive immunity and no memory cells are built.
Again, this is because the bacteria has little invasive capacity.
Diphtheria is due to the local and systemic effects of DT with potent cytotoxic features.
The uptake of the toxin varies also among some patients.
So other patients have probably more local effects.
This would explain partially why the adaptive immunity is not triggered.
Diphtheria toxin is antigenic itself.
So it can stimulate the production of protective antitoxin antibodies during natural infection.
In those patients without development of natural immunity, A subunit fails to bind EF-2, probably.
One reason is that the toxin does not get into bloodstream in 6-8% cases, and so natural immunity is developed.
So there is too low effective dose of diphtheria for some patients to invade the epithelium and trigger the adaptive immune response and create memory cells.
Sources: Murray Microbiology, Sherris Microbiology and Jawetz Microbiology.
Why do 6-8% of diphtheria patients not develop natural immunity after being infected?

Couple of quick thoughts. Extoxins by definition are secreted, and making antibodies to them can be great to limit their toxic effects, but does little to diphtheria, which is what you would want to remove if it's being pathogenic.  I'm going to have to look more into the lit to see if it seems host or path specific.

@Masi Do you have a source for the 6-8%?

There are two other, but rather exotic possibilites which explain why people do not develop immunity after an diphtheria infection. These are unlikely to get to 6-8% of the cases which @Masi writes, but I am missing the reference here.
The first possibility are people with chronic renal failure. They have problems with their immune responses since their antigenpresenting cells do not get the necessary co-stimulatory signal by the T-cells. See this paper. People with other problems in their T-cells or the co-stimulatory signal would have this problem, too. See this article.
The other possibility would be the distribution of the antibodies. The diphteria toxin is made out of two subunits, A and B. B is important for making the way of A into the cell, A gets cleaved in this process and fully active. When the antibodies made in the process are mostly against A (and then against parts, which change their conformation after the cleavage), this antibodies are mostly useless to fight the toxin. See this paper.
One (but is complete speculative) possibility is on the toxin itself. It could be possible, that some people are more sensitive to the diphtheria toxin, so that the amounts necessary for the negative effects are too small to trigger an adequate immune response. This is known for the tetanus toxin, where even a survived infection doesn't provide immunity (except when people are vaccinated afterwards) as the toxin is so toxic, that it doesn't trigger the immune system. The caveat is, that the diphteria toxin is about 3 orders of magnitude less toxic than the tetanus toxin.

may I ask if there are really no survivors of tetanus whatsoever, that become immune ? Even if they are not immune, do they have antibidies for some time ? I would expect this to happen as a stochastic effect. I only know - actually from antivaxers, but the sources seem legit - that there are some unvaccinated people, especially children, who have antitoxin antibodies without a known history of tetanus.

@Barbara As I explained above, survivors do not become immune because the tetanus toxin is so toxic, that the amount necessary to poison a person (we are talking about an LD50 of 2.5-3 ng/kg) will not trigger an immne response. Can you please cite the source?

Naturally acquired immunity to tetanus toxin in an isolated community.
H Matzkin, S Regev
Infect Immun. 1985 Apr; 48(1): 267–268.
PMCID: PMC261948

[Naturally acquired tetanus antitoxin in the serum of children and adults in Mali].
Ehrengut W, Sarateanu DE, AgRhaly A, Koumaré B, Simaga SY, Diallo D.
Immun Infekt. 1983 Nov;11(6):229-32. German.
PMID: 6680401

Naturally acquired antibodies to tetanus toxin in humans and animals from the galápagos islands.
Veronesi R, Bizzini B, Focaccia R, Coscina AL, Mazza CC, Focaccia MT, Carraro F, Honningman MN.
J Infect Dis. 1983 Feb;147(2):308-11.
PMID: 6827147

Response to single dose of tetanus vaccine in subjects with naturally acquired tetanus antitoxin.
Dastur FD, Awatramani VP, Dixit SK, D'Sa JA, Cooverji ND, Anand MP.
Lancet. 1981 Aug 1;2(8240):219-22.
PMID: 6114281

New concepts on tetanus immunization: naturally acquired immunity.
Veronesi R, Cecin H, Corrêa A, Tavares J, Moraes C, Bertoldo OJ.
J Hyg Epidemiol Microbiol Immunol. 1975;19(1):126-34.
PMID: 1092755

In this article they look at the development of natural immunity to diptheria in those who were vaccinated. I could not find any studies on people who had acquired it naturally.
http://www.sciencedirect.com/science/article/pii/S0264410X97001485
They found that the development of immunity to diptheria vaccine depended on several factors:

Time lapsed since last vaccination
Females had lower immunity rates
Number of previous vaccinations
Last vaccination within the first 3 years of life
Age

What this may mean for individuals who are affected is that similar factors could play a role preventing them from acquiring immmunity to diptheria. Indeed, some of the factors like last immunization and number of vaccinations are logical since diptheria may evolve or there may be different strains so the body needs to have the lastest antibodies for immunity.

