text:
How do high-throughput/NGS sequencers calculate quality scores?
I am confused as to how quality scores are actually calculated by DNA sequencers like Illumina. For each base call, some quality predictor value is computed, based on various properties of the sequencing machine, like intensity of light during the read.
Do we know exactly how these quality scores are computed? Exactly how many factors go into computing these QUAL values?

only have experience with Illumina platforms here's a link to the basics Illumina quality info More detailed Illumina info Take a look at the refs in that document to go deeper. (Am assuming you don't mean variant call quality scores which, in the pipeline I use, is all handled post sequencing)

@user3234810 Thanks. But I was looking for more information than that. There's some relationship between "signal-to-noise" and quality scores. How exactly Illumina calculates these, I don't know.

The quality score calculations are different for different types of machines. Specifically interested in Illumina?

@WYSIWYG Actually, any sequencer would do. I just mentioned Illumina as a starting point.

@ShanZhengYang I would suggest that you restrict your question to one kind of machine (or kinds of machine with same base calling technique). You can stick to just Illumina. Moreover, even for illumina there are different base calling approaches.

@WYSIWYG That's reasonable. Let's keep the discussion focused on base calling with Illumina.

@ShanZhengYang You can have a look at my answer

I'm restricting this answer to Illumina. Even then, I don't know about the exact details of the raw data analysis (it is a proprietary software).
Basically Illumina records the sequence based on photographic images. Each nucleotide has a distinct fluorescent label. In a cycle, a nucleotide is pumped and unincorporated nucleotides are washed off (this is repeated for all nucleotides). A laser excites the fluorophore and the emitted light is recorded in the form of a photograph. The template DNA is present in the form of clusters of strands (at a given location), which enables easy visual identification of the fluorescence.
Base calling is done using image analysis. Each image is analysed for intensities of different colours and based on this the quality score is calculated. The quality score is basically the log likelihood of a occurrence nucleotide at a given position (based on its colour intensity) compared to other nucleotides.
This is the most simple explanation of how Illumina does base calling. There are different kinds of errors and biases and there are different statistical approaches to correct for them.
Have a look at following references for more details:

Ledergerber, Christian, and Christophe Dessimoz. "Base-calling for next-generation sequencing platforms." Briefings in bioinformatics (2011): bbq077.
Illumina MiSeq Imaging and Base Calling course
Genome Analysis Wiki


text:
Looking for university/graduate-level texts on RNA
Although I was not a biology major in college, I took the biology introduction sequence, as well as organic chemistry and biochemistry.
I would like to learn more about RNA and ribozymes. What texts/textbooks are currently used? Perhaps it's best to begin with a genetics textbook.
The scope of the book should cover be at a undergraduate level or higher, and should cover the dynamics and purpose of ribozymes.

I'd start with the most recent edition of Watson's "Molecular Biology of the Gene". The problem with RNA books is you go too old (which may still be relatively new), you could be in the dark ages of RNA. I'd say newer is better, and there's a new edition of Molecular Biology of RNA set to release in '16. Textbooks are perhaps more unreliable than literature in this respect given some of the good ones date back to 2011.

Jennifer Doudna is probably the preeminent researcher in RNA today. I would say that reading her papers would give you graduate level coverage of the topic. Watson's MBOG may be a little too generic if you are focused solely on RNA, and there are better choices of advanced level genetics texts if your interest in more general genetics.

Please read the tag-wiki for book-recommendation. You should address all the mentioned points in detail, otherwise your question would be considered broad/opinion based.

@AMR "there are better choices of advanced level genetics texts if your interest in more general genetics." Do you have a suggestion? Thanks

I hesitate to recommend this Text because it is difficult to read... but Lewin's Genes XI. This is the Amazon.com page. Even in their description they say it is designed for Upper Level or Graduate Genetics, and they are not exaggerating. The material is excellent, but it is difficult to use as a textbook. They will make references to topics in other sections, but they reference by name, so you have to go to the TOC to figure out where in the book you need to go...

... I had the physical edition... An electronic version may be easier if they properly designed it with links. The Kindle version is overpriced compared to paperback or used copies. Watson is probably the way to go if you need an introduction, I was responding to your suggestion that it should be at a graduate level. Our graduate level genetics course is using Genetics, From Genes to Genomes by Hartwell, however I have not yet reviewed it so can't comment definitively.

As suggested by others, you can start with some basics on molecular biology. Genes - Benjamin Lewin and  Molecular Biology of the Gene - James Watson et al. are good books for the basics.
I haven't seen any book dedicated to RNA-biology and most of my understanding has come from reviews.
You can start by studying RNA secondary (and higher order) structures which is essential for understanding how riboswitches function. I would suggest that you first begin with the wikipedia article on this (it is not that great). The above-mentioned books would also cover the basics. You may then have a look at this review which is about thermodynamic and kinetic aspects of RNA-hairpins:
       Structures, Kinetics, Thermodynamics, and Biological Functions of RNA Hairpins
For Riboswitches you can refer to these reviews, which are quite comprehensive:

Ribozymes, riboswitches and beyond: regulation of gene expression without proteins
Riboswitches: Emerging Themes in RNA Structure and function

This is another comprehensive review on ribozymes:
        Ribozyme Structures and Mechanisms

PS: Some of these articles may not be freely available. You can mail the corresponding author (email address would be mentioned in the article) requesting for a reprint.

source: Stack Exchange

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text:
What are the ants underneath leafs in my garden doing?
So a few days ago I spotted a couple of ants underneath some leafs of a major branch of a tree in my garden. Yesterday I had the impression the amount of leafs being occupied by ants has increased a lot what then made me curious. So I spent quite some time yesterday observing one of the minor branches the ants had been very active on by that time. What I figured so far:
Underneath each leaf the ants are gathering, is an insect that looks sort of similar to a fruit fly (gonna call it fruit fly for simplicity, despite it certainly is something different).
Around that insect are varying amounts of dots, which could be eggs or larvae. The ants seem to collect something from the larvae and also seem to be interacting with the fruitfly.

At some point I spotted on the far end of the minor branch 2 living fruitfly. They seemed to be not capable of flight despite having wings. So I concluded they must just have been hatched. They seemed to try escaping the branch, as they pretty directly were just running up all the branch. Having almost made it from the minor to the major branch, the 2 fruitfly came across an ant, which immediately attacked both of them on contact. I was expecting the ant to carry them away then. While being attacked, both fruit fly tried to hide in the attatchment point of a leaf. The ant was circling around the attatchment point of the first fruitfly I was wondering why it did not carry that fly away, since it could clearly geto to that fly. After roughly a minute the ant turned back to their hide, having fully ignored the second fly, after attacking it once, and also leaving the first fly motionless at the attatchment point it was trying to find cover in.
But what happened a few minutes later is what left me astonished.
A few minutes after the 2 fruitfly had been attacked, roughly at the same time, they started moving again. But different then before (kinda looked as if they had been injured but not killed by the ant). They did not seem like trying to escape the branch anymore. But just slowly moving to the next leaf in range continuing for 1 to 2 centimeters going underneath the leaf and then stopping there. Pretty much being in a position, as a fruitfly is positioned underneath the other leafs, where the ants are gathering .
After like 4 or 5 hours 1 ant for the first time scouted the leaf these 2 flys went on. And in fact, other than attacking them again, this ant interacted with the 2 fruitfly1 like the ants under the other leaves interact with the fruitfly positioned on those leaves.

By now (over 12 hours later) the 2 fruitfly are still there I just checked and the small fruitfly that was only being attacked once, disappeared. The other one still being at the very same spot it moved to yesterday, tho. I would consider them being dead. But I am not even sure about that.
So what exactly are the ants I observed there doing?
If any other pictures would be helpful ask for it, I can take them later today.
Also I have a speculation what it could be that was going on here, but not sure if that would anyhow improve this OP.
Oh, since I can't identify the species, it might be useful to know at least: this is happening in Bavaria - Germany

1 well with 1 of them, the other that had just been attacked once, was simply being ignored

From what you described, it seems to me the "fruitflies" are aphids and the ants are farming them. This is a widespread and common phenomenon known as ants-aphid mutualism.
P.S.
I elaborate a bit. Aphids feed on plant sap, rich in sugar, which they don't digest completely. The excretions (poop) are thus still rich in sugar (you may have noticed how your car windows get sticky sometimes under tress - that's aphids poop, I believe). Some ant species co-evolved with particular aphids and collect their excretions, a valuable sugary energy source. In turn, ants protect aphids from predators and they move them around to cover other good plant spots for aphids to suck sap and even move them to different plant individuals. This mutualistic interaction between aphids and ants is quite common and causes a lot of economic losses to the agriculture sector.
The behavior you observed of an ant attacking aphids was probably more the ant checking them and trying to evoke a pooping response. Sometimes they get them between their jaws and carry them around. Aphids also have quite complex social structure, with an optimal spatial organization. Hard to say if ants are moving them around to reach this optimal "farm density" or for other reasons.
TL;DR ants farm aphids as humans farm cows. When ants interact with aphids they are mostly checking them and trying to get their sugary poop.
/Emilio

Yeah, I can Identify the "fruitflys" as one of the kinds being found in that wikipedia article you linked. But could you please elaborate a bit more on what is going on there? I.e. where were those individuals coming from that had been attacked in my observation and i.e. why had they been attacked? And why the attack seemingly caused a change in their behavior?

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text:
Is there a name for dominant-intraspecific competition?
Some ecological competition dynamics have particular names (e.g.: scramble competition, contest competition, ...). I wonder if there's such a name for competition dynamics where the interspecific interaction is weaker than the intraspecific one.
By weaker I mean that the non-diagonal elements of the community matrix are lower than the diagonal ones.

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text:
Cis-AB phenotype verification
I know that my blood type is AB. I wanted to know if I am cis-AB since cis-AB seems to have a different approach in blood transfusion.
Is there a lab test that can verify is a person is under cis-AB blood group phenotype?

First,do you have any probe that your type is AB chimera transferase? I discovered it because my mother is type AB and my brother type O. I have 2 sisters and my self cis-AB (my younger sister and me rh-). If you carried a cis-AB allele and another allele was  B1, surely you got A and B type compatible, but if you carried an A1 or O1 allele, surely you got O type compatible or worse luck. For example, I have a very rare multi-blood genotypes (rh D- C-G-, K1-, M+N-S+s+ and another unknown antigen). Actually, it doesn't matter if you are cis or trans AB phenotype, the most important thing is to know if another 34 blood groups and 200 minor groups and 600 blood antigenes have a rare combination that makes blood incompatibily or autologous like Bombay phenotype or autotransfusion like me.
If you want to be sure about your genotype, you must make dna test with SNPs of 10 cis-AB alleles


text:
How is achieved the loss of heat through vasodilation?
I know it is the widening of blood vessels, loosing heat in this way. But is it achieved through: sweat evaporation, the increase of cardiac rhythm, the increase of respiratory/ breathing rhythm or frequent urination?

It's unclear, are you asking what is/causes vasodilation or how it contributes to heat loss in the body?

@Nathan the loss of heat through vasodilation is achieved through____???

See help pages regarding homework questions.

Sweat evaporation is the most correct answer you have mentioned.  Vasodilation increases blood flow, allowing for more blood to be cooled be vessels closer to the surface of the skin.  It's increasing the surface area the blood interacts with, which always allows for faster heat transfer.


text:
How a vegan can consume all the needed varied proteins / amino acids?
I would like to ask if there are some proteins that the human body needs and can being endowed only from meat?
According this:

Other protein sources, such as fruits, vegetables, grains, nuts and
  seeds, lack one or more essential amino acids. Vegetarians need to be
  aware of this. People who don’t eat meat, fish, poultry, eggs, or
  dairy products need to eat a variety of protein-containing foods each
  day in order to get all the amino acids needed to make new protein.

How a vegan can complete these missing proteins?

this might be better for the cooking exchange.https://cooking.stackexchange.com/ Otherwise this borders on medical advice or at least nutritional advice.

Proteins are made up of amino acids. It isn't particular proteins that are necessary in diet, but particular amino acids. For humans, these come primarily from breaking down the proteins in foods we eat.
Essential amino acids are the amino acids that humans cannot synthesize; other amino acids can be synthesized from these, but they do not need to be part of the diet. Not all sources of protein have sufficient quantities of all of the essential amino acids. When people refer to a protein source as "incomplete" they mean that particular source is low on one or more of the essential amino acids.
Meat products are typically "complete" because they contain all of the essential amino acids together. Therefore, if you subsisted on various foods but only got your protein from one animal source, you would be okay.
Some plant products do not have all the essential amino acids in large concentrations. However, if you combine protein sources from different "incomplete" plant sources that together cover these deficiencies, there is no disadvantage compared to a single "complete" source.
You also have a fairly substantial reserve of amino acids in the form of all the proteins in the body, which are constantly broken down and recycled. The daily protein intake is just a tiny fraction of the total amino acid content in the body.
Here is a paper that talks about some of these issues, and addresses some of the myths about balancing proteins. The quick summary is that problems develop if you get your sole protein from a source that is low in a particular essential amino acids over a long time period, but there is no need to ensure every meal contain all the amino acids.
It is possible for people on unusual protein diets, such as vegans, to develop a particular amino acid deficiency. There are many many guides on the internet for protein sources to mix to avoid this problem. A common combination is a legume (beans, peanuts) and a grain (wheat, rice). There are also some vegetable sources that provide complete protein nutrition - soy, for example, mostly works as long as it is not truly the only source.
References:
Young, V. R., & Pellett, P. L. (1994). Plant proteins in relation to human protein and amino acid nutrition. The American journal of clinical nutrition, 59(5), 1203S-1212S.

Does the human body know to construct all the needed proteins from the 20 amino acids? That sounds impossible. Why not to use the consumed proteins? Or it's impossible for them to penetrate the plasma membrane?

That's exactly the information contained in DNA: information on which amino acids to assemble and which order, and both directly and indirectly, how much of each protein to make. That's actually much simpler than trying to detect and incorporate foreign proteins. Foreign proteins could also be harmful, and they vary far too much between different organisms. This is how biology works from bacteria to plants and animals. Think about how similar cars are, and yet, if you have an engine from a BMW and a transmission from Toyota, good luck putting them together in that Ford body.

You probably meant "how can a vegan consume all the needed amino acids".
Proteins are made of amino acids chained together in a dehydration reaction. Digestion breaks the proteins, allowing the amino acids to be reused.
The most obvious and easy way to get all the amino acids: meat.
For vegans, rice and beans is a common way to get all the needed amino acids. Even today it remains a staple in many poor countries where meat isn't always readily available.


text:
What is Genome Folding?
Why does genome folding have such great interest?
For protein folding I could say that's important because protein's functionality closely depends on its folded state, since it affects its mechanical properties etc.
But genome? What does it even mean to be folded? Where does it happen? Any reference to papers would be appreciated.

probably supercoiling see: https://www.ncbi.nlm.nih.gov/books/NBK6243/. supercoiling is important to regulate transcription. Offcourse protein folding is important but to produce protein we need RNA and to produce RNA we need transcription. By tightly wouding DNA around proteins "we" can prevent RNA polymerase from transcribing the DNA and thereby silencing genes

They are not talking about supercoiling, at least solely. You said that protein function depends on its 3D structure. Well, the function of DNA  often depends on its spatial organization as well. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4792841/

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text:
How to surpass cell death?
Is it possible to surpass/decay cell death.  For example to disable the process muscles cells death, by tweaking the transduction pathways:

If it's not possible in our age Medicine, what it would take to do such thing in theory. The idea is to tweak the cell dying mechanisms for example to preserve neural and muscle cells for longer time. I am also curious how to disable a pathway or part of it.

Or maybe we could block cell death to increase cell death?!

Yes; It is possible to inhibit cell death.
There are several possibilities, of which many - as correctly recognized by you - involve changes in the activity of the cell death pathway (or related ones);
For a long (but still incomplete) list of commercially available drugs that inhibit cell death, please see: https://www.sigmaaldrich.com/life-science/cell-biology/cell-biology-products.html?TablePage=9559839
P.S.: Note that selectively inhibiting a pathway (note: not only cell-death) in only one cell type (or tissue - as you hinted at) usually requires a lot of tests and experimentation and isn't trivial.

How does the process of disabling a pathway work?

the processes will be highly drug and target specific


text:
Detecting cancer in the hyperplasia phase using image processing and SEM
I was wondering if it possible or have someone tried before to use SEM or some other spectroscopy to detect an cancer evolvement in its hyperplasia phase:

It sounds like a good way to do it? I guess that's how biopsy works, but maybe there is a way to do test people in the risk groups using this method.

Your "SEM" link links to the same image you included below.

Not exactly spectroscopy, but microscopy is common for detecting pre-cancerous tissue as part of the standard Pap Test given to women at regular intervals throughout their life:
https://en.wikipedia.org/wiki/Pap_test
This is typically done by a team of cytologists (with pathologists confirming results, particularly in abnormal cases), but is beginning to have automated screening (with human oversight).
One of the problems with any form of screening is that the potentially problematic tissue needs to be observed, which is typically quite an invasive procedure. A potential melanoma is usually cut out prior to analysis, and I expect that any procedure involving a scanning electron microscope will also require tissue removal prior to analysis.
A more interesting development in the area of cancer screening is in looking for cell-free genomic DNA in blood; blood tests are much better tolerated for screening purposes in comparison to other tissue removal. With high-throughput short-read sequencing, it's possible for some cancers to see DNA changes before their effects are detectable through histological methods.
Here's a review paper on cfDNA screening, which is is generally negative about the whole thing:
http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1002205
And one that is generally positive:
http://cancerres.aacrjournals.org/content/76/14_Supplement/LB-136.short


text:
What would it take to create life?
Assume we know the right DNA sequence of Mycoplasma Genitalium (MG) and we would like to create Life from scratch.
Also assume that matter has been created and we have the knowledge base as today.
How could we practically or theoretically take such a sequence and create a new MG?
I saw this in case you want to read more:
https://www.quantamagazine.org/first-support-for-a-physics-theory-of-life-20170726/

What do you mean by "from scratch"?

@canadianer given the chemical elements we know today.

You mean chemically synthesize the genome and every other component of the cell?

@canadianer yes, how to create life? Given the Big Bang occurred.

The first step would be a definition of life.

@John how a cell was created at the Big Bang?

It wasn't, there is about 10 billion years between the big bang and the first life. the earth is only about 4.5 billion years old.

I wouldn't say that recreating an organism from a known genome is creating life from scratch.  That would require designing a genome for an organism that doesn't exist in nature.

@AlwaysConfused At a minimum you would need some transcription machinery, and probably translation as well (unless you are able to transcribe your translation machinery).

@Bryan Krause: I suppose you might boodstrap things by inserting your created genome into an existing cell, thus using its machinery to create the first new creature.  But I think we're quite a ways from even doing that.

@jamesqf People are doing that; see this answer and the references therein. If memory serves me right, that group is actually working with Mycoplasma genitalium.

@jamesqf Yeah having an entire functioning cell's machinery and just replacing the DNA is definitely the easiest way to go (and the approach people in the field are taking, like canadianer mentions), even if it might be difficult to use a different species' machinery. The problem with simplifying it more than that is even bacteria and archaea have evolved well past the likely initial stages of life back in the putative RNA world. Everything in a cell is highly interconnected functionally.

@canadianer: While that's certainly interesting, I'm not sure that it counts as creating life.  For an analogy, it'd be rather like making a hot rod by stripping all the unnecessary pieces off a car, as opposed to designing & building a car from scratch.


text:
RAD sequencing: choosing the appropriate enzyme?
I’m studying Darwin’s finches genome and I say in some articles that the researchers used restriction enzymes to cut the DNA in their double digest RAD protocol. They are using EcoRI and MseI (GAATTC and TTAA), the two enzymes similar and used in Peterson, B. K., J. N. Weber, E. H. Kay, H. S. Fisher, and H. E. Hoekstra. 2012. Double digest RADseq: an inexpensive method for de novo SNP discovery and genotyping in model and non-model species. PLoS ONE 7:e37135. (they are using EcoRI and MspI (GAATTC and CCGG).
Considering the huge list of restriction enzymes how to choose the appropriate enzyme? Is it a complete guess? The size of the genome of finches is about 1.07Gb. Do I have to take this in consideration?
The reference genome is available Zhang, G., P. Parker, B. Li, H. Li, and J. Wang. 2012. The genome of Darwin’s Finch (Geospiza fortis). GigaScience.

maybe R.EcoRII or FokI/Taq52I?