All the points above are interesting, but they are only important for answering the question why people get diphtheria and not why they are not developing immunity after having the disease. Evolution of strains is not a problem, since the vaccine is directed against the toxin and not against some fast changing component. Otherwise we would need a new vaccination every year (or at least every few years) which is not the case.

The question asks why do some people not develop immunity. My answer consists of reasons why this may be the case-- at the macro level (for vaccinations). I did not go into molecular mechanisms of why diptheria does not result in immunity in the 6-8% because I could not find any references in the literature. If you imagine the evidence that would need to be gathered to establish this, you would realize this is a tall order. Evolution of strains is documented in the literature -- see this article for insight http://jid.oxfordjournals.org/content/181/Supplement_1/S168.full .

Thats why I asked Masi for the reference on this quote. There are some possible mechanisms why people are not developing a immune response, I will write about this later. The evolution of the strains is obviously not causing problems, the vaccination seems to work.

Just wanted to add that this is a common problem with vaccines.

...consider an actual measles outbreak in Colorado in December 1994.5 Out of 625 children exposed to the disease, 17 got measles. Of those 609 who had previously been vaccinated, only 10 (or 1.6%) developed measles. Of the 16 children who were not immunized, 7 (or 44%) developed measles. Thus, the risk for immunized children was less than 2% while the risk for unimmunized children was 44%.

Most vaccine development struggles to reach high immune efficacy; You usually can't just inject some dead bacteria or virus and expect to get an immune response.
In particular I think there has been adaptations in the immune system to DT such that it tends to stimulate an immune response.  This is pretty much a reaction to the peptide sequence itself.  We know this because since the 1980s there has been concern that the live toxins in DPT vaccines might be causing health problems with young children.  (They don't).  As such, acellular vaccines were developed where just a few proteins were included - the cell was not used, and DT was produced where only a fragment was added or the toxin was rendered inactive by mutagenesis. DT is such a reliable component that by itself it can illicit an 88% immunity rate.
These DT fragments are formulated with other bacterial components to create new vaccines.
The failure of the vaccine on occasion is most likely the result of individual variations in immune loci. The immune system is highly complex and also highly variable from individual to individual even amongst close relatives.  their immune activation or their defenses (complement and immunoglobin pathways) may make some individuals more susceptible to diphtheria than others.
The science of vaccine formulation is highly empirical; I don't think it is understood why some molecules evoke a broadly distributed reaction and others do not.  Even so the diphtheria toxin is one of the more universal immune stimulants known.  I don't think that a completely universal adjuvant (something added to a vaccine to stimulate an immune response) is known.

This is a common problem with vaccinations, they have no 100% succes rate. For the diphtheria number Masi mentioned it would be interesting to know if these are immunized and so on...

expanded answer


text:
S. pyogenes' skin infection diagnostics
S. pyogenes is "flesh-eating" bacteria.
It results from life-theatening myonecrosis caused by this organism.
S. pyogenes avoids phagocytosis (mediated primarily by capsule, M and M-like proteins, C5a peptidase), adhere to and invade host cells (M protein, lipoteichoic, F protein), and produce toxins (streptococcal pyrogenic exotoxins, steptolysin S, streptolsin O, streptokinase, DNases).
Suppurative diseases: pharyngitis, soft-tissue infections.
Erysipelas: localised skin infection with pain, inflammation, lymph node enlargement and systemic symptoms.
Cellulitis: infection of the skin that involves the subcutaneous tissues.
Necrotising fasciitis: deep infection of skin that involves destruction of muscle and fat layers.
I think these are most its skin infections. But what about its diagnostics?
I think take biopsy from living tissue, not from necrotic.
If pus, then probably from it.
I think we can do Gram staining, recognise gram-positive cocci like in a string
Then, we can do hydrogen peroxide test - if no bubbles, then suspicion to S. pyogenes, since catalase negative.
The do optochin test which is positive for S. pyogenes.
What is the correct procedure for doing skin infection diagnostics for group A streptococci?

S. pyogenes cultured on Blood Agar should show beta-hemolysis. B-hemolytic colonies can be further identified as S. pyogenes by the results of negative catalase (hydrogen peroxide) test, positive L-pyrrolidonyl arylamidase (PYR) reaction (1) and sensitivity to Bacitracin (2). See https://www.inkling.com/read/medical-microbiology-murray-rosenthal-pfaller-7th/chapter-19/streptococcus-pyogenes
PCR may also be used: http://www.sciencedirect.com/science/article/pii/S0923250805000215


text:
Beginning of the urogenital system
Are any invertebrate nephridia (proto/meta) homologous with vertebrate kidneys in the sense that embryologically they also begin together with the genital system?  When did the embryologic association between reproduction and osmoregulartion/metabolite elimination begin in terms of evolution?