Why would you choose these?

R.EcoRII because of its molecular mass (45.2 kDa), it targets CCWGG, C-terminal domain of restriction endonuclease and apologies, I meant Tsp49I rather than Taq52I and this because of its relatively high pH optimum, reaching enzyme activity peak at rather "high" temperatures, its a thermostable neoschizomer


text:
Capture recapture for only two visit assuming a open population model
I have a study system where I’m doing a capture recapture analysis. I mark fish in one year and I’m recapturing a subset of them the next year.
I only have 2 capture events. Since a lot of time has passed, relative to the fish, between the two episode of recapture, I cannot assume a closed population model. Is there an alternative?
What mark-recapture model would be best for this situation given that I want to compute a recapture probability?

I would assume your goal is to estimate the population size, is that right? Do you have any idea of the migration rate in and out of your population?

Oh! Sorry, I forgot to mention that it's the recapture probabilities that I want. No I don't have the migration rate.

If the migration is 0, then it is the standard model. If the migration rate is 1, then the probability of recapture is 0. There is no way to estimate the recapture probability without having any information on the migration rate.

What do you mean then by the standard model?

I randomly referred to one of the multiple existing models. But it was misleading. Sorry about that. If you only want to estimate the probability of recapture knowing the population size, then this probability is just the fraction of those marked and the probability to recapture a given number of them follows a binomial or hypergeometric distribution depending on whether there is replacement. I am not sure I understand your question...

What fish are we talking about and in what ecosystem? Is it a migratory species in a river system (eg salmon) or not (eg pike)?

It's Three-spined stickleback in Canada, freshwater

In a classic closed population model, you can estimate population size with k=2 (where k is the number of events) but it's impossible to separate survival from recapture probability.

Seeing this formula you could expect to be able to estimate recapture probability dividing R by S but it would be an error since S = M*survival (ø) *probability of recapture (p) . Therefore it's imposible to separate p from ø when k<2.
Hope it helps !
Cheers

If you have unique ID's on each of the fish (instead of just marked and not marked) then you could use the Cormack-Jolly-Seber open population model.

Welcome to Biology.SE. Please provide some background to your answer, for example by providing an explanatory reference (and please also briefly describe what you reference which would be the CJS open population model in this case). I suggest you take the [tour] and have a look at how to provide what we consider good answers or your answer might be downvoted. Thank you.


text:
In a fitness landscape, is fitness relative or absolute?
I was asked if the fitness of a fitness landscape is absolute or relative.
Fitness landscapes are usually graphed with a fitness function that uses either phenotypes or genotypes in relation to fitness or one of its component.
More specifically, if the fitness measured is survival, and it's computed based on a quadratic model, does that means that every individual survival probability is an absolute measure of "fitness" (survival)?
Or since it's computed from a model, would it be better to find the relative contribution of a variable on the predictor in the model and say that the "fitness" is relative to a trait if it's computed with multiple traits?
How does the mean fitness of the population influence the model, which will determinate the fitness of all individuals? Is this "mean contribution of the population's fitness" a relative measure of fitness?
My specific questions are:

What type (relative vs absolute) of fitness is shown in a fitness landscape?
Does the type of fitness change if you change way to model it (For example, I want to know specifically for a quadratic model vs a spline)?
Does the type of fitness change if you change way to model it (For example, I want to know specifically for a quadratic model vs a spline)?
When using a mark recapture model (you use the survival of each individual to find a fitness function) is the survival estimated by the model relative or absolute? Does the mathematical formulation of the model changes something?

In the image below, I've graphed all the points (black line) and I've removed the 3 lowest values of y for the 3 largest x values (red line). If I was calculating the fitness of the individuals with or without the 3 smallest points for the 3 largest x values, then the fitness of all the other individuals would be affected (except at x~38 and y~38).

x = c(1:100,101,102,103)
y =  c(x[1:100]+rnorm(100, sd = 6), 50,60,30)

x = c(1:100,101,102,103)
y =  c(x+rnorm(103, sd = 6))

summary(lm(y~x))
plot(y~x)
abline(lm(y~x),col = "red")
points(38,38,col="blue")

Another example with crossbills:

Would you say it's relative or absolute fitness. Here the fitness measure is "performance" of eating certain types of seed.
In this article they are saying (Morrissey & Sakrejda 2013):

Regression analyses are central to characterization of the form and
  strength of natural selection in nature. Two common analyses that are
  currently used to characterize selection are (1) least squares–based
  approximation of the individual relative fitness surface for the
  purpose of obtaining quantitatively useful selection gradients, and
  (2) spline-based estimation of (absolute) fitness functions to obtain
  flexible inference of the shape of functions by which fitness and
  phenotype are related. These two sets of methodologies are often
  implemented in parallel to provide complementary inferences of the
  form of natural selection.

Are least squares-based approximation of the individual always computing relative fitness surfaces? For spline, is it always absolute values?

I put the 2 questions in bold. The rest is more of an explanation or avenue of research.

This graph is just an example of a linear regression. Both lines are identical, but the red one, I removed the 3 "outliers" at the far right. That way you see how the line shifts and how it affects the expected value on the left and the right of the $(38,38)$ point

From the website: [...]The potential benefits of specializing on a key conifer species, the diversity of key conifer cones, and the method that crossbills use to extract seeds from these cones, it is perhaps not surprising that crossbills have diversified into several forms, many of which appear to be more or less specialized for foraging on a single or a few key conifers. While the association between bill depth and cone size is pretty striking, there's more evidence inside each bill that some degree of specialization is occurring.

By experience, most of the time, authors are talking about relative fitness. To
confirm my feeling, I looked at the three randomly chosen theory papers from the first page of results that Google Scholar returned when searching for fitness landscape and they all use fitness as a relative measure. The papers are Derrida and Peliti (1991), Merz and Freisleben (2000) and Woodcock and Higgs (1995).
However, I do not think this is in the definition of a fitness landscape. One could work with absolute fitness and still call his model a fitness landscape. I think that therefore the answer is specific to every model considered. Note that even the "landscape axes" for which a fitness value is assigned can be of different nature. Typically, one can associate phenotypic or genotypic and/or even environmental axes.

In the three articles, only one was talking about relative fitness. I don't understand what do you mean by 'they all use fitness as a relative measure'. Is it relevant to determine the type of fitness if it was estimated from a model?

I considered their definition of the letter $w$, not whether they commented much on it. But it is not impossible that I'd made mistakes. Do you think two of them use absolute fitness? If yes, please tell me which one(s) and I can have a second look at it.


text:
What is the difference between absolute and relative fitness?
It's seems to me that the definition of relative and absolute fitness is not that clear.

Absolute fitness[edit]
The absolute fitness (W) of a genotype is defined as the proportional
  change in the abundance of that genotype over one generation
  attributable to selection. For example, if  ${\displaystyle n(t)}$ is
  the abundance of a genotype in generation t in an infinitely large
  population (so that there is no genetic drift), and neglecting the
  change in genotype abundances due to mutations, then[4]
  ${\displaystyle n(t+1)=Wn(t)}$. An absolute fitness larger than 1
  indicates growth in that genotype's abundance; an absolute fitness
  smaller than 1 indicates decline.
Relative fitness[edit]
Whereas absolute fitness determines changes in genotype abundance,
  relative fitness (w) determines changes in genotype frequency. If N(t)
  is the total population size in generation t, and the relevant
  genotype's frequency is ${\displaystyle p(t)=n(t)/N(t)}$, then
  ${\displaystyle p(t+1)={\frac {w}{\overline {w}}}p(t)}$, where
  ${\displaystyle {\overline {w}}}$ is the mean relative fitness in the
  population (again setting aside changes in frequency due to drift and
  mutation). Relative fitnesses only indicate the change in prevalence
  of different genotypes relative to each other, and so only their
  values relative to each other are important; relative fitnesses can be
  any nonnegative number, including 0. It is often convenient to choose
  one genotype as a reference and set its relative fitness to 1.
  Relative fitness is used in the standard Wright-Fisher and Moran
  models of population genetics.
Absolute fitnesses can be used to calculate relative fitness, since
  ${\displaystyle p(t+1)=n(t+1)/N(t+1)=(W/{\overline {W}})p(t)}$ (we
  have used the fact that ${\displaystyle N(t+1)={\overline {W}}N(t)}$,
  where  ${\displaystyle {\overline {W}}}$ is the mean absolute fitness
  in the population). This implies that ${\displaystyle w/{\overline {w}}=W/{\overline {W}}}$, or in other words, relative fitness is
  proportional to ${\displaystyle W/{\overline {W}}}$. It is not
  possible to calculate absolute fitnesses from relative fitnesses
  alone, since relative fitnesses contain no information about changes
  in overall population abundance

That's good when we are talking about genotypes or phenotypes. But
when we are using models, e.g. fitness landscapes, how can we
translate that? For example, if I have a linear fitness landscape
(made with a linear function), then the "fitness" value that I find
with the model are "expected fitness" or $\widehat y$. Thus in this
case, it's the "fitness of all possible phenotypes, based on the
population fitness and phenotypic information". Are we calling this
relative or absolute?
When fitness, or one of its components, is calculate from a model
(say a mark-recapture model), which type of fitness is computed? In
Marc Kéry and Michael Schaub (2012) Bayesian Population Analysis using WinBUGS: A Hierarchical Perspective, they are showing models
to compute survival probabilities based on a recapture history.
Would that be relative or not?
What are the distinction of the 2 definitions, and are they too restrictive when we want to extend them to models that calculates the fitness of a all the individuals in a population?

See also, Endler, J.A. (1986) Natural Selection in the Wild.
On page 168 of the book:

Mean absolute fitness: $\overline {W} = [∑ƒ(X)W(X) ]/[∑ƒ(X)]$
ƒ(X) frequency of genotype or phenotype X
Absolute fitness: $W(X)$
Relative fitness: $w(X)= W(X) /\overline {W}$
Therefor, $\overline {w}(X)=1$

Relative fitness can also be measured with reference to a particular phenotype (or genotype), in which cas $\overline {w}$ is not necessarily 1; this is the most common method used for polymorphic traits. If the population is sampled twice (or more) within a generation so that individuals in the second sample represent a subset of those sampled in the first sample (as in a capture-recapture or cohort study), then absolute fitnesses can be calculated. Examples are the probability of surviving between samples, or the probability of mating. On the other hand, if samples are made without replacement, or if samples are made of juveniles and adults at a single time, then only relative fitness can be calculaqted; information on total numbers and mean fitness is lost (see discussions in O'Donald 1971, Horns and Harrison 1970, and Manley 1974).)

On page 42 of the same book:

Adaptedness and Adaptation. Adaptedness is the degree to which an
  organism is able to live and reproduce in a given set of environments:
  the state of being adapted (Dobzhansky 1968a,b). Adaptation is the
  process of becoming adapted or more adapted (ibid.). Unfortunately,
  adaptation.is also used in the sense of an adaptive trait (Lewontin
  1978), confounding the end product with the process (see also Dunbar
  1982). An adaptive trait is "an aspect of the developmental pattern
  of the organism surviving and reproducing" (Dobzhansky 1956, 1968a).
  There are problems in defining precisely what adaptednedd is so that
  it can be measured (Dobzhansky 1956, 1968a,b; Stern 1970; Lewontin
  1978; Dunbar 1982). One solution is to define it in the sense of
  absolute (rather than relative) fitness (Table 2.1). In this case it
  can be measured by the average absolute lifetime contribution to the
  breeding population by a phenotype or a class of phenotypes. It thus
  becomes intimately related to the actual (R) or intrinsic $(r_{m})$
  rate of increase, or "Malthusian parameter," and these have actually been used as measures of fitness for populations and species, though there are some problems (Fisher 1930; Dobzhansky 1968a,b; Dunbar 1982). Adaptedness has also been defined as the mean absolute fitness (Sober 1984). [...]

Bonus: I'm trying to recreate the equation from Lande and Arnold 1983. But it's not working. I don't know what is not correct (the line where you see     (mean.rel.fit = mean(w.relative.fit)), this result should give 1, but it's not in my case. I don't know why):
# W: Absolute fitness
# w: relative fitness

set.seed(12)
nb.data = 5000
y = rnorm(nb.data,10,2)
x = 1:nb.data

# This should look normal
hist(y,
     breaks = 30)

# To have a mean of 0 for phenotypes scale the phenotypes
z.raw = y
z = scale(z.raw,
          center = TRUE,
          scale = TRUE)

hist(z,
     probability = TRUE, # In stead of frequency
     breaks = "FD",      # For more breaks than the default
     col = "grey", border = "black")
lines(density(z),   # Add the kernel density estimate (-.5 fix for the bins)
      col = "firebrick2", lwd = 3)

# Normally distributed trait, Phenotypic distribution (normal)
p.z =function(z) {
  z.mean=mean(z)
  sigma = sd(z)
  1/sqrt(2*pi) * exp((-1/2)*((z-z.mean)/sigma)^2)
}

# This is not working! It's suppose to be normal
hist(p.z(z),
     breaks = 30)
rnorm(nb.data,10,2)

# Linearly distributed absolute fitness function
W.z =function(z) {
  slope = 1
  intercept = 0
  e=(z*slope+intercept)
  (e-min(z))/(max(z)-min(z))
}

# There is a linear relationship between trait z and Absolute fitness W
plot(z,W.z(z))

de = density(z,
             n = 600000)
require(zoo)
# If n = 600000 in the density function, then it should ~=1
sum(diff(de$x[order(de$x)])*rollmean(de$y[order(de$x)],2))

duplicated(round(z,1))
df.z = as.data.frame(table(round(z,1)))
values = as.numeric(as.character(df.z$Var1))
frq = as.numeric(as.character(df.z$Freq))
frqcy = function(len){frq[1:len]}

f = function(values)(W.z(values)*frqcy(length(values)))
(mean.absolute.fitness = integrate(f,
                                   subdivisions = 2000,
                                   rel.tol = .Machine$double.eps^.05,
                                   lower = min(z),
                                   upper = max(z))
)

# Relative fitness
w.z <- function(z) {
  W.z(z)/mean.absolute.fitness$value
}
(w.relative.fit = w.z(z))

# This should be 1
(mean.rel.fit = mean(w.relative.fit))

w.relative.fit
f2 = function(z)(z*w.z(z)*p.z(z))

(mean.absolute.fitness = integrate(f2,
                                   lower = min(z),
                                   upper = max(z))
)

I'm not totally convinced in this post. The definition on Wikipedia changed. It is no longer "the ratio between the number of individuals with that genotype after selection to those before selection". Also, it seems there is a confusion with the fitness components and the measure of fitness when looking at relative vs absolute. In my mind, the absolute fitness can be larger than 1 for sure.

Relative fitness is "relative" so that it's supposed to be between 0 and 1. That's a ratio.

Exactly, so the relative fitness is based on the absolute fitness in which the most "fit" is used to bound the relative fitness between 0 and 1. It's not necessarily based on the most frequent (the most frequent genotype or phenotype is not necessarily the most fit...)


text:
Is natural selection a force?
I often hear that natural selection, or simply, selection is a "force".
e.g.:

the forces of directional selection on correlated life history
  characters, and an adaptive topography

Source: Lande, R. (1982). A quantitative genetic theory of life history evolution. Ecology, 63(3), 607–615.

because, as is becoming increasingly appreciated, long-term studies (>
  one year) are necessary to understand the selective forces affecting
  territoriality (e.g. see MacLean and Seastedt 1979).

Source: Millington, S. J., & Grant, P. R. (1983). Feeding ecology and territoriality of the Cactus Finch Geospiza scandens on Isla Daphne Major, Galápagos. Oecologia, 58(1), 76–83. http://doi.org/10.1007/BF00384545

See also this one:

Selection is a vector having intensity and direction.

Source: Simpson, G. G. 1944. Tempo and mode in evolution. Columbia University Press, New York.

But I've also heard that selection is not a force and that should be thought as a "process" taking the analogy of a chemical reaction.

Natural selection is, in a sense, a "force" that can "act" on gene
  frequencies or trait value distributions, and this is the most common
  sense in which "act" and "force" are used. But this is only a vague
  and most improper analogy with physics. [...] The use of "force" in describing natural selection is an instance of confusion between the change in an object and the changes in relationships among objects, and can also be an artifact of typological (class) thinking.

Source: Endler, J. A. (1986). Natural Selection in the Wild. Princeton University Press.

It also seems that the way we can calculate selection (using the famous Lande and Arnold 1983 paper), using a vector field, which can be thought as a field of forces. Is there a conclusion to this debate?
Is selection a process or a force?

I'm voting to close this question as off-topic because it is about linguistics, not biology.

If the debate was only about semantics and not biology, then we would reconsider the term "natural selection" which is not the purpose of this question. If you want to talk about the semantics, see Darwin's letter when he says that "I suppose natural selection was bad term; but to change it now, I think, would make confusion worse confounded. Nor can I think of better; Natural preservation would not imply a preservation of particular varieties & would seem a truism; & would not bring man's & nature's selection under one point of view." My point is a clarification on a biological concept.

You may think your point is about biology but the people who answered all discuss semantics. Like many questions about evolution it is unsuitable for SE Biology in that it doesn't have a real scientific answer, and the intension in posing the question is more to initiate a discussion than to answer a problem. Tests of concept. How will you decide which answer is correct? How will accepting an answer as correct alter your future research or thinking?

Artificial preferential selection of your clothes in the morning is not a force. the force is the weather. You need to read background texts. A force is not a selection. A force is a pressure and it has encourages selection.

The main difficulty in this question is to define the terms process and force. As such it is as much a question of linguistic than a biology question.
Process
merriam-webster list a number of definitions. Below each definition I am answering wether NS would fit this definition.

progress, advance

No, NS is not a progress

something going on

Well... I guess, yes!

a natural phenomenon marked by gradual changes that lead toward a particular result.

Yes!

a continuing natural or biological activity or function

Yes!

a series of actions or operations conducing to an end

Not sure, how action is defined here...

the whole course of proceedings in a legal action

Nope!

the summons, mandate, or writ used by a court to compel the appearance of the defendant in a legal action or compliance with its orders

Nope!

a prominent or projecting part of an organism or organic structure a bone process a nerve cell process

Nope!

conk

What?
Force
From dictionnary.com, a force can be defined as

physical power or strength possessed by a living being

Nope!

strength or power exerted upon an object; physical coercion

Nope!

strength; energy; power; intensity

Hum.... no!
In physics a force is typically defined as (from wiki)

[..] a force is any interaction that, when unopposed, will change the motion of an object.

Then, no!
Conclusion
Really it is all a matter of what you want to call a process or a force. We know how NS is defined. The rest of the work is pure terminology about what you like to call a process and a force. There is no debate here. There is only people using different definition and allowing themselves to use some terms with a loose definition.
Process
I am personally quite happy calling NS a process following certain of the above definitions.
Force
I am personally not 100% happy about calling NS a force because the term 'force' already has a definition in science under which NS is not a force. Many people call NS a force because it leads to a directional effect on allele frequency. If you vision, the allele frequency as a position and moving through allele frequencies a movement, then NS is a force acting on the object that is the allele frequency. However, this is just an analogy.
Note by the way that diffusion equations can be used to describe change in allele frequency due to genetic drift (diffusion term) and NS (drift term) just like they are used to describe movement of particles. Btw, the fact that genetic drift matches the diffusion term and NS matches the drift term in diffusion equation makes me think that "genetic drift" would better be named "genetic diffusion".

Interesting. I would also call natural selection a process that, in order to work, has to fill 4 main criteria. I find it funny that 99.9% of the articles in biology talking about selection, call it a "force". I'm not sure why people prefer this way to define natural selection.

I'm curious about the way you would write a sentence such as "selection is pushing the distribution" or "selection acts against" or anything similar to this. Basically, based on a definition of selection, what would be the preferred way of talking about it? Is selection described as a force since Lande and Arnorld's paper on selection gradients?


text:
Some sort of Lymantriidae caterpillar?
I found this larva in Sweden in July. It was about 15 mm long. It reminded me of Orgyia antiqua that I've seen before, but smaller and with a somewhat different colouration.

http://en.wikipedia.org/wiki/Lymantria_dispar_dispar

I think it's indeed a young, and possibly worn, specimen of Orgyia antiqua (also Rusty Tussock Moth or Vapourer, see also UKmoths). This species is relatively common in large parts of Sweden. However, the tufts and "tail" are usually more pronounced, but there is probably intra-species variation, and old, worn individuals can have sparser tufts. As you say, they are usually longer than 1.5cm but there is large variation, sexual dimorphism and younger larvae (early instars) are natually smaller.