I dont think invertebrates have urogenital system.

So which one, excretory or reproductive, is homologous to the vertebrate urogenital system... I understand that invertebrate is a polyphyletic category of exclusion, but I'm talking about the closest related animal phyla to vertebrate... I guess I should'look deeper into lancets and hagfish...

The urogenital system as a cohesive functional unit probably evolved very early in vertebrate history. Hagfishes and lampreys have separate systems for reproduction and excretion. More derived groups of fishes use kidney tubules and ducts for sperm delivery outside the body (Helfman et al. 2009).
The vertebrate nephron may be homologous to the invertebrate nephridia (Ruppert 1994). The genetics underlying the development of vertebrate female reproductive organs shows many homologies with invertebrate reproductive organs (Kobayashi and Behringer 2003)
I would hypothesize that the both the reproductive and extrectory systems of vertebrates show corresponding homologies to invertebrate organ systems (at least genetic and developmental homologies) but evolution of the urogenital organ system did not evolve until the early vertebrates.
Literature Cited
Helfman, G.S. et al. 2009. The Diversity of Fishes. Biology, Evolution and Ecology. Wiley-Blackwell, Oxford, UK.
Kobayashi, A. ad R.R. Behringer. 2003. Developmental genetics of the female reproductive tract in mammals. Nature Reviews Genetics 4: 969-980.
Ruppert, E.E. 1994. Evolutionary origin of the vertebrate nephron. American Zoologist 34: 542-553.

authors: Костя Дряхлов


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Why do cells vary in shape and function when they have the same genome and the same organelles?
Why do cells vary in shape and function when they have the same genome and the same organelles. For example: why do all cells have nuclei but red blood cell's don't; why can't the cells of a eye perform the function of the tongue; and the list goes on and on. If you say it is because of gene regulation, so then how does the RNA know to transcribe the specific genes that are necessary to that particular cell?

The shared genome also produces the different sexes, this and the multipurpose genome (or which is present in many different cell and tissues in an individual) leads to a conflict over gene optimization

There is a lot of literature available on this subject - Search for gene expression in multicellular organisms, enhancers, control elements etc.

Remember that not all cells (in the same organism) have the same DNA and organelles - most notably being red blood cells in mammals which are anuclear, have no DNA, and also lack many organelles.

Because cells are not only characterized by by their genetic material and other interior components, but also by the genes they express. Cells have to fulfill multiple different functions to be able to build complex multicellular organisms. Differently expressed genes lead to different proteins made in the cell, which leads to different morphology, shape or function. For example melanocytes in the skin are highly specialized cells which mostly make the pigment melanin. Plasma cells on the other are highly specialised for making antibodies.
It is all about regulation of genes. The RNA doesn't know or transcribe anything -
the DNA is trancribed into the mRNA (which is then further processed) and finally translated into proteins. Cells develop from precursors which proliferate and finally differentiate into highly specific cells. This progress is controlled and activated by specific transcription factors and growth factors. For example: pigment cells only develop, when a specific transcription factor is present. When this factor cannot be expressed, these cells do not develop at all.
This developmental process is shown schematically in the figure below (the figure is from the NIH website on stem cells):

Could be absolutely perfect with some sources and link for further readings imho.

@A.Bourgoin I'll look into it tomorrow.

The easy answer is: Each cell is living in its own environment and getting different signals that they act on. (Environmental cue --> Cell signal --> Cell turns on or off different genes based on these signals)
Recognizing that all cells have the same DNA is a good place to start. Imagine a single celled zygote formed from the union of one sperm and one egg...Early on, each of cell is capable of reacting in the same way to the same signals. And as the early embryo's cells begin proliferating, but before it implants in the womb, each cell is pretty much the same. And each cell has the possibility of becoming any of the myriad of cell types in the body. In fact, you can even split these early embryos apart and generate twins - two bodies (or more) instead of one.
However, soon, the embryo comes to rest against the wall of the womb and implant there. From this point on, not every cell gets the same signals. One cell is resting against the wall of the womb, another is several cell-widths away from the wall. A bit of randomness acts as the start of differentiation. The two cells start reacting to the signals in their slightly different environment and progress towards different fates. As development proceeds, these small differences become more pronounced and cells begin to commit to distinct lineages. No longer are they 'pluripotent' and able to become any given cell. The possibilities are more restricted as the environment of each cell gets more and more different. Cells 'commit' to their decisions and can't go back.
One good book you can pick up that will walk you through this idea is Neil Shubin's 'Your Inner Fish.' The overall story is about evolution of the first land quadrapeds, but he pursues a lot of different lines of evidence, and several of them involve molecular biology and cell differentiation.