(picture from wikipedia)
Swedish specimen:

( from http://krypinaturen.se/fjarilar-lepidoptera/nattfjarilar/tofsspinnare-lymantriidae/orgyia_antiqua_1878_20130626/)
Lymantria dispar is rather rare in Sweden and is only found in certain localities in the south (Blekinge, Småland coast) along with Öland and Gotland.

It's so hard when they don't look like perfect representatives of their species! But this sounds convincing enough. Thanks!

This caterpillar is known as Lymantria dispar dispar. Not to be confused with the Lymantria dispar, as the Lymantria dispar dispar is the classified as it's subspecies for the sake of further taxonomy. The Lymantria dispar dispar, is locale to Europe and North America (via migration), the latter being sourced in Asia. They only possess a minor (however it's deemed as rather significant in the animalia kingdom) difference - the female Asian Gypsy moth can fly!
In the contrary, The U. S. Department of Agriculture, defines the Asian Gypsy moth by means of flight capability partially ignoring location; "any biotype of Lymantria dispar possessing female flight capability". Which demonstrates the evident flair in confusion on this topic.
The difference in the moths visual appearance in comparison to the pictures of species you'd more commonly see (i.e. the color of its head), is possibly due to the stage of maturation of the Caterpillar or the present season. That's just my hypothesis though, i am unaware of any evidence to back that up.
Here are some further images:
http://www.papillon-poitou-charentes.org/Lymantria-dispar-Linnaeus-1758,4446.html
Reference to the facts:
https://en.wikipedia.org/wiki/Lymantria_dispar_dispar
(Edit: I was proved incorrect! However, this information would be useful for others who seek the answer!)

Are you sure? They don't look alike to me. :-/

I'm fairly certain... not all from the species look identical just like, zebras don't all have the same distribution of stripes. It's difficult to say with 100% certainty since, nothing looks exactly  same!  Sorry, if this sounds sloppy - I'm very tired :P

I think that's incorrect. The OP's caterpillar has dorsal tussocks on segments 4, 5, 6 and 12 (or abdominal segments 1, 2, 3, and 9.) Yours has none. That's a big mismatch. Note, I didn't find a match yet, either.

Also, do you have any idea why my answer on another health post is being classed as 'spam'? I followed the advice posted on getting past this issue but to no prevail?

I have absolutely no idea then... However, I'm 100% certain that it's from  the genus 'lymantria' - feel free to check through the 220 other species of that genus ;) I apologise for my mistake.

No apology necessary; this one is clearly out of my league as well. Regarding your "spam" answer, I can't see it (I'm not a mod on this site.) You can ask about it in meta, though.

So it was a harder question than I thought! Thanks for the input, anyway, I'll keep looking...


text:
Why would a horse-fly quickly dip into water?
For several years I have noticed a large horse-fly, flying very quickly down to the surface of my pond (in Sweden), touch the surface, and fly off. Sometimes it dips down a few times, taking some quick turns above the surface in between. Once, I caught it, and could see that it was a male of some Tabanus species.
(Since they are so quick, I haven't been able to tell if they are all male, but considering the size I believe they are all Tabanus sp.)
Now I want to know why they are doing it. It seems too quick for drinking water, and they shouldn't be feeding there. Could it be some sort of mating or territorial behaviour? I have only ever seen them one at a time, though. In sunny weather it seems to happen at least a few times per hour, all through the day.

Possibly to cool down if they get too hot? I seem to remember reading about this kind of behaviour in dragonflies; but am unable to locate the source.

@RHA interesting, i hadn't considered that at all! in that case it should go together with warm and sunny weather. another thing to keep track of...


text:
Meaning of "external demands" in a paper describing the gut-brain axis
From "Brain Gut Microbiome Interactions and Functional Bowel Disorders":

In response to external and bodily demands, the brain modulates individual cells (ECC – enterochromaffin cells; SMC – smooth muscle cells; ICC – interstitial cells of Cajal) within this network via the branches of the autonomic nervous system (ANS) (sympathetic and parasympathetic/vagal efferents) and the hypothalamic pituitary adrenal (HPA) axis.

What is the meaning of "external demands"? What other possible demands can the brain strive to meet by modulating the activity of the neural network of the gut?

From the context, it seems to refer to those demands outside of the human body. i.e. perceptions of the external world. Examples could include a perceived threat, diunal cycles, or stress about that public presentation you're giving later.
If you are about to be chased by a dangerous predator, a sudden urge to poop would probably impair your chances of survival. Luckily, when our sympathetic nervous system kicks in, our GI motility slows down, so our body can focus on surviving the external threat and live to poop another day.


text:
"Air sac" and "air cell" in a chicken embryo
I need to translate the Russian term "воздушный мешок". It is part of the chicken embryo, marked by number 5 in the figure below.

I found the expression air cell but also found the expression air sac in English. On one site, "air sac" is described as a synonym to the "allantoic sac":

Just to make sure: is air cell the only correct translation for the structure marked by number 5?
My sentence goes roughly like this:

...  the injections are made from the direction of the naturally-occuring air cell (?) so as to apply the material onto the chorioallantoic membrane (CAM).

air sac can also mean the air spaces created by outgrowth of the lung into the bones, which are part of the bird breathing mechanism. Air cell would this be less confusing.

According to Atlas of Chick Development by Ruth Bellairs and Mark Osmond, a book I'm using for my developmental biology course :

Air space  is the space between the two shell membranes at the blunt end of the egg. The chick pushes its beak into this space shortly before hatching and takes its first breathe of air.

Besides allantois is the extra embryonic membrane and the space enclosed by it is allantoic cavity.
Here label 2 is Allantoic cavity.

Thank you, Sanjukta! So "air cell" is also a miss, or it will be okay?

I can't assure you but from a google search the term air cell appears to be in use too.


text:
Do there exist T helper memory cells?
I'm translating a Russian text touching upon the IL-17 interleukin family, and it has a kind of typo in it. I'm not sure:

As mentioned above, IL-17 was found to be expressed at the highest levels by CD3+ Th17 cells. However, subsequent studies showed that it may be produced as well by stimulated CD8+ memory T cells, γδ T cells, Th memory cells (?) and NKT cells.

The Russian text says "Th memory", there is no "cells" there. It might be a typo.
I've read a little about T cells and became curious. Are there T helper memory cells, or does being a T helper cell exclude the possibility of being a memory cell as well?
P.S. The original Russian sentence is

Как уже было сказано выше, наибольшей экспрессией ИЛ-17 характеризуются CD4+ Th17 лимфоциты, однако последующие исследования установили, что стимулированные CD8+ Т-лимфоциты памяти, γδ Т-клетки, Th памяти и популяция NKT также способны к его продукции.

Relevant: https://www.ncbi.nlm.nih.gov/pubmed/18825747

Also relevant, and open-access: http://onlinelibrary.wiley.com/doi/10.1002/eji.201343751/full

Yes, T cells -- including T helper cells and cytotoxic T cells -- form memory cells.

CD4 memory T cells: what are they and what can they do?
Origins of CD4+ effector and central memory T cells
Immunological memory
Control of innate immunity by memory CD4 T cells


text:
What is "integrated spindle activity" in plain English?
From a research article:

To determine if a combination of spindle parameters allowed for a better group discrimination, integrated spindle activity (ISA) was calculated by integrating over time the amplitude of each detected spindle (and by dividing by non-REM sleep duration). We found that integrated spindle activity was markedly reduced in amplitude and number of detections during the first sleep episode in the schizophrenia group in relation to the comparison and depression groups (Figure 3A).

Is this ISA parameter calculated using integrals? I vaguely recall integrating functions in the university, but by now I've forgotten all - that was too long ago. And I don't know how one would "integrate" not functions (like we did in the university) but spindles. And what is the meaning of "over time"?
In short, I'm curious what this ISA parameter stands for. Is there a way to describe it in plain English?

Wouldn't this be subject to variance due to electrode impedance and inter-subject variability? It doesn't appear they normalize these measurements- unless I'm missing something>?

@LindseyCrown For the comparisons they are making it's probably fine to not normalize; in Fig 2A it looks like the spectra overall are comparable across groups. Inter-subject variability doesn't matter because that's the whole point of their comparisons: testing whether the differences between groups are large enough relative to inter-subject variability to not likely be from random chance.

Integrated spindle activity is just this paper's measure of the intensity of spindles. It isn't really a term of art, there is no defined thing "integrated spindle activity," it is just a description for their method of quantifying spindles, or in other words operationalizing their definition of spindle activity.
Spindles are brief bouts of (relatively) high-frequency oscillatory activity that occur occasionally during sleep - often they are called "sleep spindles."
Figure 1 of the paper you link shows their method for detecting and measuring these spindles.

Ferrarelli, F., Huber, R., Peterson, M. J., Massimini, M., Murphy, M., Riedner, B. A., ... & Tononi, G. (2007). Reduced sleep spindle activity in schizophrenia patients. American Journal of Psychiatry, 164(3), 483-492.
In summary, the top trace is a raw EEG trace. Spindles are present in this trace, but the authors want to quantify spindle activity in some way. By filtering between 12-15Hz, the spindles become more obvious (middle): they are the high-amplitude things bracketed by vertical lines.
On the bottom, they have rectified and smoothed the signal to approximate the amplitude of the spindles (that is, they aren't interested in the area under the curve in the middle plot, which has negative and positive going components, they just want a measure of the whole event).
They are defining the integrated spindle activity as the integral (i.e., the area under the curve, just like in calculus) of bouts of activity that exceed some threshold, indicated by the area shaded blue.
In summary, to answer your question, there isn't really a better or simpler English way to say "integrated spindle activity" without losing information for the reader - they are indeed referring to mathematical integration. You could say something like "total spindle activity" but then it is much less clear how exactly you are quantifying spindle activity. Probably the best plain English description of integration is the 'area under the curve' of a function or measurement, though this isn't a perfect mathematical description.
As someone who is familiar with general methods for analyzing electrophysiological data, it was pretty clear to me what they meant by "integrated spindle activity" before opening the paper - this is a fairly common way to report the amplitude of oscillatory activity, because it captures both average amplitude and duration in a sensible way.

A pretty good approximation is to say that they are summing the activity  of (rectified) spindle events, since we are talking about discrete signals.

And what is the meaning of "over time"?

This procedure presupposes that they have identified the beginning and end of a spindle event, hence the integration is done within that interval.
There are plenty of ways to calculate a discrete integral, for example by using Riemann sums or just taking the regular sum, but none of the details matter much for all practical purposes in signals such as those dealt with in the cited paper.


text:
Is there a taxon that "adaptively" radiates faster?
It seems that there are some taxa that have a greater potential to radiate through adaptations. Off my head, I can think of birds:

Darwin's finches
Hawaiian honeycreepers
House finches (Carpodacus mexicanus)
Manakin (or other passerine birds)

Also, there are some fish:

Cichlid fish (Lake Victoria in east Africa)
Threespine Stickelback

Plants:

Hawaiian silverswords
Erythranthe lewisii (Lewis' monkeyflower, great purple monkeyflower)

Lizard(s):

Anolis lizards

Insects:

Heliconius butterflies
Drosophila (Hawaiian Drosophila particularly)
Spider (Maybe peacock spider)
Leaf beetle

Generally:

Angiosperm plants
Dinosaurs
Marsupial mammals
etc.

So, is there a group of organisms (taxa could be any level: family, gender, species...) that is consistently radiating more than other?
By radiation I take the points that Grant defines here:

These examples have the following in common: (1) they comprise
  several to many species, (2) the species vary morphologically in
  conspicuous ways, and relatedly, (3) they occupy a diversity of
  ecological niches. Most of the species were (4) derived from a single
  ancestor in their current environment, and (5) most diverged
  relatively rapidly.

Threespine Stickelback and Brassica (and other domesticated species) are other examples.

Book recommendation: The Ecology of Adaptive Radiation by Schluter

Mammals have 2x times larger genomes than birds and lizards, and they radiate faster, which is why there are whales, moles, seals, bats. They have larger genomes partly because mammals have developed anucleated blood cells which are smaller and more flexible than birds, and if birds had very large genomes their blood cells would be less performent. Otherwise there could be burrowing and oceanic birds.

@com.prehens.ible I understand you did not write an answer but just a comment, but really I would need to see a reference stating that 'genome size is correlated with speciation rate and this correlation has to do with blood cells' to believe your comment.

@Remi.b do you think that domesticated species could be thought as adaptive radiation?

Beausoleil, Do you mean phenotype of breeds or species domestication? Remi,esesntially, birds have no choice about accumulating genes. they can't do it well because it clogs their capillaries: (iii) Estimates of speciation interval in mammals correlate positively with genome size. (iv) Genome reductions are inferred at the base of particular species radiations and genome expansions at the base of others. Not a single mammal has a smaller genome than a bird, i.e. a thimble sized vole's is larger than an emu's.

@M.Beausoleil Yes, sounds legitimate to me to not refuse the term to domesticated species. Franske et al. (2011) talk about adaptive radiation of cabbage.

@com.prehens.ible Oh.... sounds very interesting. Thank you. I managed to find a few reference on the subject (e.g. Kraaijeveld (2010)). I'll study this a little bit, sounds quite extraordinary. If you happen to have a reference for the idea that speciation rate is slow in brids than in mammals becuase of small genome size and genome size is smaller in birds than mammals because they have nucleated RBC, I'd be happy to have a look at it.

You are probably right Remi, We learned that there were many dormant genes that were shed if the genome became compact, except that was 20 years ago, today they talk mostly about gene repetitions. Anyways, birds could not radiate to whales because of the egg laying issues more than the chromosomes, else penguins perhaps could have made it to whale type ecologies.

The species from your list have some common traits:

Fast metabolism of themselves, food and fertilizers
sexual reproduction is more complex than crabs and coral
complex ecosystems and fast changing ecology
lots of ecological competition generally advanced compared to ferns, moss and crabs
More Possibility to travel through gene bottlenecks
recent in fossil history
prevalently small
possibility of population explosions
generalist and robust flexible habits and traits like tree nests, live birthing, flying, fangs, close inter-animal relations i.e. with bees,

If you study animals that have sedate speciation habits like platipus, they are limited in many of the common traits from that list.
The animal is therefore mostly dependent on it's ecosystem's stability, richness and opportunities, as well as the specie's own physical wealth, opportunism and stability. Those species have very complex and flexible ecology cycles working over them at a high rate. The rate of change of the ecology is also dictated by the other's organisms ability to radiate in record times, so today's species are in an arms race of the fastest rates of change in predator-prey-reproduction traits, with all the tools of the trade, i.e. fast movement, strong protection, freaky efficient cell-type mutations, locomotive, feeding, protective and spacial habits that by themselves can define the base of the most prevalent recent families.
Some species RNA is more susceptible to change and has to be be counterbalanced with different checks, it's to keep up with the arms race of competition in the complex ecology spaces of most of the planet.

You only need two things to radiate rapidly, fast reproduction and opportunity, many of the species mentioned changed rapidly becasue they had access to a wide open environment with little or no competition. They are also small quick reproducing, the faster you breed the faster you can change. A rodent can go through 60 generation in the time an elephant goes through one, that is 60 times as many changes that can occur. Small organisms tend to breed faster so in general small things evolve faster. This is believed to be part of the reason birds survived when other dinosaurs did not.
Another noted factor is generalists tend to survive change better than specialists which means they tend to get to radiate more, they are not necessarily radiating faster they just tend to survive whatever changes opens up niche space for more speciation. Specialists are more likely to go extinct, so generalists end up with more opportunity to radiate.
Now another important facet is preadaptations that can affect oppurtunity. For instance animals with hox genes have a big advantage in creating different body plans over ones without, like nematodes, but note this is only an advantage in this one facet of change, nematodes are arguable one of the most successful lineages ever, they just all have similar body plans. Some argue that having exons/introns helps by more dna to experiment with to get useful mutations, but right now this is just supposition.
Another example of a preadaptation is mammals could not radiate into large sizes until dinosaurs were not around, for instance it was easier for a large dinosaur to expand into large insectivore niche by changing diet than it was for insectivore mammals to evolve large size and all the adaptations to go with that. the dinosaur just had better preadaptations to fill the niche.


text:
Is survival probability the same thing as relative fitness?
I created a model where I calculate the survival probabilities from a Mark-recapture design.
I'm wondering if I can call the survival probabilities as "relative fitness".

Phenotype or genotype: $X$
  Absolute fitness: $W(X)$
  Relative fitness: $w(X)=\frac{W(X)}{\bar W}$

Since relative fitness is a ratio, I would have the tendency to say that it's the same thing as survival probability (keeping in mind that survival is only one component of fitness, so conceptually not exactly the same thing).
If I refer to this article, since I'm computing survival probabilities per individual, I would just need to call it "individual fitness".
It seems that "relative fitness" is more appropriate with a certain categorical phenotype: the relative fitness of tall vs short plants. If you have a continuous trait, how is the relative fitness interpreted?


text:
Do humans have chemosensors for nutrients or chemicals?
I'm reading about chemoreceptors on Wikipedia, and see that the typical ones are mentioned: taste, smell, CO₂.  I would like to learn more about the other kinds of chemoreceptors that humans may possess. I'm particularly interested if these can detect chemical compounds, or lack of thereof in food.
Here's an example:
Do omnivore mammals vary food preferences based on dietary needs?

There's "rapid recognition of Indispensible Amino Acid(IAA) depletion in the rat brain's IAA chemosensor, the anterior piriform cortex (APC)"

Reading the article above, it appears that at least rats and birds can develop aversion to food that does not contain indispensable amino acids. This is done through chemosensors in the brain. Do humans possess any similar chemosensors?
Thank you for your input!

The answer to this question would fill books. Take Pheromones, for example, this is a very complicated story by itself! Could you be a bit more specific in which particular field you're interested in?

I'm interested in digestion - are there any chemicals or chemical imbalances that can be detected in food?

Isn't our sense of smell basically from a large number of chemosensors in the nose? Am I missing something?

@Qubei You are right, it is the pattern of activation of 100+ olfactory receptors that provokes smell.

I vote to close this question. This would indeed require to write a book...

authors: Александр Пупкин


text:
Are there any culinary fruits that are not botanically fruits or accessory fruits?
Many culinary vegetables are botanically fruits. For example, the tomato, bittergourd and the cucumber are generally considered culinary vegetables, but they are botanically considered fruits.
Does the reverse also hold true, in that are there any plant parts that are considered fruits culinarily, but are botanically not considered fruits or accessory fruits?

I'm voting to close this question as off-topic because it's not about biology but about what chefs consider a fruit.

I think this would be better suited to [cooking.se] (though I'm not sure about that site's scope, you should check first). You're not really asking anything biological here, you're asking about misnomers that chefs might be using.

I'm afraid the question would be pointless on Seasoned Advice too, because our users don't know enough biology to be able to compare both categorization systems. From our point of view, you wouldn't be asking anything about cooking :( I won't close it outright if you ask it, but I don't know how it will be received by the community in terms of voting, close votes and, most importantly, providing answers.

I think there aren't any, with two tentative positive results. Of course, it is hard to prove a negative. But here are my arguments:

Logic. there is little reason for this to happen. A culinary fruit is supposed to be sweet, and plants tend to store sugars in their botanical fruits, not in other parts (although by this logic, there should be tuber-fruits too).
Source checking. I went through two books intended as comprehensive reference works in the kitchen, The professional chef and McGee On Food and Cooking. They don't list a (culinary) fruit which I could identify as a botanical non-fruit, with one contentious case. Note that On Food and cooking's chapter on vegetables is structured according to plant part, and it has a subchapter called "fruits used as vegetables" - but it does not have a chapter of "vegetables used as fruit" or similar.
Language. People tend to mix up the two categories of "culinary fruit" and "botanical fruit" until the difference is pointed out to them. While they don't follow the correct botanical definition of fruit, a plant part seems to have to check the "used by the plant for reproduction" check box to be called a fruit, to the point where many words related to "fruit" evoke a harvest-like image such as "to come to fruition", or also words for "barren" in many languages which literally translate to "without fruit", e.g. the German unfruchtbar. So even when a food fulfills the "plant part" and "sweet snack" criteria, it is not called a fruit if it's not (commonly perceived as) a seed container.