Despite of the fact that all cells have the same genome, not all the genes contained in the cell nuclei are functional. During embryonic development, cells are subjected constantly to division and differentiation processes; this means that in the earliest stages of embryonic development, each cell of the embryo can form, by itself, a new complete body. However, these cells loose their ability of "all-forming" as the embryonic development progresses and they become able to form only certain group of tissues. Lately, they would be only able to form just one type of tissue.
All these cells have, obviously, the same genes, but what makes a cell of early stages of embryo development (stem cell) different from another of the body if they have the same genes? The answer is that although they have identical genes, differentiated cells use less genes than a stem cells would use. For this reason, only a certain number of genes of the total that a differentiated cell contains, are in use. A neuron, for example, wouldn't need a gene that produces hair protein because simply, its function isn't that, so neurons inactivate the gene of hair-producing.
There is much more to investigate and to research in this field because many questions still remain without answer such as how cells acquire certain shapes and not other or how do they form perfect 3D organized shapes (tissues and organs) and much more question in this way.


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Evolution in fruits
So, I saw a video on YouTube that says the banana we eat today is not what a banana looked like years ago. Since the banana has been genetically modified over the years, does that qualify as evolution?

Yes. Modern domesticated bananas have evolved from ancestral wild species under the influence of humans. Quoting D'Hont et al.: (1)

The [banana] domestication process started some 7,000 years ago in
  Southeast Asia. It involved hybridizations between diverse species and
  subspecies, fostered by human migrations, and selection of diploid and
  triploid seedless, parthenocarpic hybrids thereafter widely dispersed
  by vegetative propagation.

Modern bananas have undergone extensive evolution from the original wild species. The selection pressure has in part been provided by humans, who have selected the most nutritious/tasty/desirable examplars and facilitated their reproduction. This can be considered "artificial selection" as opposed to "natural selection", but does not change the fact that an evolutionary process has taken place. The UC Berkeley website "Understanding Evolution" gives the following definition of "artificial selection".(2)

A process in which humans consciously select for or against particular
  features in organisms. For example, the human may allow only organisms
  with the desired feature to reproduce or may provide more resources to
  the organisms with the desired feature. This process causes
  evolutionary change in the organism and is analogous to natural
  selection, only with humans, not nature, doing the selecting.

Thus, whether the selection is considered "natural" or "artificial", the end result is evolution.

"Modern" should be understood as "domesticated". The wild relatives and even ancestors are still there:

Yes. Good point.

It's just selective breeding, not evolution. Far from it.

I actually got an answer from watching Cosmos. It's called Artificial Selection - the reason why we have different breeds of dogs today.

You could say it clasiffies as evolution only if you accept that the artificial things humans have done to bananas are actually natural occurences. I personally don't think they are, because intent is at play here, and evolution is a natural process without intent.
Evolution is not when something gets better. That's the misconception behind your question.
If humans would just happen to eat the tasty bananas first, what would happen is negative selection and all the remaining bananas (which lived long enough to reproduce) wouldn't be tasty. Bananas would get less tasty in order to survive.
What actually happened goes against the natural process of selection, and is something completely different to the concepts of evolution which led to us evolving intelligence, for example. This is just selective breeding. Nothing as grand as evolution.
Evolution is a natural process which led to intelligent species from single-cell organisms, and is a continuous process of random mutations being selected for or against by natural causes. Evolution has no intent and is a natural random process. A grand one, as all biology depends on it, and we depend on it.
Genetic engineering, on the other hand, has intent to improve things, and happens on a much smaller scale than the natural process of evolution. Genetic engineering of any kind, whether it be tinkering with the genes or just inbreeding to create a new breed, is artificial and is being done by an intelligent creature as opposed to nature. Calling genetic engineering a tool for evolution is the same mistake that eugenics proponents made.

I must disagree with this answer - I have updated my own in response.

I still disagree with you, as I believe evolution is a grand process that can only be tied to natural selection, not artificial selection. But then again, whenever you reach humans in evolutionary biology you're bound to be up against something that is completely different from the several billions of years prior to development of human intelligence.

I agree somewhat with the "humans are different" idea, but I still think declaring humans and human influence as "unnatural" is rather arbitrary. Species affect each other's evolution all the time, and I see no reason why the level of cognitive abilities of humans should change the name we use for that process. I see your point though.

Evolutionary biologists consider artificial selection to be a valid input into the process of evolution.  Evolution is the gradual change itself, over time, and the varieties it produces are selected against by various criteria.

By this argument human are almost incapable of evolution, since it is humans who decide who they mate with.