The contentious case coming from the books is rhubarb. The professional chef lists it as a fruit, while McGee calls it "a tart stand-in for fruit" in the vegetable chapter, and mentions it again in the fruit chapter, as "a vegetable that often masquerades as a fruit". Kitchen terminology is by no means standardized, so if you were to question random cooks about rhubarb categorization, I guess you'd get a mixture of "a fruit" , "a vegetable" and "I don't know" answers.
An idea I had while writing the answer: maybe you can count ginger. Ginger has many uses in the kitchen, but it is available as a candied snack, which is else only common for fruit. McGee lists it as a spice, although he explicitly speaks of "the dried spice" without giving a category for the fresh rhizome. I think most cooks won't dub ginger "a fruit" but would be willing to include candied ginger in a bowl of mixed candied fruit.
Some petals and leaves are also made into jams, which would support a fruit categorization. Nevertheless, I've never heard of them being referred to as fruits. Prominent examples are rose petals, violet petals and verbena leaves (although one could argue that preserving verbena produces a herb jelly, not a jam).
This answer encompasses Western cooking traditions. It is possible that other cuisines have a different view of what a "fruit" is - for example aloe is frequently used in sweet preparations, maybe the leaf flesh is eaten as fruit somewhere.
So in the end, it comes mostly to your willingness to stretch the definition of a culinary fruit. It is certainly not the case for the most commonly eaten fruits.


text:
What are haplotype blocks and what is the effect of hybridization on these?
In this PDF, there is a quick definition of haplotype blocks.

A haplotype block is a set of closely linked alleles/markers on a
  chromosome that, over evolutionary time, tend to be inherited
  together.

Also look at this definition:

We defined a haplotype block as a region over which a very small
  proportion (<5%) of comparisons among informative SNP pairs show
  strong evidence of historical recombination. [We allow for 5% because
  many forces other than recombination (both biological and artifactual)
  can disrupt haplotype patterns, such as recurrent mutation, gene
  conversion, or errors of genome assembly or genotyping.]

Although in the abstract they say:

haplotype blocks: sizable regions over which there is little evidence
  for historical recombination and within which only a few common
  haplotypes are observed.

But the first definition confuses me because it really looks like the definition of linkage disequilibrium:

linkage disequilibrium is the non-random association of alleles at
  different loci in a given population.

Which means that they are inherited together (non-randomly inherited).
The other definitions don't seem to agree in the same paper...
Just as a reminder a haplotype is: "The set of alleles found on a single sequence is referred to as a haplotype."
(Hahn, M. W. 2018. Molecular Population Genetics. Sinauer Associates, Incorporated, Sunderland, Massachusetts.)
So:

What are haplotypes blocks precisely and compared to LD? How to estimate haplotypes blocks?
Why is this an important concept (what is it informing us, why would want to study that specifically)?
What influences haplotypes blocks and how is it useful to get some information when doing genomic analysis (can we account for that)?

Here are 2 relevant resources on the subject:

Daly, M. J., J. D. Rioux, S. F. Schaffner, T. J. Hudson, and E. S.
Lander. 2001. High-resolution haplotype structure in the human
genome. Nature Genetics 29:229–232.
Patil, N., A. J. Berno, D. A.
Hinds, W. A. Barrett, J. M. Doshi, C. R. Hacker, C. R. Kautzer, D. H.
Lee, C. Marjoribanks, D. P. McDonough, B. T. N. Nguyen, M. C. Norris,
J. B. Sheehan, N. Shen, D. Stern, R. P. Stokowski, D. J. Thomas, M.
O. Trulson, K. R. Vyas, K. A. Frazer, S. P. A. Fodor, and D. R. Cox.   2001. Blocks of limited haplotype diversity revealed by high-resolution scanning of human chromosome 21. Science
294:1719–1723.


text:
Is it possible to calculate the evolutionary response to nonlinear selection gradient as a change in variance of phenotypes?
I often see the breeders equation written like this:
$R = h^2s = \frac{V_a}{V_z}s = V_a\beta$ or $\Delta \bar z  = G\beta$
But is it possible to get something like this:
$\Delta \sigma_z  = G\gamma$
In this case, it would be the change in variance of the population due to nonlinear selection.
Basically, it would me that the response of selection is a direct measurement of the change in $V_z$. So to come back to this equation: $R = \frac{V_a}{V_z}s$, it would mean that $\gamma$ is related to $V_z$ somehow. But is there a way to predict what would be the response?
Is it possible to also predict the total response of a non-linear selection gradient if there are multiple traits?
When one wants to calculate the total response to selection, it is needed to account for the correlated effect of selection on other traits (correlational selection):
$R_1 = V_{a,1} *z_1 +\text{COV}_{V_{a,12}} * z_2$
$R_2 = \text{COV}_{V_{a,21}} * z_1 +V_{a,2}* z_2$
In matrix form:
$
\begin{bmatrix}
    R_{1}    \\
    R_{2}
\end{bmatrix}
=
\begin{bmatrix}
    V_{a,1}       & \text{COV}_{V_{a,12}} \\
    \text{COV}_{V_{a,21}}       & V_{a,2}
\end{bmatrix}
* \begin{bmatrix}
    \beta_{1}    \\
    \beta_{2}
\end{bmatrix}
= \boldsymbol{R}=\boldsymbol{G} \boldsymbol{\beta} $
How would that be translated to non-linear selection?
EDIT:
I think this answer is here:
$\Delta \sigma_a^2 = \frac{\sigma_a^4}{2}(\gamma - \beta ^2 )$
But this equation predict a change in genetic additive variance not phenotypic variance. Would it be possible to simply take $h^2=\frac{V_a}{V_z}=\frac{\sigma_a^2}{\sigma_z^2}$ and get the change for phenotypic variance?
This could also represent an answer:
$\boldsymbol{G}^* -\boldsymbol{G}=\boldsymbol{G}(\boldsymbol{\gamma}-\boldsymbol{\beta}\boldsymbol{\beta}^T)\boldsymbol{G}$

By non-linear selection, do you mean cases where fitness of an individual is a non-linear function of its phenotype or do you mean cases where fitness of an individual depends upon the genetic diversity in the population?

That's what I mean:
$w = \alpha_0 + \beta X + \frac{1}{2}\gamma(X-\bar{X})^2+ \epsilon $
w: fitness, $\beta$ is the linear selection gradient and $\gamma$ is the nonlinear selection gradient. Like in Lande Arnold 1983.

Now, if you would predict the response of selection on the next generation of phenotypes, you can use the breeders equation as shown above. But what about the nonlinear selection gradient $\gamma$? Can we predict it?


text:
When doing crosses (Punnett square) with drosophila, how can you be *sure* your parents are *pure lines*?
In plants, when someone wants to confirm that the parents are pure lines (homozygous) for the alleles studied, the person can self pollinate the plant to make sure that the descendants are identical to the parental plant. (See How to confirm pure-breeding parents)
In drosophila, self-reproduction is not possible so how to make sure that the parental strains you are breeding are indeed homozygous for an allele (in an efficient way, I don't want to breed drosophila for 'a lot of successive generations')?
E.g., assuming N is dominant and n recessive, if I have a male (NN) and a female (NN), then the F_1 is all (NN). But, if it happens that I have females that are (Nn) then, all offspring will look like (phenotype) their parents (NN and Nn), but they will have different genotypes. To make sure that the parents are homozygous, should I also verify with the F_2 or the F_1 is good enough? In other words, what is the most efficient way to verify that the parents are indeed homozygous?
F2 of F1 (NN) cross from parents (NN) = (NN) (should I be doing a third cross to make sure?)
F2 of F1 (NN and Nn) cross from parents (NN and Nn) = (NN, Nn and nn) => some males (Nn) will mate with females (Nn) giving (NN, Nn and nn) thus confirming that I didn't start with pure lines.
Thus, it really seems to be a long process to find the homozygous parents in the first place as you never know in advance if you have homozygous parents when you breed them. You have to pick individuals that you think are homozygous and test them until all the offspring are identical to the parents no matter how long you do it. Is that correct?
Another point here would be to calculate the level of 'confidence' in which we have a pure line. Can we calculate that (and what would be the test to verify that)?

A very similar question that came up yesterday: https://biology.stackexchange.com/q/104329/59521

I looked at the answer and it says 'it is always risk that the population is not 100% pure'. My question therefore is how can we calculate our confidence in assuring that we generated a pure line? Basically, how many generations would be needed to be 'convinced' that we have a 'pure line'. Basically, how could I 'confirm' that I indeed have a pure line in an efficient way? Another answer was 'buy it from a supplier' but that is not the type of answer that I expect! I'm curious in knowing whether there is a systematic way for testing a pure line (with relative certainty) What is the standard?

One is usually acting on the assumption of random mating, which implies a sufficiently big population to avoid genetic drift - this includes such rare situations as you described (when all the males are NN, but an substantial part of females are Nn). As for the calculations - I suggest that you ask more specific questions, and show how you tried to do this calculation.

I added a simple calculation to the linked question. It is not exactly what you ask, but I hope it helps.


text:
What is allelic effect sizes and direction?
In a paper, Berkley, C. A., and C. Lexer. 2008. Admixture as the basis for genetic mapping. Trends in Ecology & Evolution 23:686–694, the definition of Genetic architecture is given. It says:

Genetic architecture: the number and genomic location of loci that
  contribute to variation in a trait, as well as the allelic effect
  sizes and direction, the genotypic effects (additivity and dominance)
  and the extent of epistatic interactions among loci.

What is the allelic effect sizes and direction?
I found that allelic effect sizes is the same thing as penetrance. But the direction?

These two concepts are different from penetrance.
Allelic effect size
An allelic effect size is the magnitude of the effect of an allele on a phenotype.
The detailed definition seems a little bit trickier than it sounds I think (and I would love confirmation by other users on what follows and or a reference). For example, a phenotypic trait might be influenced by 20 QTL. At one such QTL (say QTL8), you may observe two alleles in the population: QTL8_A and QTL8_B. The effect size is the absolute phenotypic difference between two individuals differing exclusively at QTL8. I suppose it is also possible to define an allelic effect size as the average difference between the phenotype of QTL8_A and QTL8_B over all possible genetic background (eventually weighted by the average frequency of each background in the population at a given instant). In the case of a QTL that contains more than two alleles, then the allelic effect size can be defined either between each pair of alleles or between one allele and the average effects of all the others. Strong epistasis make the whole thing more complicated if one wants to average over all possible genetic backgrounds.
Direction of an allelic effect
The direction of an allelic effect is the direction (add or subtract) that an allele has on a phenotype.
Talking about direction makes sense only in the absence of sign epistasis.

Do you have a reference that talks about this?

Nope! The term is often encountered but I am not I ever saw a nice and complete definition of it (although it probably exists). This is the reason why I am asking for confirmation from other users. Sorry, cannot do better!


text:
How to derive the Equilibrium value $\hat F$ equation
In population genetics, there is a relationship between $\hat F$ and $Nm$.
$\hat F=\frac{1}{1+4Nm}$
In population genetics textbook, (i.e. Hartl, D. L., and A. G. Clark. 2007. Principles of population genetics. Fourth edition. Sinauer Associates Incorporated, Sunderland, Massachusetts.) it reads that using the equation below:
$F_t= \bigg(\frac{1}{2N}\bigg)(1-m)^2+\bigg(1-\frac{1}{2N}\bigg)(1-m)^2F_{t-1}$

Set $\hat F = F_t = F_{t-1}$. After expanding the squared terms on the right-hand side, and assuming
  that $m$ is small enough and $N$ large enough, and that terms  in
  $m^2$ and $m/N$ can be ignored, some rearrangement leads to:
$\hat F=\frac{1}{1+4Nm}$

I tried redoing it algebraically, without success. So do you know how to get to "$\hat F=\frac{1}{1+4Nm}$"
$(1-m)^2 = 1-2m+m^2$
$F_t= \bigg(\frac{1}{2N}\bigg)(1-2m+m^2)+\bigg(1-\frac{1}{2N}\bigg)(1-2m+m^2)F_{t}$
$F_t-\bigg((1-2m+m^2)-\frac{(1-2m+m^2)}{2N}\bigg)F_{t}= \frac{(1-2m+m^2)}{2N}$
$F_t(1-(1-2m+m^2)-\frac{(1-2m+m^2)}{2N})= \frac{(1-2m+m^2)}{2N}$
$F_t(-2m+m^2-\frac{(1-2m+m^2)}{2N})= \frac{(1-2m+m^2)}{2N}$
$F_t(\frac{2N(-2m+m^2)}{2N}-\frac{(1-2m+m^2)}{2N})= \frac{(1-2m+m^2)}{2N}$
$F_t(\frac{2N(-2m+m^2)-(1-2m+m^2)}{2N})= \frac{(1-2m+m^2)}{2N}$
$F_t= \frac{(1-2m+m^2)}{2N} * (\frac{2N}{2N(-2m+m^2)-(1-2m+m^2)})$
$F_t= \frac{1-2m+m^2}{(-4Nm+2Nm^2)-1+2m-m^2}$
Then $m^2= 0$
$F_t= \frac{1-2m}{(-4Nm)-1+2m}$
$F_t= \frac{1}{(-4Nm)-1+2m} -\frac{2m}{(-4Nm)-1+2m}$
??
$F_t= \frac{1}{(-4Nm)-1+2m}$
Magic
$\hat F=\frac{1}{1+4Nm}$

Sign problem
When you go from
$F_t(1-(1-2m+m^2)-\frac{(1-2m+m^2)}{2N})$
to
$F_t(-2m+m^2-\frac{(1-2m+m^2)}{2N})$
You make a mistake in the sign. It should be
$F_t(2m-m^2-\frac{(1-2m+m^2)}{2N})$
Approximations
I will assume this error of sign propagate to inverse your end result. You hence should get
$F_t= \frac{1}{4Nm+1-2m} -\frac{2m}{(-4Nm)-1+2m}$
$\frac{2m}{4Nm+1+2m}$ is negligible compared to $\frac{1}{4Nm+1+2m}$, so you can indeed remove it. You get
$F_t= \frac{1}{4Nm+1-2m}$
Also, $2m$ is negligible compared to $4Nm$, so again you can remove it. You end up with
$F_t= \frac{1}{4Nm+1}$
Tadaa!

Yup! Good old sign problems. Thanks for the help.


text:
How to calculate relative fitness from absolute fitness with recapture data?
In Grant 1986, it says:

For this analysis the absolute fitness of an individual id scored as 0 if it disappeared and 1 if it survived, and these scores are then converted to relative fitness values by dividing them by the mean absolute fitness.

Grant, P. R. 1986. Ecology and Evolution of Darwin's Finches

If we have this dataset (for example):
   id x1 x2 x3 x4 x5
1   1  0  1  0  0  0
2   2  0  0  1  1  0
3   3  1  0  1  1  0
4   4  1  0  1  1  1
5   5  1  0  1  0  0
6   6  0  0  0  0  1

Imagine that id is a column of individuals and the rest (x#) are the absolute fitness. Then, how would you calculate the relative fitness? For an example, what would be the relative fitness between x3 and x4?
X1 is the first event of capture. I.e. I went on the field and capture birds for examples and noted who was there (0). I went on the field on X2, X3, etc. and noted which bird was there.

I don't fully understand the data set. Can you please explain what each column $x_n$ mean?

I edited the question

An individual cannot have more than one value of absolute fitness. I still don't fully understand the data. I don't understand how can an individual disapear at reappear. I suppose the data just say present/absent (or found/not found). I don't understand why knowing an individual is present at time $t_2$ give us as information about its fitness. Do you know or is it part of what is unclear to you too?

Let's say you're calculating the fitness of an individual from one year to another (say X3 to X4). ID 2 to 4 are surviving, but ID 5 is not. Than the absolute fitness for year x4 would be 1,1,1,0 (for ID 2 to 5). I wonder how to calculate a relative fitness. Like the citation basically.

Well for one thing each individual lived at least as long as the interval between first and last capture - e.g. although individual #5 was not captured at time point X2 you know it was alive then because it was captured both at X1 and X3. I don't see where fitness comes in to this - you can score relative lifespan but longevity is a poor proxy for fitness

OK, but if you refer to the citation, it is possible, right? How then it's possible to calculate relative fitness with absolute fitness in this fashion?

My guess would be that the capture-recapture analysis will give you an estimation of the survival rate (1/0) for each individual for each time point (taking non-observations into account), along with an average survival rate at each time step (often the purpose of a capture-recapture study). With this information, you can divide the absolute fitness at each time (survival, 1 or 0) by the average survival at that time point to obtain a measure of relative fitness. So for a timestep where few survived, rel fitness will be >1 (e.g. 1/0.2), and when all survive rel fitness will be 1 (1/1).

So the dataset is this:
  id   x3 x4
   2    1  1
   3    1  1
   4    1  1
   5    1  0

Lets assume that we caught the entire population so that we know that a 0 is really a dead organism (the estimate is proportional to lifetime fitness). Furthermore, there is no density-dependent selection and the generations are non overlapping.
The survival for next year would be the fitness value of all individual. So in year x4, the absolute fitness would be W = c(1,1,1,0). Then the mean absolute  fitness would be: W_bar = (1+1+1+0)/4 = 3/4. Then to get w, the relative fitness, you divide W by W_bar. w = c(4/3, 4/3, 4/3, 0). Therefor, if you calculate mean(W/W_bar), it should give you 1.
This is as in Endler, J. A. 1986. Natural Selection in the Wild. Princeton University Press, p. 168.

Not sure I get your question here, with your capture history you coulde estimate a survival for the populaiton. Therefore you could add covariable to your model like body mass and make a realtion between higher survival and bigger weight by example. A proxy of absolute fitness coulde be surviving until sexual maturity or something like that ... So what your question (objective )

To illustrate my comment:
   id x1 x2 x3 x4 x5 group
1   1  0  1  0  0  0   1
2   2  0  0  1  1  0   0
3   3  1  0  1  1  0   1
4   4  1  0  1  1  1   1
5   5  1  0  1  0  0   0
6   6  0  0  0  0  1   1

Lets say the 1 are the bird with dark wing and the zero the bird with white wing. So You can easily run a model in MARK or Rcapture (or others...) to estimate survival for each group.
Let's say you obtain a survival between X2 and X3  of 0.70 for the dark wing and of 0.85 for the white wings. Assuming that they have the same number of offspring, you can calculate the relative fitness for the white wing :
w(white)= 0.7/0.85 = 0.83

Is that what you want to do ?

Not exactly, I wanted to calculate relative fitness values, like the Grants. I mean, look at the citation in the yellow box. That's what I mean.

What's your fitness proxy ?

Survival, like what the Grants used.


text:
How are haplotype blocks different from genes?
According to Cardon et al. 2003, a haplotype block is

A discrete chromosome region of high linkage disequilibrium and low
  haplotype diversity. It is expected that all pairs of polymorphisms
  within a block will be in strong linkage disequilibrium, whereas other
  pairs will show much weaker association. Blocks are hypothesized to be
  regions of low recombination flanked by recombination hotspots.

It seems obvious that the parts of the genome that compose genes will have a somewhat similar behavior.
So what are the differences between haplotype blocks and genes? Are genes a kind of haplotype block?
Cardon, L. R., and G. R. Abecasis. 2003. Using haplotype blocks to map human complex trait loci. Trends in Genetics 19:135–140.

Haplotype blocks may cover more than just one gene.
While positions within a gene are also in high linkage disequilbrium (or well correlated) with each other, this phenomena of high LD may extend beyond the gene body and overlap with the next gene.  A good visual representation of this comes from Jeffreys et al. in the figure below:

Red means more LD, black means zero LD.  Each point in the heatmap is essentially a pairwise correlation between two points in the genome.  Therefore regions of red represent regions of high LD or haplotype blocks.  Going from left to right we can see that each gene appears to be in its own block of high LD.  However, the genes PSMB9 and TAP1 appear to be in the same block.  Other examples exist as well, a great source is this review.

OK! Cool! But in the end, is a gene a haplotype block? I guess there are cases where there are haplotype blocks that span many genes, but genes themselves seem to have the same characteristics of a haplotype block.

Yes genes could likely be considered haplotype blocks, although this distinction does not add any understanding about genes.  Perhaps similar to calling a square a rectangle, the distinction is true but rather redundant.